Association of obesity with recurrent stroke and cardiovascular events.

BACKGROUND AND PURPOSE: The relation between obesity and stroke recurrence is still under debate. In this study, we investigated whether initial obesity was associated with recurrent stroke and major cardiovascular events over a long period of time. MATERIALS AND METHODS: Five-years follow-up data of the Ege Stroke Registry for stroke recurrence and cardiovascular events related to obesity were analyzed. Data include age, gender, stroke severity, neuroimaging studies, cardiovascular risk factors. Within the inclusion period, all of the included patients were followed until censoring (10th of December 2011) or readmission because of recurrent stroke, cardiovascular event or death, whichever came first. The Kaplan-Meier method was used for survival analysis. Cox proportional hazard model was applied to identify predictors of stroke and all major vascular events. RESULTS: Of 9285 eligible patients for evaluation, 5158 (56%) were male and 3068 (33%) with a prior stroke were obese at baseline. Among 2198 patients with recurrent stroke, 843 (38%) had obesity while 2229 (62%) had no obesity (HR, 1.36; 95% CI, 1.23-1.50; P<0.001). Overall major vascular events (recurrent stroke, cardiovascular events, and death) occurred in 1464 obese patients (48%) and in 2182 non-obese patients (35%) (HR, 1.69; 95%CI, 1.55-1.84). Cox hazard model showed that being obese was associated with increased recurrent stroke risk compared with those without obesity (HR, 0.85; 95%CI, 0.76-0.94; P<0.001), being obese was not associated with cardiovascular events (HR, 1.09; 95%CI, 0.95-1.26; P=0.22). CONCLUSIONS: Our results showed that obesity is a significant risk factor for recurrent stroke, although obesity was not associated significantly with myocardial infarction and death after 5-years of first stroke. Further clinical goal-directed weight reduction outcome trials in this area will be critical to validate the most effective approaches and, ultimately, to guide policy is certainly needed.

Limb shaking transient ischemic attacks: A follow-up of 28 patients.

BACKGROUND: Limb shaking transient ischemic attack (LSTIA) is an uncommon picture of carotid-occlusive disease. The symptoms are a seizure like activity and misdiagnosed as partial motor seizures. We here present a series of patients in our registry who had limb-shaking activities and their long-term outcome after treatment of their disease. METHODS: A total of 28 patients with limb shaking symptoms were recruited among 798 patients with TIA in our stroke registry. Risk factors and etiology of LSTIA were examined within hospitalization. After the initiaition of treatment patients were followed for a median of 6months. RESULTS: Limb-shaking was observed mainly on the hand-arms (46%), and secondly on the legs (39%). We found five different DWI lesion patterns in patients with LSTIA, including unilateral or bilateral either cortical or borderzone ischemic hyperintensities. Carotid endarterectomy was performed in 9 (32%) patients and carotid angioplasty-stent (CAS) in 10 (36%), and after 6-months of follow-up none of the patients had LSTIA. Limb shaking continued only in a patient with chronic carotid occlusion who received only conservative treatment. CONCLUSIONS: Limb shaking TIA point to carotid artery disease in the majority of patients and vertebrobasilar artery disease in one third. Fast and timely treatment with either surgical or CAS eliminates the attacks and also reduce their risk of stroke.

Effect of ARMS2 gene polymorphism on intravitreal ranibizumab treatment for neovascular age-related macular degeneration.

