Biomedical subjects
Publications and source records attributed to Oh Young Bang.
Spontaneous middle cerebral arterial dissection (MCAD) is a rare cause of ischemic stroke. We report two cases of isolated spontaneous MCAD causing ischemic stroke. MCAD should be considered when a young patient has a middle cerebral artery territory infarct with stenosis at the origin of the middle cerebral artery. We discuss noninvasive radiological techniques for the diagnosis of MCAD.
BACKGROUND AND PURPOSE: The pathogenesis of internal border-zone (IBZ) and cortical border-zone (CBZ) infarcts is unclear. Both types of infarct have been combined into a single group in most previous reports, which has produced conflicting results. We hypothesized that different pathogenic mechanisms underlie IBZ and CBZ infarcts. METHODS: We reviewed 946 consecutive patients with ischemic stroke within the middle cerebral artery territory. IBZ and CBZ infarcts were selected based on diffusion-weighted imaging templates to identify vascular territories. Baseline patient characteristics, clinical courses, and neuroradiological features were compared between patients with IBZ and CBZ infarcts. RESULTS: We identified 45 IBZ and 75 CBZ infarct patients. Compared with the CBZ infarct patients, IBZ infarct patients had a higher degree of stenosis or occlusion in either the middle cerebral or internal carotid artery (P=0.008) and exhibited a rosary-like pattern of infarction more frequently (P<0.001). In contrast, concomitant small cortical infarcts were observed more frequently in CBZ infarct patients (P<0.001). Clinical deterioration during the first 7 days of admission and poor outcome after 3 months after stroke was more prevalent in IBZ infarct patients than in CBZ infarct patients (P=0.002 and P=0.003, respectively). CONCLUSIONS: IBZ infarcts are caused mainly by hemodynamic compromise, whereas embolic pathogenesis appears to contribute greatly to the genesis of CBZ infarcts. Patients with IBZ infarcts showed poor early and late clinical courses. Our findings suggest that different therapeutic approaches may be required to prevent early clinical deterioration in patients with different types of border-zone infarcts.
OBJECTIVE: To compare clinical and angiographic characteristics and stroke patterns between spontaneous intracranial vertebral artery dissection (VAD) and vertebral large artery disease (LAD) (atherosclerosis). DESIGN: Retrospective study. SETTING: Tertiary referral center for cerebrovascular diseases. Patients Twenty-two patients with spontaneous VAD and 25 with LAD in the intracranial portion of the vertebral artery. MAIN OUTCOME MEASURES: We compared (1) clinical characteristics, including epidemiologic data, vascular risk factors including inflammatory markers, the presence of headache, and stroke syndromes and severity; (2) stroke pattern on diffusion-weighted imaging, which was classified as vertebral perforator infarct, basilar perforator infarct, small scattered infarct, large scattered infarct, and territorial infarct; and (3) angiographic findings, ie, the distribution of involved arteries, degree of stenosis, and the involvement on the anterior circulation and calcification of vertebral artery. RESULTS: Although patients with VAD were younger, and more often had headaches and fewer vascular risk factors than those with LAD (P<.01 in all cases), these clinical features were also observed in some LAD patients. Diffusion-weighted imaging data showed that vertebral perforator infarct and small scattered infarct were most common in the VAD group, while territorial infarct and large scattered infarct were most common in the LAD group (P = .02). On angiography, LAD more frequently had anterior circulation arterial involvement (P = .002), higher degree of stenosis (P = .002), and calcifications (P = .008). CONCLUSION: Our findings indicate that results of diffusion-weighted imaging and noninvasive vascular studies might provide clues to the clinical characteristics in differential diagnosis between VAD and LAD.
In some cases, it is difficult to differentiate essential tremor (ET) from Parkinson's disease (PD), especially in the early stages of the disease. We investigated cardiac sympathetic dysfunction using (123)I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy in 22 patients with ET, in comparison with early PD and tremor-dominant PD (TDPD). The mean ratio of (123)I-MIBG uptake in the region of interest in the heart to that in the mediastinum (H/M ratio) was significantly greater in patients with ET (1.99 +/- 0.21) than in those with either TDPD (1.28 +/- 0.11) or early PD (1.28 +/- 0.17; each P < 0.001). The H/M ratio in all patients with ET was greater than two standard deviations above the range of the ratio in the patients with early PD or TDPD.
