Stroke is a common cause of death in South Korea. The etiology of stroke affects prognosis, outcome, and management. Trials of therapies for patients with acute stroke should include measurement of responses as influenced by the subtypes of stroke. Stroke can be classified into ischemic and hemorrhagic stroke. Ischemic stroke classification denotes five subtypes of ischemic stroke : ① large-artery atheromatous disease, ② cardioembolism, ③ lacunes, ④ stroke of other causes, and ⑤ transient ischemic attack. Hemorrhagic stroke can be classified into ① intracerebral hemorrhage, ② subarachnoid hemorrhage, and ③ other hemorrhages. Stroke is a syndrome with various etiologies, and proper classification is important for the treatment and prognosis. Risk factors for stroke such as hypertension, heart disease, smoking, diabetes, and hypercholesterolemia should be controlled properly. Clinical trials testing new treatment for acute stroke are on-going worldwide, and it is appropriate to standardize the classification of stroke.
Cause of Death ; Cerebral Hemorrhage ; Cerebrovascular Disorders* ; Classification* ; Heart Diseases ; Hemorrhage ; Humans ; Hypercholesterolemia ; Hypertension ; Ischemic Attack, Transient ; Korea ; Prognosis ; Risk Factors ; Smoke ; Smoking ; Stroke ; Subarachnoid Hemorrhage

No abstract available.
Gait*

Reviewing of each parameters of MRI and PET scan in thirteen acute ischemic stroke patients according to their ROIs based on the lesion in MRI, lesion-cores and lesion-peris in MRI are relatively well correlated with infarction and ischemia of the PET criteria respectively. Among the parameters of PET scan, CMRO2 values seem to be bst correlated with T1 and T2 changes of the lesions in MRI of acute ischemic stroke. As those parameters of both imaging techniques are more related with the pathologic site than the type of the stroke, the changes of the parameters in stroke are greater when the lesion is located in cerebral cortex than in white matter. It is assumed that T2 change occurs in the early stage of the ischemic insult followed by more prominet T1 change with increase of water content which leads to the infarction of the tissue, but further confirmation is needed.
Cerebral Cortex ; Humans ; Infarction ; Ischemia ; Magnetic Resonance Imaging* ; Positron-Emission Tomography ; Statistics as Topic* ; Stroke*

Persistent trigeminal artery is an embryonic remnant of the anastomotic channel linking the internal carotid artery and the basilar artery. Cases of vertebrobasilar insufficiency caused by the persistent trigeminal artery with internal carotid artery stenosis has been described previously, but vertebrobasilar insufficiency entirely due to in situ stenosis of the persistent trigeminal artery has not been reported. A 71-year-old man presented with frequent dizzy episodes. The brain MRI showed no parenchymal lesions. MR angiography showed poor visualization of vertebrobasilar system. He was diagnosed as having vertebrobasilar insufficiency. Cerebral angiography revealed that there was complete occlusion at the vertebrobasilar junction, and the basilar artery was supplied by the persistent trigeminal artery which had severe stenosis at its origin. There was no stenosis of the internal carotid artery of both sides. We believe that this is the first report of vertebrobasilar insufficiency due to stenosed persistent trigeminal artery, without internal carotid artery stenosis.

BACKGROUND: Cerebral cortical dysplasia (CD) is one of the important causes of intractable epilepsies and characterized histologically by disorganized cortical lamination and cytomegalic dysplastic neurons. Although various cytoskeletal abnormalities have been found in dysplastic neurons of CD, the pathogenetic role of dysplastic neurons has rarely been investigated. METHODS: In this study, immunohistochemical analysis was performed using antibodies against non-phosphorylated high- or medium-molecular weight neurofilament protein and microtubule-associated protein 2 (MAP-2) in surgical specimens of CD. In order to know the possible relationship of dysplastic neurons with cytoskeletal abnormalities and various neurotrophin receptors, NGFR p75, trkA, trkB, and trkC immunoreactivities were also analyzed. RESULTS: Dysplastic neurons showed strong immunoreactivities for non-phosphorylated high- or medium-molecular weight neurofilament protein and MAP-2, which might reflect abnormal outgrowth and altered plasticity of the dysplastic neurons. TrkB and trkC were strongly expressed in dysplastic neurons and NGFR p75 was also strongly expressed in some dysplastic neurons. CONCLUSIONS: Since it has been known that brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) have effects on the differentiation of neuronal precursor cells from the cortex and on dendritic and axonal arborization, increased expression of trkB and trkC may play a role in cytoskeletal abnormalities and altered synaptic transmission in dysplastic neurons.
Antibodies ; Axons ; Brain-Derived Neurotrophic Factor ; Epilepsy ; Malformations of Cortical Development* ; Microtubule-Associated Proteins ; Neurons* ; Plastics ; Receptors, Nerve Growth Factor ; Synaptic Transmission

