The pneumonia score: a simple grading scale for prediction of pneumonia after acute stroke.
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Biomedical subjects
Sang-Wuk Jeong
Publications and source records attributed to Sang-Wuk Jeong.
Granulocyte colony-stimulating factor induces sensorimotor recovery in intracerebral hemorrhage.
Granulocyte colony-stimulating factor (G-CSF) has been used in the treatment of neutropenia in hematologic disorders. The neuroprotective and anti-inflammatory effects of G-CSF were reported in various neurological disease models. In this study, we examined whether G-CSF induces functional recovery after intracerebral hemorrhage (ICH). ICH was induced using collagenase injection in adult rats. Either G-CSF (50 microg/kg, i.p.) or saline was given from 2 h after ICH and every 24 h for 3 days. 72 h after ICH induction, the rats were sacrificed for histological analysis and measurement of brain edema. Behavioral tests were performed before and 1, 7, 14, 21, 28, and 35 days after ICH. We also measured the blood-brain barrier (BBB) permeability using Evans blue dye injection method. G-CSF-treated rats recovered better on rotarod and limb placing tests, starting from 14 days throughout 5 weeks after ICH. The brain water content and BBB permeability of G-CSF-treated group decreased in the lesioned hemispheres compared with those of ICH-only group. In G-CSF-treated group, the number of TUNEL+, myeloperoxidase+, and OX42+ cells was smaller than that of ICH-only group in the periphery of hematoma. These findings suggest that G-CSF induces long-term sensorimotor recovery after ICH with reduction of brain edema, inflammation, and perihematomal cell death.
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Aphasia following striatocapsular infarction may be explained by concomitant small cortical infarct on diffusion-weighted imaging.
BACKGROUND: The underlying mechanism of aphasia following striatocapsular infarction (SCI) remains controversial. We hypothesized that aphasia resulting from SCI might be associated with concomitant cortical lesions, which can be demonstrated by diffusion-weighted imaging (DWI). METHODS: We analyzed 24 patients with left SCI who underwent DWI and MR angiography within 2 days after the onset. Aphasia was assessed by the modified Korean version of the Boston Diagnostic Aphasia Examination test. RESULTS: DWI showed the presence of additional ischemic lesions involving the cortical areas in 13 of 24 SCI patients (54%). Ten patients (42%) showed aphasia. All 10 patients with aphasia had cortical lesions in addition to SCI (p = 0.0002), whereas 21% (3/14) of the nonaphasic patients had additional cortical lesions. Conventional MRI did not reveal the presence of corresponding acute cortical lesions in any of the aphasic patients. There was no difference between the patients with and without aphasia in terms of their stroke etiology. CONCLUSIONS: Our data suggest that aphasia due to SCI in the acute stage may be attributed to direct cortical injury, whose presence can be demonstrated by DWI, even though it might be invisible on conventional imaging.
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Prognostic factors for the surgery for mesial temporal lobe epilepsy: longitudinal analysis.
PURPOSE: Determining long-term prognostic factors of surgery for mesial temporal lobe epilepsy (MTLE) is important for identifying ideal candidates and predicting the prognosis for individual patients. We tried to identify the prognostic factors of anterior temporal lobectomy (ATL) for MTLE with longitudinal multivariate analysis. METHODS: Two hundred twenty-seven patients with MTLE were included in this study. The primary outcome variable was patient status 1-5 years after surgery: seizure free, or not. Clinical characteristics and recent diagnostic modalities were considered as prognostic factors. Univariate and standard multiple logistic-regression analysis for outcome at 1 and 5 years after surgery and the generalized estimation equation (GEE) model for longitudinal multiple logistic regression of the 5-year follow-up period were used. RESULTS: The seizure-free rate at 1 year was 81.1% and decreased to 75.2% at 5 years after surgery. By the univariate or standard multiple logistic-regression analysis, age at surgery or hippocampal sclerosis on magnetic resonance imaging (MRI) ipsilateral to surgery was significant for the postsurgical outcome. However, the longitudinal analysis by the GEE model revealed that younger age at surgery [odds ratio (OR), 0.59; 95% confidence interval (CI), 0.43-0.81], absence of secondarily generalized tonic-clonic seizure (2 degrees GTCS; OR, 0.45; 95% CI, 0.26-0.79), and hippocampal sclerosis on MRI (OR, 2.44; 95% CI, 1.11-5.26) were significant predictors of a good surgical outcome. CONCLUSIONS: Age at surgery, presence of 2 degrees GTCS, and hippocampal sclerosis on MRI are independent prognostic factors for ATL in MTLE. These findings suggest that MTLE is a progressive disorder, and surgical outcome is better when early ATL is performed.