Age-related macular degeneration (AMD) is a leading cause of blindness in developed countries. The ARMS2 gene has been found to be associated with AMD. Currently, intravitreal ranibizumab (IVR) treatment is one of the widely used treatments for neovascular AMD. The aim of this study was to investigate the association between the genotype of ARMS2 rs10490924 polymorphism and IVR treatment responsiveness in patients with neovascular AMD. The study included 39 patients with advanced neovascular AMD (patient group) and 250 healthy individuals with exome sequencing data (control group). The patient group was divided into three subgroups: GG (N = 10), TG (N = 14), and TT (N = 15). Before IVR treatment, all patients had intraretinal or subretinal fluid or both. They received three monthly IVR-injection treatments. One month after the third injection, the patients were evaluated as either "responders" or "non-responders" based on the presence or absence of intraretinal or subretinal fluid or both. The patient subgroups TG and TT had an 8.56- and 39-fold higher risk of AMD, respectively, than patient subgroup GG had. The allele frequency was 0.537 and 0.10 in the patient and control groups, respectively. Within the patient subgroup TT, there was a significant difference between the "responders" and "non-responders" (P = 0.025). In conclusion, in neovascular AMD patients undergoing IVR treatment, TT genotype tended to be a better predictor of good short-term treatment response, compared to the GG and TG genotypes. Further studies using confirmed genetic biomarkers for individualized optimal treatments are required.

No relationship between lipoprotein-associated phospholipase A2, proinflammatory cytokines, and neopterin in Alzheimer's disease.

OBJECTIVE: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a reported risk factor for dementia. However, the relationship between Alzheimer's disease (AD) and Lp-PLA2 is still debatable and, to the best of our knowledge, no study has evaluated the associations between levels of Lp-PLA2, proinflammatory cytokines, and neopterin in AD. METHODS: In total, 59 patients with AD and 38 non-demented individuals were included in the case-control study. Fasting serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), neopterin, and Lp-PLA2 were determined using ELISA. The associations between AD and each of the variables were analyzed by logistic regression. RESULTS: The median Lp-PLA2 levels in AD and controls were similar (P=0.29, not significant). Median serum neopterin and IL-6 levels were significantly higher in patients with AD than in controls (P=0.0001 and P=0.03, respectively). In regression analyses, median neopterin levels, a lower level of education, and female gender were significantly associated with AD when compared with controls (OR, 31.44, 95% CI 3.59-275.28, P=0.002; OR, 4.35, 95% CI 1.13-16.61, P=0.032; OR, 7.25, 95% CI 1.88-28.00, P=0.004, respectively). CONCLUSION: In contrast to previous evidence suggesting its role in dementia and AD, Lp-PLA2 enzyme levels were higher in the controls, and no relationship between Lp-PLA2 and either proinflammatory cytokines or neopterin was identified in AD. Elevated neopterin levels may be considered inflammatory markers of AD.

Multiple variant type thalamic infarcts: pure and combined types.

BACKGROUND AND PURPOSE: Variant topographic patterns of thalamic infarction with distinct manifestations have been classified into three territories: anteromedian, central, and posterolateral. The purpose of this study was to determine clinical, etiological, and radiological features of multiple variant thalamic infarcts. METHODS: We reviewed 8400 patients with a first clinical stroke included in the Ege Stroke Registry between 2000 and 2013. Among 80 patients with an acute multiple thalamic infarcts confirmed by MRI, we selected all patients with lesions outside the classical territories and studied their clinical, etiological, and radiological features. RESULTS: Among 8400 patients with first-ever stroke in our registry, 21 patients (26% of all multiple thalamic infarcts) showed infarction outside the classical territories, allowing us to delineate three variant distributions; (i) unilateral multiple variant infarcts [seven patients (9%) in the anteromedian, central, and posterolateral territories] presented with predominantly decreased vigilance (66% with right lesions, 75% with left lesions), cognitive impairment including amnesia (71%), aphasia (57%) in left-sided or bilateral lesions, and executive dysfunction (43%). The most frequent stroke mechanism was cardioembolism (43%). (ii) Bilateral multiple variant infarcts [five patients (6%)], with lesions on the variant territories of the thalamus, resulting in a variety of neurological and neuropsychological signs, consciousness disturbances (80%), sensory-motor deficits (80%). Cardioembolism (60%) was the most frequent etiology. (iii) Combined multiple variant and classical infarcts [nine patients (11%)], characterized by hemihypesthesia (89%) as the most frequent manifestation, followed by hemiataxia (78%), and cognitive deficits. Cardioembolism (56%) and large-artery disease of the vertebrobasilar system (33%) were the main stroke mechanisms. CONCLUSIONS: We described multiple variant topographic patterns of thalamic infarction with distinct manifestations and etiologies. We thought that multiple variant infarcts are the result of variation in thalamic arterial supply or reflect a source of embolism.