OBJECT: To analyze clinical'data about the patients presenting with altered consciousness in the emergency room and to plan adequate evaluations and managements. BACKGROLTND. Clinical analysis of comatose patients is necessary. We have a few reports but they don't give enough clues to evaluate the patients rapidly and systematically. METHOD: We included the patients with altered consciousness on the base of the daily reports of emergency room, and reviewed the medical records of the patients. We analyzed the age, sex, visiting date, the patterns of discharge of emergency room, underlying causes, and consequences of the patients. The validity of the contents of daily reports was tested by pilot study. In pilot study, we examined all patients entering emergency room for a week, and compared contents of daily reports with the data acquired from direct examination. RESULTS: The pilot study revealed that the method of patient selection had no problem statistically. The nwnber of patients with altered consciousness entering emergency room, was 594 for one year. The causes of altered consciousness consisted of metabolic problem (35.4%), hemorrhagic stroke (21.2%), malignancy (9.26%), nonhemorrhagic stroke (8. 1%), and others. The causes of metabolic coma werehepatic encephalopathy (69.5%), glucose and electrolyte problem (12.9/o), drug intoxication (6.67%), uremic encephalopathy (6.19%) and alcohol related illness (4.76%). Metabolic coma patients showed better prognosis than others, and hemorrhagic stroke and malignancy showed poor prognosis. The ischemic stroke patients were older than others. Considering the age of the patients, the younger men had better clinical courses than elderly. Significant seasonal variation was notfound. CONCLUSION: The patients visitmg emergency room with altered consciousness had various causes. The most common cause was metabolic origin followed by hemorrhagic stroke. Under the influence of the improvement of socioeconomic status and longevity, the distributions of the underlying disease have changed. The prognosis and consequence of them relied on underlying diseases and age.
Aged ; Coma ; Consciousness* ; Emergencies* ; Emergency Service, Hospital* ; Glucose ; Humans ; Longevity ; Male ; Medical Records ; Patient Selection ; Pilot Projects ; Prognosis ; Seasons ; Social Class ; Stroke

BACKGROUND AND PURPOSE: Current therapy for acute ischemic stroke is highly focused on neuroprotective agents, and many ion channel blockers have been challenged for experimental models. In this study, we tried to reveal the neuroprotective effect of lamotrigine, a voltage-sensitive sodium channel blocker, for transient global ischemia of Mogolian gerbil. METHODS: Lamotrigine (50mg/kg) was administered via gastric tube 30 minutes before and after global ischemia (for 10 min) under body temperature monitoring. Sham-operated and non-treated ischemia group were compared. Seven days after reperfusion, gerbils were killed with perfusion/fixation technique and representative sections were cut through the hippocampus. Hematoxylin-Eosin staining was done for microscopic examination and number of viable neurons in CA1 area was counted. RESULTS: Neuronal density was different between sham-operated (n=11), non-treated ischemic (n=11), and lamotrigine-treated (n=26) group (107.8+13.1/mm vs. 21.5+23.0/mm vs. 82.0+13.1/mm, p<0.01). Both pre-(n=17) and post-treated group (n=9) showed significant neuroprotective effect compared with non-treated group. Neuronal density of pre-treated group was slightly higher than in post-treated group, though statistically not significant (84.6+13.0/mm vs. 77.3+12.7/mm, p=0.13). CONCLUSION: These results show that lamotrigine may have some effects reducing the delayed neuronal death in transient global ischemia. Considering the mechanism of action, we suggest that activation of voltage-sensitive sodium channel and release of glutamate at early phase of ischemia may be related to the delayed neuronal death.
Body Temperature ; Cerebral Infarction ; Gerbillinae ; Glutamic Acid ; Hippocampus ; Ion Channels ; Ischemia* ; Models, Theoretical ; Neurons ; Neuroprotective Agents* ; Reperfusion ; Sodium Channels ; Stroke