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Human neural stem cell transplantation reduces spontaneous recurrent seizures following pilocarpine-induced status epilepticus in adult rats.
Transplantation of neural stem cells (NSCs) can replace lost neurons and improve the functional deficits. Cell transplantation strategies have been tried in the epileptic disorder, but the effect of exogenous NSCs is unknown. In this study, we attempted to test the anti-epileptogenic effect of NSCs in adult rats with status epilepticus. Experimental status epilepticus was induced by lithium-pilocarpine injection, and beta galactosidase-encoded human NSCs were transplanted intravenously on the next day of status epilepticus. Spontaneous recurrent seizures were monitored with Racine's seizure severity scale. Immunohistochemistry with anti-beta gal, Tuj-1, NeuN, GFAP, CNPase, GluR2, parvalbumin, and GABA were performed and extracellular field excitatory postsynaptic potentials (fEPSP) were recorded. Human NSCs suppressed spontaneous recurrent seizure formation and transplanted NSCs were differentiated into GABA-immunoreactive interneurons in the damaged hippocampus. Amplitude of fEPSP in the hippocampal CA1 was reduced, which was reversed by picrotoxin. These findings suggest that NSCs could be differentiated into inhibitory interneurons and decrease neuronal excitability, which could prevent spontaneous recurrent seizure formation in adult rats with pilocarpine-induced status epilepticus.
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Human neural stem cells improve sensorimotor deficits in the adult rat brain with experimental focal ischemia.
Ischemic stroke is caused by the interruption of cerebral blood flow that leads to brain damage with long-term sensorimotor deficits. Stem cell transplantation may recover functional deficit by replacing damaged brain. In this study, we attempted to test whether the human neural stem cells (NSCs) can improve the outcome in the rat brain with intravenous injection and also determine the migration, differentiation and the long-term viabilities of human NSCs in the rat brain. Focal cerebral ischemia was induced by intraluminal thread occlusion of middle cerebral artery (MCA). One day after surgery, the rats were randomly divided into two groups: NSCs-ischemia vs. Ischemia-only. Human NSCs infected with retroviral vector encoding beta galactosidase were intravenously injected in NSCs-ischemia group (5 x 10(6) cells) and the same amount of saline was injected in Ischemia-only group for control. The animals were evaluated for 4 weeks using turning in an alley (TIA) test, modified limb placing test (MLPT) and rotarod test. Transplanted cells were detected by X gal cytohistochemistry or beta gal immunohistochemistry with double labeling of other cell markers. The NSCs-ischemia group showed better performance on TIA test at 2 weeks, and MLPT and rotarod test from 3 weeks after ischemia compared with the Ischemia-only group. Human NSCs were detected in the lesion side and labeled with marker for neurons or astrocytes. Postischemic hemispheric atrophy was noted but reduced in NSCs-ischemia group. X gal+ cells were detected in the rat brain as long as 540 days after transplantation. Our data suggest intravenously transplanted human NSCs can migrate and differentiate in the rat brain with focal ischemia and improve functional recovery.
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HMG-CoA reductase inhibitor, atorvastatin, promotes sensorimotor recovery, suppressing acute inflammatory reaction after experimental intracerebral hemorrhage.
