Reversible Cerebral Vasoconstriction Syndrome After Heart Transplantation: A Case Report.

BACKGROUND: Reversible cerebral vasoconstriction syndrome (RCVS) is a transient cerebrovascular disorder putatively caused by some immunosuppressive agents. CASE REPORT: We recently encountered a 47-year-old female patient diagnosed with dilated cardiomyopathy who developed RCVS after heart transplantation. A triple-drug regimen consisting of tacrolimus, mycophenolate mofetil, and a corticosteroid was started after surgery. On postoperative day (POD) 11, the patient developed a severe headache, although computed tomography of the head demonstrated no signs of hemorrhage or infarction. At first, both a painkiller and migraine drugs were regularly administered to the patient. On POD 21, however, she developed an unbearable headache with a visual field defect and mild hemiparesis of the right hand. Magnetic resonance imaging (MRI) of the brain revealed a cerebral infarction in the left occipital lobe with diffuse vasoconstriction of both the middle and posterior cerebral arteries. A diagnosis of RCVS was made and tacrolimus, a drug suspected to cause RCVS, was discontinued. In its place, two doses of basiliximab followed by everolimus, both of which are alternatives for tacrolimus, were given. The corticosteroid dose was also increased. Furthermore, to release vasoconstriction, both verapamil and diltiazem were administered. On POD 27, cerebrovascular constrictions were shown to be relieved on brain MRI and the patient's neurological symptoms subsequently almost completely diminished. CONCLUSION: RCVS should always be considered as a cause of headache in heart transplant recipients because tacrolimus, an immunosuppressive agent, may trigger RCVS. This will allow rapid intervention that is essential for avoiding irreversible neurological deficits.

Baseline NIH Stroke Scale Score predicting outcome in anterior and posterior circulation strokes.

OBJECTIVE: The NIH Stroke Scale (NIHSS) may not appropriately assess the spectrum of posterior circulation (PC)-related neurologic deficits. We determined the cutoff baseline NIHSS score that predicts independent daily life activity during the chronic stage in anterior circulation (AC) vs PC ischemic strokes. METHODS: A total of 310 consecutive patients hospitalized within 3 days after the onset of an ischemic stroke were prospectively enrolled in the study. Patients on thrombolytic therapy were excluded. In all patients, infarcts and vascular lesions were identified primarily using magnetic resonance techniques. A favorable outcome was defined as a modified Rankin Scale score of < or =2 at 3 months poststroke. RESULTS: In 101 patients with PC stroke, the total baseline NIHSS score was lower (p < 0.001), and the subscores of ataxia (p < 0.001) and visual fields (p = 0.043) were higher than in 209 patients with AC stroke. Multivariate-adjusted OR for the favorable outcome in patients with PC vs AC stroke was 2.339 (95% CI 1.331-4.109, p = 0.003). A low baseline NIHSS score was independently predictive of a favorable outcome in both patients with PC (OR 1.547, 95% CI 1.232-1.941) and AC (1.279, 1.188-1.376) stroke. The optimal cutoff scores of the baseline NIHSS for the favorable outcome were < or =5 for patients with PC stroke (sensitivity, 84%; specificity, 81%) and < or =8 for patients with AC stroke (sensitivity, 80%; specificity, 82%). CONCLUSIONS: The cutoff score of the baseline NIH Stroke Scale (NIHSS) for a favorable chronic outcome was relatively low in patients with PC stroke compared to patients with AC stroke. The NIHSS appears to have limitations with respect to its use when comparing the neurologic severity of PC and AC stroke.

Serial changes in cerebral blood flow and flow-metabolism uncoupling in primates with acute thromboembolic stroke.