Association of uric acid and carotid artery disease in patients with ischemic stroke.

BACKGROUND AND PURPOSE: Some previous studies reported an independent association between uric acid and coronary artery disease, while little is known on the association among uric acid and carotid artery disease (CAD). To address this issue, we investigated the association between CAD and higher uric acid level because of the well-known importance of the carotid artery pathologies for ischemic stroke. METHODS: Between 2009 and 2012, we conducted a study among 406 consecutive first-ever ischemic stroke patients to assess the relationship between uric acid and carotid artery. A mean intima-media thickness IMT was calculated for the wall of the left and right common carotid arteries (CCA) and IMT of the bifurcation of the carotid arteries. CAD was assessed by neuroimaging techniques in patients with carotid artery stenosis more than 50%. Logistic regression models were used to determine the relation among pathological changes of the carotid artery and higher uric acid level. RESULTS: In patients with hyperuricemia, the frequency of age (>60 years), hypertriglyceridemia, higher apo B, renal failure were significantly higher than those with normal uric acid level. CAD was more frequent in patients with hyperuricemia than those with normal uric acid level (OR, 1.8, 95% CI, 1.1-3.1; P = 0.01). In patients with higher uric acid level, the mean of the IMT of the CCA and of the bifurcation of the carotid artery were higher than those with normal uric acid level (P = 0.001 for each). Covariance matrix analysis displayed a strong correlation between CAD and age (>60 years) (P < 0.05), sex (P < 0.01), hyperuricemia (P < 0.01), hypertension (P < 0.05), and hypercholesterolemia (P < 0.05). In the models of regression analysis, a strong association was found among patients with CAD and sex, renal failure, hyperuricemia, number of plaques, and size of plaques. CONCLUSION: Our study demonstrated that higher uric acid level is strongly associated with CAD. Elevated uric acid might be injurious for large cerebral arteries with some probable confounding risk factors. Further prospective large clinical trials will determine whether lowering uric acid level reduces the frequency of CAD and ischemic stroke.

The clinical spectrum of intracerebral hematoma, hemorrhagic infarct, non-hemorrhagic infarct, and non-lesional venous stroke in patients with cerebral sinus-venous thrombosis.

BACKGROUND AND PURPOSE: The clinical spectrum of different neuroradiological features of cerebral sinus-venous thrombosis (CSVT) varies considerably. We sought the relationship between different neuroradiological aspects and clinical presentations in these patients. METHODS: The diagnosis of cerebral sinus-venous thrombosis has been confirmed by conventional angiography, MRI combined with MR venography following established diagnostic criteria. We analyzed clinical data, symptoms and signs, imaging findings, location and extent of the thrombus, and parenchymal lesions, retrospectively. RESULTS: There were 220 consecutive patients with cerebral sinus-venous thrombosis; 98 (45%) had non-lesional sinus-venous thrombosis (NL CSVT), 51 (23%) had non-hemorrhagic infarct (NHI), 45 (20%) had hemorrhagic infarct (HI), and 26 (12%) had intracerebral hemorrhage (ICH). In patients with hemorrhagic lesion (HI+ICH), advanced age, headache (99%), behavioral disturbances (55%), consciousness disturbances (35%), seizures (41%), and language deficits (42%) were significantly higher than the other patients (NL+NHI) (P < 0.001). High blood pressure at admission, puerperium, sigmoid and straight sinus thrombosis, multiple sinus and vein involvement were more frequent in patients with hemorrhagic lesion than those with non-hemorrhagic lesion. Patients with hemorrhagic lesion were more dependent or died (32%) than the other patients (12%) (P < 0.001), and most of the patients with NL and NHI had no disability compared with the other patients at the 3 month of follow-up (96% and 65%; P < 0.001). CONCLUSION: Headache, convulsion, behavioral disorder, seizures, and speech disorders were the most frequent clinical symptoms of patients with hemorrhagic CSVT. Specific risk factors, including pregnancy/puerberium, early and extended thrombosis of large sinus, and presence of high blood pressure at admission, are associated with hemorrhagic lesion and unfavorable outcome.