BACKGROUND AND PURPOSE: Statins have neuroprotective effects on ischemic stroke. They modify the endothelial function, increase blood flow, and inhibit thrombus formation, which are independent of lipid-lowering effects. However, whether statins have a protective effect toward hemorrhagic stroke is yet unknown. To test this possibility, we attempted to determine the effect of atorvastatin on experimental intracerebral hemorrhage (ICH). METHODS: ICH was induced using stereotaxic infusion of collagenase into the left basal ganglia in adult rats. Atorvastatin (1 mg/kg or 10 mg/kg) or phosphate-buffered saline was administered for 2 weeks. To monitor the sensorimotor deficits, limb placing and Rotorod tests were performed. Hematoma volume, brain water content, and hemispheric atrophy were analyzed. Immunohistochemical staining for myeloperoxidase (MPO), microglia (OX42), inducible nitric oxide synthase (iNOS), or endothelial nitric oxide synthase (eNOS) was performed. Perihematomal cell death was determined by TUNEL staining. RESULTS: The atorvastatin-treated ICH group showed better performance on Rotorod and limb placing tests when compared with the vehicle-treated group (P<0.01). The hematoma volumes between groups were not different, but the brain water content and hemispheric atrophy were reduced in the atorvastatin-treated ICH group. Atorvastatin reduced TUNEL-positive cells, iNOS expression, and MPO-positive or OX42-positive cells in the perihematomal regions in a dose-dependent manner, whereas it increased eNOS expression. CONCLUSIONS: The present study shows that atorvastatin reduces the perihematomal cell death via antiinflammation, which is associated with sensorimotor recovery after experimental ICH.
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Diffusion-weighted MRI and 99mTc-HMPAO SPECT in delayed relapsing type of carbon monoxide poisoning: evidence of delayed cytotoxic edema.
BACKGROUND: Carbon monoxide (CO) is a common cause of poisoning, and its sequelae include a progressive (25%) and a delayed relapsing form (75%). We report the diffusion-weighted MRI (DWI) findings in the delayed relapsing form of CO poisoning and characterize the types of edema. METHODS: From November 1, 2000 to June 1, 2003, 5 consecutive patients (2 men, 3 women, range of age: 54-67 years), who had the delayed relapsing type of CO poisoning, underwent DWI, conventional MRI, MR angiography and SPECT. CO poisoning was diagnosed by the presence of a typical clinical history, an abnormally increased level of serum carboxyhemoglobin and MRI findings. Apparent diffusion coefficient (ADC) values were measured in all of the abnormal lesions with visual inspection of DWI and T(2)-weighted echo-planar imaging. RESULTS: DWI showed high signal intensities in bilateral periventricular white matter, in the splenium of the corpus callosum, in internal capsules, and brainstem showing moderately decreased ADC values. In the globus pallidus, the ADC values were rather increased with low signal intensities on DWI. Brain SPECT showed decreased perfusion in bilateral white matter and some parts of the cerebral cortex, which correlated well with the DWI findings. CONCLUSIONS: We suggest that prominent, symmetric restricted diffusion can occur in periventricular white matter, brainstem, and corpus callosum after the delayed relapsing type of CO poisoning. Delayed cytotoxic edema can occur in this setting, which provides a new guidance for the pathogenesis of CO poisoning and the differential diagnosis of white matter diseases.
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Clinical and radiologic differences between primary intracerebral hemorrhage with and without microbleeds on gradient-echo magnetic resonance images.
BACKGROUND: Microbleeds on gradient-echo magnetic resonance (MR) imaging reflect bleeding-prone microangiopathy. The microbleeds are frequently detected in patients with primary intracerebral hemorrhage (PICH). However, some patients do not have microbleeds. OBJECTIVE: To clarify the risk factors associated with microbleeds in PICH, thus providing insight into the pathogenesis of PICH. DESIGN: Prospective study. SETTING: Neurology department of a tertiary referral center. Patients A consecutive series of 107 patients with PICH. INTERVENTIONS: Gradient-echo MR imaging to determine distribution patterns and numbers of microbleeds. MAIN OUTCOME MEASURES: Clinical variables and the associated MR imaging abnormalities in patients with PICH with and without microbleeds. RESULTS: Patients with PICH who had microbleeds were significantly older (65.9 +/- 10.9 years) than those without microbleeds (53.9 +/- 13.0 years; P<.001), and previous stroke, medication with antithrombotics or anticoagulants, lacunes, and leukoaraiosis were more common in patients with microbleeds. However, potential triggering events tending to raise the blood pressure were more common in cases of PICH without microbleeds (18 [56.3%] vs 10 [15.4%]). In logistic regression analysis, age (odds ratio and 95% confidence interval: 1.07, 1.01-1.14), advanced leukoaraiosis (7.79, 1.05-57.74), number of lacunes (1.66, 1.21-2.28), and potential triggering events (0.18, 0.04-0.90) were independent risk factors associated with the presence of microbleeds in patients with PICH. CONCLUSIONS: Primary intracerebral hemorrhage without microbleeds was more common in younger patients with precipitating events, whereas PICH with microbleeds was more common in elderly patients with prominent ischemic change and frequent use of antithrombotics or anticoagulants. Our findings might help to determine the pathogenetic type for secondary prevention.