Stroke is the second leading cause of mortality world-wide and is well suited for prevention because it has a high prevalence, high burden of economic cost, well-defined modifiable risk factors, and effective prevention measures. Atherosclerosis is one of the major mechanisms of ischemic stroke, but the apparent differences in risk factors for intra- and extracranial atherosclerosis are unclear and the mechanisms that underlie strokes in patients with intracranial atherosclerosis are not well known. Consequently, patients with intracranial stenosis receive the same treatment as those with carotid -atherosclerosis. Several novel substances have emerged recently as risk factors for atherosclerosis. Specifically, it has recently been suggested that both the metabolic syndrome, which refers to a constellation of metabolic risk factors that are linked to insulin resistance, and vascular inflammation are associated with increased risk of coronary heart disease and stroke. The results of the studies reviewed here suggest that these factors play a differential role in the development of atherosclerotic stroke between the intra- and extracranial arterial systems.
BACKGROUND: Information on the mechanism of recurrent stroke may help physicians treating patients with ischemic stroke. However, the mechanisms of recurrence in each stroke subtype are not well known, especially in Asians. OBJECTIVE: To compare the mechanisms of the index and recurrent stroke. DESIGN: Analysis of data from a prospective acute stroke registry. SETTING: University hospital. PATIENTS: Using the clinical syndrome, diffusion-weighted imaging, and vascular studies, we divided 901 patients into 5 groups: large-artery atherosclerosis, cardioembolism, small-artery disease, parent-artery disease occluding the deep perforators, and no determined cause. The patients with large-artery atherosclerosis were subdivided into 2 groups: intracranial and extracranial. MAIN OUTCOME MEASURES: The mechanisms of recurrent vascular events (strokes or coronary heart disease) in subtypes of ischemic stroke were compared. RESULTS: Ninety-three recurrent vascular events (86 strokes and 7 instances of coronary heart disease) were evaluated. The pattern of recurrent stroke differed for the intracranial and extracranial groups; unlike the patients with intracranial large-artery atherosclerosis, recurrent strokes in the extracranial group were often unpredictable with respect to the site of recurrence and degree of preexisting stenosis. None of the patients in the extracranial group had recurrences that were caused by intracranial large-artery atherosclerosis or vice versa. In patients with small-artery disease and stroke with no determined cause, intracranial stenosis was often found at the time of recurrence. CONCLUSIONS: From prognostic and therapeutic perspectives, patients with atherosclerosis should be divided into those with intracranial large-artery atherosclerosis and extracranial large-artery atherosclerosis. In addition, intracranial large-artery atherosclerosis may be important in the development of small-artery disease and stroke with no determined cause, especially in the population with a higher frequency of intracranial large-artery atherosclerosis.
Mesenchymal stem cell (MSC) transplantation improves recovery from ischemic stroke in animals. We examined the feasibility, efficacy, and safety of cell therapy using culture-expanded autologous MSCs in patients with ischemic stroke. We prospectively and randomly allocated 30 patients with cerebral infarcts within the middle cerebral arterial territory and with severe neurological deficits into one of two treatment groups: the MSC group (n = 5) received intravenous infusion of 1 x 10(8) autologous MSCs, whereas the control group (n = 25) did not receive MSCs. Changes in neurological deficits and improvements in function were compared between the groups for 1 year after symptom onset. Neuroimaging was performed serially in five patients from each group. Outcomes improved in MSC-treated patients compared with the control patients: the Barthel index (p = 0.011, 0.017, and 0.115 at 3, 6, and 12 months, respectively) and modified Rankin score (p = 0.076, 0.171, and 0.286 at 3, 6, and 12 months, respectively) of the MSC group improved consistently during the follow-up period. Serial evaluations showed no adverse cell-related, serological, or imaging-defined effects. In patients with severe cerebral infarcts, the intravenous infusion of autologous MSCs appears to be a feasible and safe therapy that may improve functional recovery.