Assessment of myocardial ischaemia using tissue Doppler imaging in pseudoexfoliation syndrome.

PURPOSE: Pseudoexfoliation (PEX) syndrome is characterized by the widespread deposition of abnormal extracellular fibrillary material on many ocular and extraocular tissues. We aimed to investigate the association between PEX syndrome and subclinical myocardial ischaemia, using tissue Doppler echocardiography. METHODS: Thirty-two patients with pseudoexfoliation syndrome (mean age: 66±9 years, 22 men) and 25 healthy individuals (mean age: 67±8 years, 13 men) were included in the study. Patients with overt coronary artery disease, congestive heart failure, valvular heart disease, cardiomyopathy, and left ventricular hypertrophy were excluded from the study. Tissue Doppler imaging was performed at the septal, lateral, anterior, and inferior mitral annuluses. Differences between the groups were evaluated by the unpaired t-test and the Mann-Whitney U-test, with a P-value of <0.05 considered significant. RESULTS: Baseline clinical characteristics, two-dimensional, and Doppler echocardiography parameters were similar in the PEX and control groups. Peak systolic velocities at the septal, lateral, anterior, and inferior annuluses were significantly lower in patients with PEX syndrome (P<0.001, 0.01, 0.02, and 0.02, respectively). The early diastolic velocity at the septal annulus, and the ratio of early/late diastolic velocity at the lateral annulus were significantly lower in the study group (P=0.03). CONCLUSION: PEX syndrome is a common disorder of extracellular matrix. Our data suggest that there may also be an association between PEX syndrome and subclinical myocardial ischaemia in patients who have no signs and symptoms of ischaemia. Thus, we think that ophthalmologists should consider informing their PEX syndrome patients' general practitioners about a possible cardiac risk.

Spinal ischaemic stroke: clinical and radiological findings and short-term outcome.

BACKGROUND AND PURPOSE: The mechanism and pathogenesis of ischemic spinal stroke remain largely undetermined because most clinical studies have included mostly patients without a systematic study of associated vascular and concomitant disease of the vertebral body. Therefore, we assessed the pathogenetic mechanisms and short-term outcomes of the patients with spinal stroke based on clinical data and magnetic resonance imaging findings. METHODS: We studied clinical, imaging, and outcome data for 36 patients with acute spinal stroke admitted between 1998 and 2008. There were 16 men and 20 women (mean age 73, range 56-85 years). RESULTS: Twelve patients (33%) had anterior spinal artery patterns, 8 (22%) had anterior and 6 (17%) had posterior unilateral infarct, 5 (14%) had posterior spinal artery infarct pattern, 3 (8%) had central involvement, and 2 (5%) had transverse syndrome. Twelve patients (33%) had no cause of stroke. Patients with central infarct and transverse infarct had a high frequency of peripheral vascular disease and prolonged hypotension, and one patient each had a chronic spinal disease. The onset of all other infarcts was associated with mechanical triggering movements in 12 patients (41%, P<0.05), and with diseases of the spine in 19 (66%; P<0.001), with the clinical picture suggesting root involvement at the level of the spinal cord ischemia. The short-term outcomes were favorable in two-thirds of patients, while 25% of them did not show any recovery on leaving the hospital. CONCLUSION: The most common type of spinal cord ischemia is bilateral or unilateral anterior spinal artery infarcts due to radicular artery disease with acute or chronic spinal disease and followed by central and transverse infarcts due to extensive spinal cord hypoperfusion and arteriopathy.

Cerebral cortical and deep venous thrombosis without sinus thrombosis: clinical MRI correlates.