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Distribution and in situ proliferation patterns of intravenously injected immortalized human neural stem-like cells in rats with focal cerebral ischemia.
Neural stem cells are considered as a candidate for cell replacement therapy in various neurological diseases. To investigate whether human neural stem cells can migrate into the adult ischemic rat brain, we transplanted immortalized human neural 'tem-like' cells intravenously 24 h after focal cerebral ischemia. The intravenously injected human neural stem-like cells were found around the infarcted area, differentiated into neurons and astrocytes in the lesioned areas, and survive up to 56 days after transplantation. The number of the injected cells increased between 7 and 14 days after transplantation with incorporating BrdU. Our findings show that intravenously injected human neural stem-like cells may incorporate into the ischemic brain, and undergo proliferation responding to the endogenous mitotic signal during the acute period of focal ischemia.
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Diffusion changes suggesting predominant vasogenic oedema during partial status epilepticus.
Diffusion-weighted imaging (DWI) has demonstrated a focal area of cytotoxic oedema during partial status epilepticus (PSE). However, vasogenic oedema related to the breakdown of the blood-brain-barrier (BBB) and ictal hyperperfusion could be the predominant DWI findings in the epileptogenic area during PSE. We report a case of PSE with ictal aphasia, right hemiparesis, and repetitive focal motor seizure of the right side. T2-weighted image (T2WI) and apparent diffusion coefficient (ADC) maps obtained during PSE showed an increased signal in the left temporo-parietal area, indicative of vasogenic oedema. EEG documented the ictal activities and single photon emission tomography (SPECT) showed asymmetrically increased perfusion in the corresponding area. Follow-up T2WI, DWI, and ADC maps obtained 3 months later showed the disappearance of the previous abnormalities. However, T2WI showed cortical atrophy and newly developed white matter changes in the corresponding area. This case shows that DWI findings may be variable during PSE, dependent on the predominance of cytotoxic and vasogenic oedema.
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Celecoxib induces functional recovery after intracerebral hemorrhage with reduction of brain edema and perihematomal cell death.
The selective cyclooxygenase-2 (COX-2) inhibitor has been reported to have antiinflammatory, neuroprotective, and antioxidant effects in ischemia models. In this study, the authors examined whether a selective COX-2 inhibitor (celecoxib) reduces cerebral inflammation and edema after intracerebral hemorrhage (ICH), and whether functional recovery is sustained with longer treatment. ICH was induced using collagenase in adult rats. Celecoxib (10 or 20 mg/kg) was administered intraperitoneally 20 minutes, 6 hours, and 24 hours after ICH and then daily thereafter. Seventy-two hours after ICH induction, the rats were killed for histologic assessment and measurement of brain edema and prostaglandin E2. Behavioral tests were performed before and 1, 7, 14, 21, and 28 days after ICH. The brain water content of celecoxib-treated rats decreased both in lesioned and nonlesioned hemispheres in a dose-dependent manner. Compared with the ICH-only group, the number of TUNEL-positive, myeloperoxidase-positive, or OX42-positive cells was decreased in the periphery of hematoma and brain prostaglandin E2 level was reduced in the celecoxib-treated group. Celecoxib-treated rats recovered better by the behavioral tests at 7 days after ICH throughout the 28-day period, and the earlier the drug was administered, the better the functional recovery. Evidence of similar effects in an autologous blood-injected model showed that direct collagenase toxicity was not the major cause of inflammation or cell death. These data suggest that celecoxib treatment after ICH reduces prostaglandin E2 production, brain edema, inflammation, and perihematomal cell death in the perihematomal zone and induces better functional recovery.
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Continuous cytosine-b-D-arabinofuranoside infusion reduces ectopic granule cells in adult rat hippocampus with attenuation of spontaneous recurrent seizures following pilocarpine-induced status epilepticus.