The authors recently developed a primate thromboembolic stroke model. To characterize the primate model, the authors determined serial changes in cerebral blood flow (CBF) and the relation between CBF and cerebral metabolic rate of glucose (CMRglc) using high-resolution positron emission tomography. Thromboembolic stroke was produced in male cynomolgus monkeys (n = 4). Acute obstruction of the left middle cerebral artery was achieved by injecting an autologous blood clot into the left internal carotid artery. Cerebral blood flow was measured with [15O]H2O before and 1, 2, 4, 6, and 24 hours after embolization. CMRglc was measured with 2-[18F]fluoro-2-deoxy-D-glucose ([18F]FDG) 24 hours after embolization. Lesion size and location 24 hours after embolization was determined by the 2,3,5-triphenyltetrazolium chloride (TTC) staining method. The results are summarized as follows: (1) 1 hour after embolization, CBF in the temporal cortex and the basal ganglia decreased to < 40% of the contralateral values. In these regions, regarded as an ischemic core, CBF decreased further with time and CMRglc at 24 hours also decreased. Infarcted lesions as indicated by being unstained with TTC were consistently observed in these regions. (2) In the parietal cortex and several regions surrounding the ischemic core, CBF was > 40% of the contralateral values 1 hour after embolization and recovered gradually with time (ischemic penumbra). In these regions, CMRglc at 24 hours increased compared with that in the contralateral regions, indicating an uncoupling of CBF and CMRglc. No obvious TTC-unstained lesions were detected in these regions. The authors demonstrated a gradual recovery of reduced CBF, an elevated CMRglc and a CBF-CMRglc uncoupling in the penumbra regions of the primate model. Positron emission tomography investigations using this model will provide better understanding of the pathophysiology of thromboembolic stroke in humans.

Group disability income: new policies emphasize employee appeal.

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Experimental thromboembolic stroke in cynomolgus monkey.

To develop an experimental model of thromboembolic stroke without intracranial surgery, an autologous blood clot was delivered to the middle cerebral artery (MCA) via the internal carotid artery in cynomolgus monkeys. Male cynomolgus monkeys, in which a chronic catheter had been earlier implanted in the left internal carotid artery, were used. The clot was flushed into the internal carotid artery under sevofluorane anesthesia. A neurologic deficit score was assigned after MCA embolization. After 24 h, cerebral infarct size and location were determined by the TTC staining method. Cerebral blood flow (CBF) was measured prior to and after MCA embolization, using positron emission tomography (PET). After embolization, long-lasting and profound extensor hypotonia of the contralateral upper and lower limbs, and mild to severe incoordination were observed. Contralateral hemiplegia was observed over the following 24 h. In gross morphologic observation of the brain, the lesions involved mostly the caudate nucleus, putamen, globus pallidus and insular cortex. CBF was maximally reduced in the left MCA territory, but not in the right MCA territory. This model is relevant to thromboembolic stroke in human in neurologic dysfunction and histopathologic brain damage.

Expression cloning of Xantivin, a Xenopus lefty/antivin-related gene, involved in the regulation of activin signaling during mesoderm induction.

In a screening for activin-responsive genes, we isolated a Xenopus lefty/antivin-related gene, called Xantivin (Xatv). In the animal cap assay, the expression of Xatv was induced by activin signaling, and in the embryo, by nodal-related genes. Overexpression of Xatv in the marginal zone caused suppression of mesoderm formation and gastrulation defects, and inhibited the secondary axis formation induced by Xnr1 and Xactivin, suggesting that Xatv acted as a feedback inhibitor of activin signaling. However, in the animal cap, Xatv failed to antagonize Xnr1 and Xactivin. This result suggested that Xatv has different responses in the marginal zone and in the animal region, and antagonizes to a higher degree activin signaling in the marginal zone.

Two novel nodal-related genes initiate early inductive events in Xenopus Nieuwkoop center.

In vertebrates, Nodal-related protein plays crucial roles in mesoderm and endoderm induction. Here we describe two novel Xenopus nodal-related genes, Xnr5 and Xnr6, which are first zygotically expressed at the mid-blastula transition, in the dorsal-vegetal region including the Nieuwkoop center. Xnr5 and Xnr6 were isolated by expression screening of a library enriched with immediate-early-type transcripts, and are strong inducers of both mesoderm and endoderm. They also induce the other nodal-related genes in the animal cap. In embryos, cerberus-short (nodal-specific inhibitor) can inhibit Xnr1 and Xnr2 express to the same extent goosecoid, but not Xnr5 and Xnr6 transcription. Xnr5 and Xnr6 are regulated completely cell autonomously, differently from other Xnrs in the cell-dissociated embryos. The expression of Xnr5 and Xnr6 is regulated by maternal VegT and (beta)-catenin, but does not require TGF-(beta) signaling. Therefore, expression of Xnr5 and Xnr6 is controlled by different mechanisms from other Xnr family genes.

Effects of single and repetitive spreading depression on cerebral blood flow and glucose metabolism in cats: a PET study.