BACKGROUND: Cortical and/or deep vein thrombosis (CDVT) without dural sinus involvement is uncommon and presents diagnostic difficulty for many reasons. Our aim is to determine the relationship between magnetic resonance imaging (MRI) findings and clinical findings in patients with CDVT. METHODS: Forty-six patients with venous stroke proved on MRI included in our Registry, corresponding to 0.1% of 4650 patients with stroke, were studied. Magnetic resonance angiography (MRA) was performed in all patients, and 18 of them had follow-up MRA. Outcome was evaluated by using the Glasgow Outcome Scale at the time of discharge and during follow-up. RESULTS: Thirty-two patients presented cortical venous stroke; 21 of them had involvement of the dorsomedial venous system, six had a defect in the posteroinferior venous group, and five had a defect in the anteroinferior venous group. Thirteen patients presented simultaneous involvement of the superficial and deep venous system; seven with a defect in the parietal and internal cerebral veins (three with involvement of vein of Gallen), four with a defect in the temporooccipital (vein of Labbé) and basal vein of Rosenthal, two with a deficit in the anterior frontotemporal and uncal-pterygoid venous system. One patient had deep venous thrombosis primarily localized to the thalami bilaterally and the basal ganglia on the right because of occlusion of the thalamostriate veins. The main presenting symptoms of CDVT were headache, focal neurologic signs, partial complex or secondary generalized seizures, and consciousness disturbances in those with deep venous thrombosis, presented alone or in combination at onset. CDVT was more than twofold more frequent in women than in men. Pregnancy, puerperium, oral contraceptive use, and infections were the most common predisposing factors. CONCLUSION: Computerized tomography, conventional MRI and diffusion-weighted imaging showing ischemic and/or hemorrhagic lesion that does not follow the boundary of classical arterial boundaries without signs of sinus thrombosis, and partial or generalized seizures followed by focal neurologic signs may predict CDVT. The outcome of patients with cortical venous stroke was good, but not in those with cortical plus deep venous infarction.

Lesion patterns and etiology of ischemia in the anterior inferior cerebellar artery territory involvement: a clinical - diffusion weighted - MRI study.

The topography and mechanism of stroke in the anterior inferior cerebellar artery (AICA) territory are delineated before, but the detailed clinical spectrum of lesions involving AICA territory was not studied by diffusion weighted imaging (DWI). We reviewed 1350 patients with posterior circulation ischemic stroke in our registry. We included patients if the diagnosis of AICA territory involvement was confirmed, and DWI, and magnetic resonance angiography were obtained in the 3 days of symptoms onset. The potential feeding arteries of the AICA territory were evaluated on magnetic resonance imaging (MRI) using a three-dimensional rotating cineoangiographic method. There were 23 consecutive patients with lesion involving AICA territory, six with isolated lesion in the AICA territory, six with posterior inferior cerebellar artery, 11 with multiple posterior circulation infarcts (MPCIs). The clinical feature of isolated AICA infarct was vertigo, tinnitus, dysmetria, ataxia, facial weakness, facial sensory deficits, lateral gaze palsy, and sensory-motor deficits in patients with pontine involvement. Patients with largest lesion extending to the anterior and inferolateral cerebellum showed mixed symptomatology of the lateral medullary (Wallenberg's syndrome) and AICA territory involvement. Patients with MPCIs presented various clinical pictures with consciousness disturbances and diverse clinical signs because of involvement of different anatomical structures. Large-artery atherosclerotic disease in the vertebrobasilar system was the main cause of stroke in 12 (52%) patients, cardioembolism (CE) in one (4%), and coexisting large-artery disease and a source of CE in four (17%). The main cause of stroke was atheromatous vertebrobasilar artery disease either in the distal vertebral or proximal basilar artery. The outcome was usually good except those with multiple lesions. The new MRI techniques and clinical correlations allow better definition of the diverse topographical and etiological spectrum of AICA territory involvement and associated infarcts which was previously based on pathological and conventional MRI studies.

The mechanism of ischemic stroke in patients with dolichoectatic basilar artery.