Brief or prolonged seizures induce various patterns of plasticity. Axonal or dendritic remodelling and development of ectopic granule cells have been described in the hilus and molecular layer of the adult rodent hippocampus. Hippocampal cell proliferation also occurs after seizures. However, whether the seizure-induced cell proliferation plays a pathological or reparative role in the epileptic brain is unknown. In this study, we attempted to suppress the seizure-induced cell proliferation with the antimitotic agent cytosine-b-D-arabinofuranoside (Ara-C) and to examine the development of spontaneous recurrent seizures (SRS). Experimental status epilepticus was induced with pilocarpine, and Ara-C or vehicle alone was infused continuously with an osmotic minipump. SRS were video-monitored. BrdU immunohistochemistry was used for the spatial and temporal analysis of hippocampal cell proliferation, and double labelling with NeuN, calbindin and GFAP antibodies was performed for the differentiation of BrdU-positive cells. Timm staining was also performed for evaluation of mossy fibre sprouting (MFS). With continuous Ara-C infusion, the likelihood of developing SRS was decreased and, during the latent period, the development of ectopic granule cells in the hilus and new glia in the CA1 area was reduced when compared with the vehicle-infused group, while MFS was not altered. The results suggest that the hippocampal cell proliferation plays a pro-epileptogenic role rather than a compensatory role, and that the epileptogenic process may be associated with the generation of new glia in the CA1 area and/or new neurons in the dentate gyrus, particularly the ectopically located hilar granule cells.
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Hyperglycemia exacerbates brain edema and perihematomal cell death after intracerebral hemorrhage.
BACKGROUND AND PURPOSE: Hyperglycemia has a deleterious effect on brain ischemia. However, the effect of hyperglycemia in intracerebral hemorrhage (ICH) is not well known. We investigated the effect of hyperglycemia on the development of brain edema and perihematomal cell death in ICH. METHODS: Hyperglycemia was induced by intraperitoneal injection of streptozotocin (60 mg/kg) in adult Sprague-Dawley male rats. ICH was induced by stereotaxic infusion of 0.23 U of collagenase into the left striatum. Seventy-two hours after ICH, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining was performed for perihematomal cell death. We also measured brain water content to evaluate edema formation. RESULTS: The serum glucose level of the hyperglycemic group was 394.0+/-180.3 mg/dL (n=31), and that of the normoglycemic group was 97.5+/-27.4 mg/dL (n=31). The size of hemorrhage was similar between groups, without any significant difference (n=8 in each group). The brain water content of hyperglycemic rats (n=17) increased in both lesioned (81.0+/-0.5%) and nonlesioned hemispheres (78.7+/-0.6%) compared with the normoglycemic group (n=17; lesioned: 78.9+/-0.8%; nonlesioned: 77.3+/-1.1%). In the hyperglycemic group, more TUNEL-positive cells were found in the perihematomal regions (n=6). CONCLUSIONS: Hyperglycemia caused more profound brain edema and perihematomal cell death in experimental ICH.
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Human neural stem cell transplantation promotes functional recovery in rats with experimental intracerebral hemorrhage.
BACKGROUND AND PURPOSE: Cell transplantation has been used to reduce behavioral deficit in cerebral ischemia. However, there is no report about cell transplantation in experimental intracerebral hemorrhage (ICH). We hypothesize that intravenously transplanted human neural stem cells (NSCs) can migrate and differentiate into neurons or glial cells, thereby improving functional outcome in ICH. METHODS: Experimental ICH was induced by intrastriatal administration of bacterial collagenase in adult rats. One day after surgery, the rats were randomly divided into 2 groups to receive intravenously either immortalized Lac z-positive human NSCs (5x10(6) cells in 500 microL, n=12) or the same amount of saline (n=13). The animals were evaluated for 8 weeks with modified limb placing and rotarod tests. Transplanted NSCs were detected by X-gal histochemistry or beta-gal immunohistochemistry with double labeling of GFAP, NeuN, neurofilament, or CNPase. RESULTS: Intravenously transplanted NSCs migrated selectively to the perihematomal areas and differentiated into neurons (approximately 10% of beta-gal+ cells) and astrocytes (approximately 75%). The NSC-transplanted group showed better functional performance on rotarod test after 2 weeks and on modified limb placing test after 5 weeks compared with the control group (P<0.05), and these effects persisted for up to 8 weeks. There was no difference in the final hemispheric area between the 2 groups. CONCLUSIONS: Intravenously transplanted NSCs can enter the rat brain with ICH, survive, migrate, and improve functional recovery. Transplantation of human NSCs can be used to restore neurological deficits in experimental ICH.