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BACKGROUND: Global aphasia without hemiparesis (GAWH) is a rare stroke syndrome. This study localized the lesion and examined the pathogenic mechanism in Korean patients with GAWH, and investigated whether areas of extensive hypoperfusion existed outside the diffusion-weighted imaging (DWI) lesions seen in these patients. MATERIAL AND METHODS: Eleven patients were diagnosed with aphasia using the Western Aphasia Battery. To identify decreased perfusion, which might be functionally relevant to aphasia but not detected by DWI, single photon emission tomography (SPECT) was performed in five patients. To uncover the possible pathogenic mechanisms of ischemic stroke, vascular and cardiologic work-ups were performed in all of the patients. RESULTS: The lesions seen on DWI varied, and included both inferior frontal and superior temporal (three), isolated inferior frontal (four) or superior temporal (one), subcortical (two), and even parieto-occipital (one) lesions. Brain SPECT did not reveal an extensive lesion of the peri-sylvian area outside the DWI lesion in any of the patients, except one with the subcortical lesions. CONCLUSION: Our results indicate that a single lesion in different locations may be sufficient to produce GAWH, and the lesion profile and stroke mechanism in GAWH are heterogeneous, suggesting that lesions to an area of complex functional anatomy result in aphasia.
BACKGROUND: The significance of occlusive lesions of the parent artery in patients with lacunar syndrome (LS) and small deep infarcts (SDIs) on diffusion-weighted imaging remains unclear. OBJECTIVE: To compare the recurrence of stroke in patients with LS and SDIs between those with vs without a parent arterial lesion. DESIGN: Analysis of data from a prospective acute stroke registry. SETTING: University hospital. PATIENTS: Using clinical syndrome, diffusion-weighted imaging, and vascular studies, we divided 173 patients into 3 groups: (1) parent arterial disease occluding deep perforators (PAD), LS with SDIs, and a parent arterial lesion (n = 32); (2) small artery disease (SAD) (n = 70); and (3) large artery disease (LAD) (n = 71). MAIN OUTCOME MEASURES: Recurrent strokes and the prognosis were registered for 1 year, and the outcome of the PAD group was compared with that of the SAD and LAD groups. RESULTS: During follow-up, there were 9 deaths (6 vascular) and 18 recurrent strokes. The recurrence rate in the PAD group (16%) was significantly higher than that in the SAD group (1%) (P =.01) but similar to that in the LAD group (17%) (P =.87). The presence of the parent arterial lesion was the only independent predictor of stroke recurrence in patients with LS and SDIs (odds ratio, 13.8; 95% confidence interval, 1.5-123.9; P =.02). CONCLUSIONS: Although LS on examination, SDIs on diffusion-weighted imaging, and a stable hospital course suggest lacunar stroke of benign course, our results indicate that the PAD group represents an intracranial type of LAD.
Estrogen is beneficial to patients with Alzheimer's disease (AD) but has a limited clinical use due to its proliferative and oncogenic effects on non-neuronal cells responsive to estrogen. In an attempt to find an estrogen substitute that retains the beneficial effects of estrogen with minimal side effects, we compared the neuroprotective and proliferative effects of genistein, a selective estrogen receptor (ER) beta-agonist, with those of estrogen. Genistein and 17beta-estradiol showed comparable levels of protection against Abeta-induced deaths of cultured SH-SY5Y human neuroblastoma cells, which were blocked by an estrogen receptor antagonist, ICI 182,780. On the other hand, 17beta-estradiol, but not genistein, induced proliferation of uterine endometrial cells. Our results suggest that genistein is a potential alternative to estrogen in the treatment of Alzheimer's disease.