To clarify the effects of spreading depression (SD) on cerebral circulation and metabolism, we elicited a single or repetitive episode of SD and evaluated CBF and CMRglc three-dimensionally in normal cats (n=4, in each group) using a high-resolution positron emission tomography (PET) scanner. SD was evoked by applying KCl to the left occipital cortex. We then monitored DC potential changes with tungsten electrodes inserted into the left temporal cortex. CBF was measured twice before and three times (immediately, 30-60 min, and 60-120 min) following KCl application using [15O]H(2)O, and CMRglc was determined using 2-[18F]fluoro-2-deoxy-D-glucose immediately following the last CBF measurement. The following results were obtained: (1) a single episode of SD produced a temporary CBF increase, followed by a long-lasting hypoperfusion in the cortex, with no significant changes to CBF observed in the subcortex; (2) no significant CMRglc changes were observed in either cortical or subcortical regions following a single episode of SD; (3) a flow-metabolism uncoupling was observed in the cortical regions concurrently with persistent hypoperfusion; (4) repetitive SD produced significant CBF changes in the cortex; and (5) the cortical CMRglc increased as a result of repeated episodes of SD, with no significant changes observed in the subcortex. Thus, we succeeded in determining three-dimensionally the effects of single and repetitive SD on CBF and CMRglc in cats using a high-resolution PET scanner. The present study provides the first direct evidence of CBF-CMRglc uncoupling occurring concurrently with persistent hypoperfusion following SD.

Spontaneous improvement in reduced vasodilatory capacity in major cerebral arterial occlusive disease.

Reduced vasodilatory capacity resulting from occlusive lesions of the major cerebral arteries may return to normal without surgical revascularisation. We aimed to determine prospectively the frequency and predictors of recovery of impaired haemodynamics as demonstrated by acetazolamide (ACZ) reactivity on single-photon emission computed tomography (SPECT). Vasoreactivity was measured by (123)I-IMP SPECT with an ACZ challenge, in 37 medically treated patients with unilateral occlusive disease of the internal carotid or middle cerebral artery at an interval of 1-2 years. Each ACZ challenge test was analysed semiquantitatively by calculating the degree of increase in cerebral blood flow (CBF) asymmetry after ACZ administration (DeltaAI). Vasodilatory capacity was abnormal initially in 20 patients (65 %); eight of whom (40 %) exhibited spontaneous normalisation on follow-up. Although the baseline characteristics did not differ significantly between patients with or without increase in reactivity, logistic regression analysis revealed that the initial DeltaAI (P < 0.05) and the type of vascular lesion (stenosis or occlusion) (P < 0.05) correlated significantly with a return towards normal of reduced ACZ reactivity. Spontaneous improvement of impaired vasodilatory capacity may not be a rare phenomenon. We found that mild reduction in the initial ACZ reactivity and a stenosis, but not complete occlusion, were independent factors contributing to normalisation of impaired cerebral haemodynamics.

[Analysis of ischemic stroke in patients aged up to 50 years].

BACKGROUND AND PURPOSE: Ischemic stroke in young adults has not fully been studied in Japan. The purpose of this study is to clarify the clinical features and pathogenetic mechanisms of ischemic stroke in young adults. METHODS: From January 1990 to June 2000, 133 (7.1%) of 1,862 consecutive patients with ischemic stroke were aged 16 to 50 years (92 men and 41 women, aged of 42.6 +/- 7.7 years). We divided the patients into three groups according to the age of stroke onset; 16 to 40 (group A, n = 38), 41 to 45 (group B, n = 33), and 46 to 50 years (group C, n = 62). Sex, vascular risk factors including hypertension, diabetes mellitus, hyperlipidemia and smoking, cerebrovascular lesions, potential cardiac sources of emboli (emboligenic cardiac diseases), and clinical categories of stroke were examined. We compared them among the three groups. RESULTS: Men predominated in the all groups. Patients in the group C had more frequently hypertension (p < .0005) and diabetes mellitus (p < .05) than those in the group A and B. The vertebrobasilar infarcts were often revealed in the group A but not in the group B and C (p < .01). No significant difference was observed about the incidence of emboligenic cardiac diseases among the three groups. Out of 46 emboligenic cardiac diseases, the most frequent one was patent foramen ovale (15 patients), whereas nonvalvular atrial fibrillation was documented only in five. Fourteen of 20 patients with significant atherosclerotic arterial lesions were found in the group C, whereas 13 of 16 patients with nonatherosclerotic vasculopathies in the group A. Ulcerated atheroma in the aortic arch was detected in two patients, both in the group C. Overall, clinical categories of stroke were identified as lacunar (Lac) in 34 patients (26%), atherothrombotic (AT) in 16 (12%), cardioembolic (CE) in 44 (33%), miscellaneous (Misc) in 27 (20%), and undetermined in 12 (9%). The most frequent cause of Misc (nine patients) was arterial dissection, occurring mostly in the vertebrobasilar system (eight of nine patients). Misc was most frequent in the group A (p < .0001), and Lac was so in the group C (p < .001). Seventy-six percent of patients in the group A and 61% of those in the group B were attributed to nonatherosclerotic causes. In contrast, 61% of patients in the group C had atherosclerotic causes. CONCLUSIONS: Incidence of athero- and arteriosclerosis as causes of ischemic stroke was apparently increased beyond 45 years of age. Patients < or = 45 years are likely to have various and unique etiologies for ischemic stroke. A specific diagnostic approach is strongly recommended for young patients with ischemic stroke.