Basilar artery dolichoectesia (BD) may cause brainstem ischemia by multiple mechanisms, including thrombosis, embolism, occlusion of deep penetrating arteries. The objective of this study was to determine and characterize clinical, imaging findings and hemodynamic mechanisms in patients with cerebrovascular event associated with BD and compare these data with those for patients with BD who did not have stroke. We studied 29 consecutive stroke, two transient ischemic attack (TIA) patients with BD who have been admitted to our stroke unit. We sought the diameter of ectasia, height of the bifurcation, lateral displacement, shape deformities, and blood flow velocity of the basilar artery (BA) by transcranial Doppler. Imaging and hemodynamic findings were compared with those found in a group of 18 patients without stroke or TIA. The main infarct localization was pons, eight (28%) with restricted single lesion, 10 (32%) with multiple lesions involving thalamus, midbrain, posterior cerebral artery (PCA) territory. Patients with BD were more probably to have had stroke fitting a clinical and imaging patterns of multiple infarcts than those with restricted infarct in territories supplied by branches of the BA (60% vs. 40%). Hypertension and atherosclerotic changes of the posterior circulation were more frequent in patients with stroke than those without (P = 0.004 and P = 0.028, respectively), whilst the incidence of other vascular risk factors were not significantly different in two groups. Patients with stroke/TIA had more often low blood flow velocity but not significant in the BA when compared with those for BD patients without cerebrovascular event (71% vs. 39%; P = 0.1). Reduced blood flow velocity in the BA was correlated significantly with distal lesions involving thalamus, midbrain and PCA territory rather than those located in the territory supplied by branches of the BA (P = 0.02). In conclusion, it seems probably that BD may cause vertebrobasilar system ischemia by multiple mechanisms, especially reduced blood flow in the BA and atheromatous changes in the vertebrobasilar system may precipitate thromboembolic stroke.

Diffusion-weighted and conventional MR imaging in neurotrichinosis.

Central nervous system involvement in trichinosis is not rare. Brain lesions in trichinosis have been defined on computed tomography and magnetic resonance imaging (MRI) as multifocal small lesions located in the cerebral cortex and white matter. We present a case of trichinosis with multifocal lesions of the brain detected by MRI and diffusion weighted MRI. Evolutions of these lesions from acute through chronic stages on follow up studies are also presented. This is the first report describing sequential MRI findings and diffusion weighted imaging appearance of brain lesions in trichinosis. Sequential evaluation of conventional and diffusion MR data allowed us to conclude that multifocal lesions in the brain were related to multiple infarctions rather than true inflammatory infiltration of the brain parenchyma.

Spectrum of superficial posterior cerebral artery territory infarcts.

Posterior cerebral artery (PCA) territory infarction is not uncommon. Published series were concentrated either on isolated deep PCA territory infarcts or on incomplete calcarine artery territory infarcts. Although, correlations between clinical symptoms, causes of stroke and outcome at 6-months in patients with superficial PCA territory stroke are less well known. We sought prospectively stroke causes, infarct topography, and clinical findings of 137 patients with superficial PCA territory infarcts with or without mesencephalic/thalamic involvement, representing 11% of patients with posterior circulation ischemic stroke in our Stroke Registry. We analyzed patients by subdividing into three subgroups; (1). cortical infarct (CI) group; (2). cortical and deep infarcts (CDI) (thalamic and/or mesencephalic involvement) group; (3). bilateral infarcts (BI) group. We studied the outcomes of patients at 6-month regarding clinical findings, risk factors and vascular mechanisms by means of comprehensive vascular and cardiac studies. Seventy-one patients (52%) had cortical (CI) PCA infarct, 52 patients (38%) had CDI, and 14 patients (10%) had bilateral PCA infarct (BI). In the CDI group, unilateral thalamus was involved in 38 patients (73%) and unilateral mesencephalic involvement was present in 27% of patients. The presumed causes of infarction were intrinsic PCA disease in 33 patients (26%), proximal large-artery disease (PLAD) in 33 (24%), cardioembolism in 23 (17%), co-existence of PLAD and cardioembolism in 7 (5%), vertebral or basilar artery dissection in 8 (6%), and coagulopathy in 2. The death rate was 7% in our series and stroke recurrence was 16% during 6-month follow-up period. Features of the stroke that was associated with significant increased risk of poor outcome included, consciousness disturbances at stroke onset (RR, 66.6; 95% CI, 8.6-515.5), mesencephalic and/or thalamic involvement (RR, 3.79; 95% CI, 1.49-9.65), PLAD (RR, 2.71; 95% CI, 1.09-6.73), and basilar artery disease (RR, 5.94; 95% CI, 1.73-20.47). The infarct mechanisms in three different types of superficial PCA territory stroke were quite similar, but cardioembolism was found more frequent in those with cortical PCA territory infarction. Although, the cause of stroke could not reliably dictate the infarct topography and clinical features. Visual field defect was the main clinical symptom in all groups, but sensorial, motor and neuropsychological deficits occurred mostly in those with CDI. Outcome is good in general, although patients having PLAD and basilar artery disease had more risk of stroke recurrence and poor outcome rather than those with intrinsic PCA disease.