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Human neural stem cells can migrate, differentiate, and integrate after intravenous transplantation in adult rats with transient forebrain ischemia.
Intraparenchymally transplanted rodent-origin neural and human-origin mesenchymal stem cells migrate and differentiate in neurological diseases. By intravenously injecting human neural stem cells, we showed that transplanted human neural stem cells migrate to the damaged hippocampus, proliferate and differentiate into mature neurons and astrocytes in the adult rat brain with transient forebrain ischemia. We also demonstrated the migratory course of implanted human neural stem cells after intravenous injection. Our findings show that transplanted human neural stem cells differentiate into mature neurons to replace lost neural cells in the adult hippocampus with human-rat neural chimeras.
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Cerebral cavernous malformations with dynamic and progressive course: correlation study with vascular endothelial growth factor.
BACKGROUND: Cerebral cavernous malformations (CCMs) are reported to exhibit a wide range of dynamic patterns including growth, regression, and de novo formation, which generally show slow and steady courses. Although the pathogenesis of CCMs is not well known, vascular endothelial growth factor (VEGF) has been suggested as a possible mediating factor. OBJECTIVES: To report CCMs showing rapid progression over a short period and to investigate these biological characteristics. DESIGN: Experimental study. SETTING: Tertiary referral center, neurology department. Patient A 40-year-old man was admitted because of a left-sided numbness, vertigo, and ataxia, which were attributed to a pontine hemorrhage. He had experienced a left-sided weakness 6 months before admission, and thereafter had complained of intermittent headache. Serial brain magnetic resonance images showed multiple intracerebral microhemorrhages throughout the cerebral hemispheres. A biopsy of the lesion confirmed the diagnosis of CCM. MAIN OUTCOME MEASURES: We investigated the expression of VEGF by immunohistochemistry of the biopsy specimen. Dynamic patterns of CCMs, obtained with spin-echo magnetic resonance images with gradient-echo sequences, were compared with serial serum VEGF concentrations, determined by enzyme-linked immunosorbent assay. RESULTS: Immunohistochemistry of the specimen displayed increased VEGF expression. Serial magnetic resonance images during 7 months showed dynamic signal changes of the preexisting lesions and 15 de novo formations in many cortices. The VEGF level in serum increased during this dynamic period and became normal during the steady and resolving stages. CONCLUSIONS: Cerebral cavernous malformations can be progressively deteriorating. The endothelial proliferation induced by VEGF is likely to be an important aspect of the pathogenetic mechanisms of CCMs.
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POEMS syndrome associated with ischemic stroke.
BACKGROUND: A syndrome variously combining peripheral neuropathy, visceromegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS syndrome) is a rare variant of plasma cell dyscrasia with multisystemic manifestations. Acute ischemic strokes in patients with POEMS syndrome have rarely been reported, and the pathophysiologic mechanism of this disease is unknown. Fibrinogen is reported to be an independent risk factor for cerebrovascular disease and is correlated with the interleukin 6 level in the plasma. The serum level of interleukin 6 is high in the active stage of POEMS syndrome. OBJECTIVE: To describe the neuroimaging findings and fibrinogen levels in patients with POEMS syndrome. DESIGN: Case series. SETTING: The neurology department of a tertiary referral center. METHODS: Three patients with an acute cerebral infarction associated with POEMS syndrome underwent magnetic resonance imaging, diffusion-weighted imaging, magnetic resonance angiography, transcranial Doppler ultrasonography, and serum fibrinogen level and serum C-reactive protein level analysis. The serum fibrinogen level before the stroke was collected retrospectively from the hospital medical records. RESULTS: There was an elevated fibrinogen level in all of the patients. In 2 patients, unilateral or bilateral end artery border-zone infarcts were observed on the brain magnetic resonance imaging scan. The serum fibrinogen level was high before the stroke in 2 patients. CONCLUSIONS: The POEMS syndrome can be associated with stroke, particularly end artery border-zone infarctions. We suggest that an elevated fibrinogen level might play a role in the pathogenesis of stroke.
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