In vitro pancreas formation from Xenopus ectoderm treated with activin and retinoic acid.

In the present study, isolated presumptive ectoderm from Xenopus blastula was treated with activin and retinoic acid to induce differentiation into pancreas. The presumptive ectoderm region of the blastula consists of undifferentiated cells and is fated to become epidermis and neural tissue in normal development. When the region is isolated and cultured in vitro, it develops into atypical epidermis. Isolated presumptive ectoderm was treated with activin and retinoic acid. The ectoderm frequently differentiated into pancreas-like structures accompanied by an intestinal epithelium-like structure. Sections of the explants viewed using light and electron microscopy showed some cells clustered and forming an acinus-like structure, including secretory granules. The pancreas-specific molecular markers insulin and XIHbox8 were also expressed in the treated explants. The pancreatic hormones, insulin and glucagon, were detected in the explants using immunohistochemistry. Therefore, sequential treatment with activin and retinoic acid can induce presumptive ectoderm to differentiate into a morphological and functional pancreas in vitro. When ectoderm was immediately treated with retinoic acid after treatment with activin, well-differentiated pronephric tubules were seen in a few of the differentiated pancreases. Treatment with retinoic acid 3-5 h after activin treatment induced frequent pancreatic differentiation. When the time lag was longer than 15h, the explants developed into axial mesoderm and pharynx. The present study provides an effective system for analyzing pancreas differentiation in vertebrate development.

Endoderm differentiation and inductive effect of activin-treated ectoderm in Xenopus.

When presumptive ectoderm is treated with high concentrations of activin A, it mainly differentiates into axial mesoderm (notochord, muscle) in Xenopus and into yolk-rich endodermal cells in newt (Cynops pyrrhogaster). Xenopus ectoderm consists of multiple layers, different from the single layer of Cynops ectoderm. This multilayer structure of Xenopus ectoderm may prevent complete treatment of activin A and subsequent whole differentiation into endoderm. In the present study, therefore, Xenopus ectoderm was separated into an outer layer and an inner layer, which were individually treated with a high concentration of activin A (100 ng/mL). Then the differentiation and inductive activity of these ectodermal cells were examined in explantation and transplantation experiments. In isolation culture, ectoderm treated with activin A formed endoderm. Ectodermal and mesodermal tissues were seldom found in these explants. The activin-treated ectoderm induced axial mesoderm and neural tissues, and differentiated into endoderm when it was sandwiched between two sheets of ectoderm or was transplanted into the ventral marginal zone of other blastulae. These findings suggest that Xenopus ectoderm treated with a high concentration of activin A forms endoderm and mimics the properties of the organizer as in Cynops.

Cytochalasin B inhibits morphogenetic movement and muscle differentiation of activin-treated ectoderm in Xenopus.

Xenopus ectodermal explants (animal caps) begin to elongate after treatment with the mesoderm inducing factor activin A. This phenomenon mimics the convergent extension of dorsal mesoderm during gastrulation. To analyze the relationship between elongation movement and muscle differentiation, animal caps were treated with colchicine, taxol, cytochalasin B and hydroxyurea (HUA)/aphidicolin following activin treatment. Cytochalasin B disrupted the organization of actin filaments and inhibited the elongation of the activin-treated explants. Muscle differentiation was also inhibited in these explants at the histologic and molecular levels. Colchicine and taxol, which are known to affect microtubule organization, had little effect on elongation of the activin-treated exp ants. Co-treatment with HUA and aphidicolin caused serious damage on the explants and they did not undergo elongation. These results suggest that actin filaments play an important role in the elongation movement that leads to muscle differentiation of activin-treated explants.

Peptide growth factors in amphibian embryogenesis: intersection of modern molecular approaches with traditional inductive interaction paradigms.