Spectrum of anterior cerebral artery territory infarction: clinical and MRI findings.

To evaluate and review the clinical spectrum of anterior cerebral artery (ACA) territory infarction, we studied 48 consecutive patients who admitted to our stroke unit over a 6-year period. We performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) in all patients, and diffusion magnetic resonance imaging (DWI) in 21. In our stroke registry, patients with ACA infarction represented 1.3% of 3705 patients with ischemic stroke. The main risk factors of ACA infarcts was hypertension in 58% of patients, diabetes mellitus in 29%, hypercholesterolemia in 25%, cigarette smoking in 19%, atrial fibrillation in 19%, and myocardial infarct in 6%. Presumed causes of ACA infarct were large-artery disease and cardioembolism in 13 patients each, small-artery disease (SAD) in the territory of Heubner's artery in two and atherosclerosis of large-arteries (<50% stenosis) in 16. On clinico-radiologic analysis there were three main clinical patterns depending on lesion side; left-side infarction (30 patients) consisting of mutism, transcortical motor aphasia, and hemiparesis with lower limb predominance; right side infarction (16 patients) accompanied by acute confusional state, motor hemineglect and hemiparesis; bilateral infarction (two patients) presented with akinetic mutism, severe sphincter dysfunction, and dependent functional outcome. Our findings suggest that clinical and etiologic spectrum of ACA infarction may present similar features as that of middle cerebral artery infarction, but frontal dysfunctions and callosal syndromes can help to make a clinical differential diagnosis. Moreover, at the early phase of stroke, DWI is useful imaging method to locate and delineate the boundary of lesion in the territory of ACA.

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.

Neurologic complications after deep hypothermic circulatory arrest: types, predictors, and timing.

To determine the nature of neurologic dysfunction after deep hypothermic circulatory arrest during aortic arch surgery, we reconsidered the cases of 154 patients who had undergone aortic arch surgery (either of the ascending or transverse aorta, or both) between November 1993 and July 1999. Temporary postoperative neurologic dysfunction was seen in 9 patients (5.8%), and another 3 patients (1.9%) experienced stroke. Patients with temporary neurologic dysfunction had no new infarct and were discharged home with no residual symptoms. Computed tomographic scans revealed that 2 patients with stroke had multiple infarcts in the brainstem, and the 3rd had bilateral border-zone infarcts. The patients with brainstem infarcts died on postoperative days 7 and 15, and the patient with border-zone infarct was discharged home with no symptoms 3 months after surgery. Univariate analysis revealed that patients with neurologic deficits had significantly higher rates of history of hypertension, concomitant coronary artery bypass grafting, cardiac ischemia times longer than 90 minutes, and chronic renal failure. A multivariate logistic regression analysis revealed that the significant preoperative variables associated with neurologic deficits were a history of hypertension and a cardiac ischemia time longer than 90 minutes. Deep hypothermic circulatory arrest is a safe and useful technique for protection of the brain during surgery for complex aortic problems. In future, some patients at extreme risk for perioperative neurologic complications might be offered novel neuroprotective agents, in combination with deep hypothermia.

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.