BACKGROUND AND PURPOSE: Because of difficulty in distinguishing between superficial perforator (SP) and internal border-zone (IB) infarcts, some studies lumped SP and IB infarcts together as so-called subcortical white matter infarcts, which might complicate the classification of infarct type and its pathogenesis. Using diffusion-weighted MRI (DWI), we made comparative analyses of clinical and neuroradiological characteristics between IB and SP infarcts to clarify the difference in underlying pathogenesis. METHODS: We selected SP and IB infarcts on DWI using templates for the identification of subcortical vascular territories. Sex, age, neurological symptoms, clinical course, risk factors, concomitant cortical spotty lesions, and degree and location of arterial occlusive disease were compared between the 2 groups. RESULTS: Among the 720 consecutive patients, 54 and 29 patients met the criteria for SP and IB infarcts, respectively. The SP group had lower initial National Institutes of Health Stroke Scale scores (2.4+/-2.1 versus 4.4+/-3.1; P=0.001), favorable clinical outcomes (P=0.001), and more frequent potential cardioembolic sources (14.8% versus 0%; P=0.046) than the IB group. Cortical spotty lesions were more frequently accompanied by SP than IB infarcts (72.2% versus 24.1%; P<0.001). IB infarcts were larger (24.2+/-10.2 versus 11.4+/-8.5 mm; P<0.001), appeared in a chainlike fashion (72.4% versus 33.3%; P=0.001), and had a higher degree of stenosis or occlusion (86.2% versus 46.3%; P=0.001) compared with SP infarcts. CONCLUSIONS: Our present study suggests that embolic pathogenesis makes a greater contribution to SP infarcts than IB infarcts. This finding may explain the difference in clinical and neuroradiological characteristics between the 2 groups.
To evaluate the differential diagnostic role of apolipoprotein E (apoE) genotype in dementia, we carried out a meta- analysis of 78 case-control series, including our own new data. The dementia subjects were grouped into Alzheimer's disease (AD) and non-AD. AD patients were subgrouped according to their subtypes, and non-AD patients into vascular dementia (VD), mixed dementia (MD), and non-AD non-VD dementia (NAVD). The apoE allele frequencies and apoE genotype-specific odds ratio (OR) of each group were estimated. The (4 allele frequency was higher in all of the dementia subgroups than in the elderly controls, and the associations with (4 allele were lower in the non-AD (OR 1.8) patients than in the AD (OR 4.2) patients. However, the apoE-related risk alsovaried as a function of the subgroup, in both the AD and non-AD groups; for AD, it was dependent on the subtype of AD (OR 2.3 - 11.3), and higher in late- onset and familial cases than in early-onset and sporadic cases, respectively; among non-AD patients, it was higher in MD (OR 2.6) than in VD (OR 1.3), and intermediate in NAVD (OR 1.9), in which a significant difference was also found between Lewy body dementia (LBD) type (OR 5.1) and non-LBD type (OR 1.3). In conclusion, variability in the apoE-related risk was found in both the AD and non-AD cases, depending on the subgroup. Therefore, precise subgrouping of both AD and non-AD patients should be performed, and this information should taken into consideration when interpreting the results of apoE genotyping.
BACKGROUND: Comparative studies of clinical and magnetic resonance imaging findings in patients with spinocerebellar ataxias (SCAs) have been seldom reported. OBJECTIVE: To investigate clinical, genetic, and neuroradiological characteristics of SCAs in Korean kindreds. SETTING: University hospital. PATIENTS AND METHODS: Molecular analysis of SCA types 1, 2, 3, 6, and 7 and dentatorubral pallidoluysian atrophy and magnetic resonance imaging were performed in 67 patients with ataxia. RESULTS: The overall prevalence of 6 types of SCAs was 54% (36 of 67 patients), irrespective of patients' family histories. The most frequent type was SCA7 (11 patients, 16%), followed by SCA3 and SCA6 (10 patients, 15% for both). Certain clinical features suggested specific gene defects, although overlap among the 6 SCA subtypes was broad: visual disturbance was noted in patients with SCA3 and SCA6, dystonia in 1 patient with SCA6, and sporadic ataxia without pigmentary retinopathy in 1 patient with SCA7. Compared with the control subjects, patients with SCAs and multisystem atrophy had a significant enlargement of the fourth ventricle and atrophy of the cerebellum (P<.01). An inverse correlation between the pontine area and the degree of cerebellar atrophy was found in patients with multisystem atrophy (r = -0.73) but not in patients with SCAs. Magnetic resonance imaging revealed significant differences in pattern of morphological alterations among patients with different SCA gene mutations. A similar finding was observed in SCA patients with atypical phenotype. CONCLUSION: The clinical and neuroradiological characteristics of Korean patients with SCAs might be helpful in detecting underlying gene mutations.