Recent discoveries of the role peptide growth factors (PGFs) play in regulating embryonic patterning and differentiation have profoundly influenced research on the molecular biology of early amphibian embryogenesis. Several PGFs have been recognized to be present as endogenous components of amphibian eggs and early embryos, while other PGFs -- which are known from heterologous systems (e.g., Drosophila) -- exert remarkable effects when injected as either protein or mRNA into eggs/embryos or when added to cultured embryonic tissue. For a variety of reasons (reviewed herein) optimism abounds that an understanding in molecular terms of the classical Spemann and Nieuwkoop tissue interactions which are generally believed to drive embryonic patterning is within reach. A critical assessment of the interpretations of some of the contemporary data on PGFs (included herein) should, however, temper some of that optimism. Likely, multiple rather than single PGFs act in a combinatorial fashion to contribute to individual patterning events. As well, substantial redundancy in PGF regulatory circuits probably exists, so the heavy reliance on tissue culture assays and overexpression studies which characterize much recent research needs to be circumvented. Potential experimental approaches for "next generation" experiments are discussed.

Patterns of gene expression in the core of Spemann's organizer and activin-treated ectoderm in Cynops pyrrhogaster.

The presumptive pharyngeal endoderm region of the Cynops early gastrula induces head or trunk-tail structures in sandwich culture. Activin-treated ectoderm can mimic this phenomenon at least at the histological level. The patterns of expression of organizer-specific genes were examined to compare these two inductive materials at the molecular level. A chordin cDNA clone from Cynops pyrrhogaster (Cychd) was isolated by reverse transcription-polymerase chain reaction (RT-PCR). Cychd mRNA was first detected in the presumptive pharyngeal endoderm and prechordal plate regions of stage 11 embryos, and was expressed continuously until stage 20. The spatiotemporal expression pattern of Cychd was similar to that of Xenopus chordin. The patterns of expression of organizer-related genes in the pharyngeal endoderm and activin-treated ectoderm were compared by RT-PCR analysis. Expression of Cychd in these two materials peaked at the time when they can induce head structures in sandwich culture. Expression of fork head and goosecoid did not change in the presumptive pharyngeal endoderm over this period. Cychd may play a key role in head formation in the Cynops embryo.

Lipoprotein disorder in brain infarction and hemorrhage.

The cholesterol, triglyceride, and apolipoprotein B content of very low-, intermediate-, low-, and high-density lipoprotein fractions (separated by ultracentrifugation) and plasma were measured in healthy controls and patients with atherothrombotic infarction (26), lacunar infarction (26), and brain hemorrhage (14). In both atherothrombotic and lacunar infarction, increased plasma and low-density lipoprotein apolipoprotein B and a decreased low-density lipoprotein cholesterol/apolipoprotein B ratio were noted. In brain hemorrhage patients, a decreased ratio was also observed. These findings suggest that increased small dense low-density lipoprotein is a characteristic risk factor for atherothrombotic and lacunar infarction.

Cloning and expression pattern of Xenopus prx-1 (Xprx-1) during embryonic development.

Homeobox genes are expressed both temporally and spatially during vertebrate development, and regulate the tissue-specific expression of other genes. A Xenopus paired-related homeobox- 1 (Xprx-1) cDNA was cloned. Xprx-1 had a paired-related homeodomain, but did not contain a paired-box. The sequence of Xprx-1 had a high level of homology with K-2(mouse) and Prx-1 (chicken), thus Xprx-1 is assumed to be the Xenopus homolog of these genes. Xprx-1 transcripts were maternally restricted, in Xenopus embryos, and a decrease in the late blastula stage was followed by an increase in zygotic transcripts after gastrulation. The transcripts were localized to the animal hemisphere of the late blastula and were concentrated in the branchial arches of the tail-bud stage embryo. In animal cap experiments, Activin A dose-dependently induced Xprx-1 gene expression. These results suggest that Xprx-1 plays a role in early Xenopus development similar to other species.

Midkine counteracts the activin signal in mesoderm induction and promotes neural formation.

Midkine (MK) is a heparin-binding growth factor that has been implicated in neural survival and differentiation, fibrinolysis, and carcinogenesis. It is expressed in the nervous system during early Xenopus development. In the present study, we demonstrated that injection of vegetal blastomeres with Xenopus MK at the 8-cell stage results in incomplete invagination. In the case of dorsal vegetal injection, hypertrophic neural tissue is produced. Animal caps isolated from embryos that have been injected with Xenopus MK and cultured with activin do not elongate, and all mesoderm markers examined, including both head and trunk/tail ones, are greatly diminished. In contrast, head-specific neural markers, XANF-1 and Xotx2, are induced, while trunk/tail neural markers, XlHbox6 and F-spondin, are decreased. Moreover, MK showes the same effects in animal caps injected with Xenopus Smad2 mRNA.