The purpose of this study was to better understand the frequency and mechanisms of stroke recurrence after the stroke with no determined cause (NC). We prospectively studied consecutive patients with acute cerebral infarcts. We divided the patients into five groups (large artery disease [LAD], cardioembolism [CE], small artery disease [SAD], two or more causes [TMC], and NC) and registered recurrent strokes and prognosis for 1 year. Those in the NC group were compared with other subtypes. A total of 204 patients were included; 56 LAD, 22 CE, 62 SAD, 27 TMC, and 37 NC. During follow-up, there were 7 deaths and 31 first recurrent strokes. Patients of the NC group showed a significantly higher rate (30%) of recurrent stroke than those of other subtypes (LAD 16%; CE 14%; SAD 2%), and it was associated with the existence of mild stenosis (</=50%) on relevant artery or the stenosis of greater than 50% on nonrelevant artery. Occlusive lesions other than significant stenosis of relevant artery may play an important role in the development of stroke recurrence in patients of the NC group. Therefore, from the therapeutic and prognostic point of view, the detection of such occlusive lesions in patients with cryptogenic stroke may be needed.
A recent clinical study showed that statins, which are inhibitors of cholesterol biosynthesis pathway, reduced the prevalence of Alzheimer's disease (AD). Animal studies that have employed high cholesterol diet indicate significant relationship between cholesterol level and senile plaque deposition. Here, we investigated the effects of lovastatin on beta-amyloid production and senile plaque deposition in an animal model of AD (Tg2576 mice). As expected, lovastatin treatment reduced plasma cholesterol level in both male and female mice. However, lovastatin enhanced the amounts of beta-amyloid and other beta-secretase derived peptides in females, but not in males. Likewise, lovastatin increased the number of plaques in the hippocampus and cortex of females, but not in males. Lovastatin did not change the amounts of full-length or alpha-secretase processed amyloid precursor protein (APP), or presenilin 1 (PS1) in either sex. Thus, lovastatin lowers cholesterol level in both genders, but enhances beta-amyloid production and senile plaque deposition only in brains of female Tg2576 mice. Our results suggest that low plasma cholesterol levels might be a risk factor for AD in females.
The role of stenting in the treatment of patients with middle cerebral artery stenosis is not defined because of the high risk and difficulty in tracking. However, recent improvements in the technology, in particular of small, flexible stents and of small, flexible stents with accumulative stenting experience in occlusive intracranial disease endovascular treatment of this disease is now possible. We treated three patients with a symptomatic stenosis of the M1 segment of the middle cerebral artery despite combination anticoagulation therapy. All patients were successfully treated with a balloon-expandable S660 coronary stent. No procedure-related complications occurred and all patients were discharged and remained neurologically stable during the follow-up period (2-12 months). We propose stenting as one of the treatment modalities in patients with symptomatic stenosis of the M1 segment of the middle cerebral artery in selected cases. However, further studies on this new procedure should be done to determine its effect on long-term stroke prevention and to compare its safety with other treatment options.
BACKGROUND AND PURPOSE: The transcranial Doppler (TCD) findings in symptomatic small deep infarction are not well known. The aim of this study was to evaluate the role of TCD in striatocapsular small deep infarctions (SSDIs). METHODS: The cerebral angiography and TCD findings were analyzed on 100 patients with symptomatic cerebral infarcts on the middle cerebral artery (MCA) territory. The sensitivity, specificity, and accuracy of TCD in detecting the MCA lesions were compared between lacunar group (the patients with lacunar syndrome and SSDIs on magnetic resonance image) and nonlacunar group. RESULTS: Thirty-eight patients were classified as the lacunar group, whereas 62 patients as the nonlacunar group. On angiography, occlusive lesion of MCA was found in 18 of the lacunar group and 24 patients of the nonlacunar group. The degree of MCA stenosis was higher in the nonlacunar group (80.8% +/- 21.2%) than the lacunar group (60.4% +/- 21.6%). The accuracy of TCD for the detection of MCA stenosis was not different between the groups. However, the sensitivity of TCD in the lacunar group was lower (72%) than in the nonlacunar group (88%), and it might have been due to the difference in the degree of MCA stenosis among the groups. CONCLUSION: Occlusive lesions of the MCA should be considered as a potential cause of SSDIs. In this respect, TCD may be used for screening candidates for conventional angiography in those patients. High rate of mild-degree stenosis of MCA in patients with SSDIs, however, caused a risk for missing such stenosis on TCD.