Effect of acetazolamide reactivity on [corrected] long-term outcome in patients with major cerebral artery occlusive diseases.

BACKGROUND AND PURPOSE: It remains unclear whether hemodynamic insufficiency plays a major role in ischemic events. We performed a prospective follow-up study in ischemic stroke patients with occlusive large-artery diseases to determine whether stroke recurrence is related to reduced vasodilatory capacity, judged with single-photon emission CT and acetazolamide (ACZ) challenge. METHODS: During the period from 1987 to 1995, we examined cerebral vasodilatory capacity with single-photon emission CT and an ACZ challenge in 105 consecutive stroke patients with severe stenosis (> 75% in diameter) or occlusion of the internal carotid artery or the trunk of the middle cerebral artery who had no or minimal infarcts on CT. According to criteria reported earlier, the patients were divided into two groups: normal (negative ACZ, n = 50) or reduced ACZ reactivity (positive ACZ, n = 55). They were prospectively followed at regular intervals for a median period of 2.7 years. RESULTS: The Kaplan-Meier analysis revealed no difference in cumulative recurrence-free survival rate between the two groups. The multivariate analysis with Cox proportional hazards model demonstrated that a high systolic blood pressure at entry into the study significantly increased stroke recurrence (coefficient = .0466; hazard ratio = 1.0477; 95% confidence interval = 1.0017 to 1.0957; P = .04), whereas antihypertensive medication significantly reduced stroke recurrence (coefficient = -1.527; hazard ratio = 0.217; 95% confidence interval = 0.0612 to 0.771; P = .02), but no other variables including ACZ reactivity affected stroke recurrence rate. CONCLUSIONS: The present results demonstrate that reduced vasodilatory capacity does not play a major role in stroke recurrence. Antihypertensive therapy appears to reduce stroke recurrence even in patients with hemodynamically significant arterial diseases.

[Pathophysiology and treatment of cardioembolic stroke].

To elucidate the pathophysiologic mechanism of cardioembolic stroke in elderly people and to devise therapeutic strategies for it, was analyzed 120 consecutive patients (77 men and 43 women aged 65 +/- 13 years) with acute cardioembolic stroke who were admitted within 7 days of the stroke onset. We compared underlying heart diseases. NIH stroke scale on admission, lesion size on computed tomography (CT), the relation between anticoagulant therapy and recurrence, complications during admission. ADL at discharge, recurrence, and death during the follow up period in three groups: patients aged less than 65 years (the young group), those aged from 65 to 74 years (the "non-old" group), and those aged more than 75 years (the "old old" group). In the "old old" group, non valvular atrial fibrillation (75.8%) was the most common underlying heart disease and so was rheumatic heart disease (33.3%) in the "non-old" group. NIH stroke scale score (median, 11) and the proportion of patients with a large lesion (> 3 cm) of CT were higher in the "old old" group than in the other two groups. Immediate anticoagulation (A/C) within 14 days of onset was performed in more than 70% of the "non-old" and the "young old" groups but in only 57.6% of the "old old" group. Stroke recurred more often in 34 patients who did not receive immediate A/C than in the 86 who did (11.8% v.s. 2.3%. Chi square test, p = 0.053). Hemorrhage during immediate A/C and other complications (infection and pulmonary embolism) were seen in 2 and 14 patients, respectively, in both the "young old" groups, but not in the "non-old" group. Good outcomes (able to walk with or without cane) were more common in the "non-old" group (78.9%) than the other groups (57.1%, Chi square test, p < (0.01). A/C after the acute stage was done in more than 80% of those in the "non-old" and the "young old" groups, but in less than 30% of those in the "old old" group (Chi square test, p = 0.0514). Survival without recurrence during the observation period (605 +/- 550 days) was significantly lower in the "old old" group than in the other two groups (log-rank test, p = 0.0091). Cardioembolic stroke in the elderly may be characterized as follows: (1) non valvular atrial fibrillation is the most common, (2) severe neurologic deficits on admission and large lesions on CT are noted, (3) complications (infection and pulmonary embolism) often occur, (4) A/C in both acute and chronic stages are done infrequently. Therefore, the indication and intensity of A/C for primary and secondary prevention and prevention of complications are important in management of cardioembolic stroke in the elderly.