Medial medullary infarction is usually manifested as hypoglossal palsy, limb weakness, impairment of proprioception, and oculomotor disturbance. We report a case with the unusual presentation of sensory ataxia. A 71 year-old male presented with ataxia and disequilibrium. Bilateral dysmetria, truncal ataxia, Upbeat nystagmus, and impaired vibration and position sense were the clinical features. However, weakness of the limbs, tongue, or face was not definite. MRI revealed bilateral lesion in the medullary tegmentum, and cortical potentials of somatosensory evoked response were absent. Recovery was fair after treatment. According to the literature, motor weakness is a cardinal manifestation in medial medullary infarction, and there has been no reported case presented as sensory ataxia preserving motor power. Current development of diagnostic tools would contribute to define a variety of clinical manifestations, topography, vascular concomitants, and prognosis in medial medullary infarction.
Aged ; Ataxia/*etiology ; Cardiovascular Diseases/diagnosis ; Case Report ; Cerebral Infarction/*complications/*diagnosis ; Diagnosis, Differential ; Human ; Magnetic Resonance Imaging ; Male ; Medulla Oblongata/*blood supply ; Syndrome

BACKGROUND: Cardiogenic embolic infarction is the most preventable type of ischemic stroke. This study was under-taken to compare the infarct size, prognosis, and risk factors between cardiogenic embolic infarction (CE) and large artery atherosclerotic infarction (LAA). METHODS:We reviewed the medical records and brain computed tomography/magnetic resonance image (CT/MRI) scans of patients with CE or LAA during the period between January 1996 and May 1998. Patients with lacunar and posterior circulation infarctions were excluded. A slice of brain CT/MRI scan showing the largest lesion was selected in each patient and the area of infarction was then measured. Prognosis was determined by the Modified Rankin Disability Scale (MRDS) and was grouped as either good (MDRS 0, 1, 2) or poor (MDRS 3, 4, 5). RESULTS: The study included 103 patients : 50 with CE (NVAF in 23, VHD with or without AF in 13, prosthetic valve in 6, and others in 8) and 53 with LAA (large artery thrombosis in 29, and artery to artery embolism in 24). The infarct size of CE (23.2+/-14.7 cm2) was significantly larger than that of LAA (11.4+/-10.5 cm2) (p<0.001). The infarct size of NVAF (29.0+/-19.1 cm2) was significantly larger than that of VHD with or without AF (19.2+/-11.5 cm2) (p<0.05). Patients with CE had a worse prognosis (poor in 46%) than those with LAA (poor in 23%) (p<0.05). CONCLUSIONS Our results showed that CE led to larger lesions and worse outcomes. Therefore, we emphasize the importance of primary and secondary preventions of stroke in patients with cardiogenic embolic sources.
Arteries* ; Brain ; Embolism ; Heart Valve Diseases ; Humans ; Infarction* ; Medical Records ; Prognosis* ; Risk Factors ; Secondary Prevention ; Stroke ; Thrombosis

Transient ischemic attack (TIA) often precede cerebral infarcts as a warning symptom. But the studies revealing the frequency and the correlation between preceding TIAs and following infarcts are rare. According to the western data, about one-quarter of the patients with cerebral infarct have been supposed to have the previous history of TIAs. We prospectively studied the exact frequency, clinical presentation, and presumed causes of TIAs preceding cerebral infarct. Ninety five patients diagnosed as acute cerebral infarction were interviewed whether they had had previous episodes of TIA. 4 check-list using ordinary language was used, and NINDS diagnostic criteria was applied on the consensus between several neurologists. Seventeen patients (18%) had history of preceding TIAs. Carotid territory was affected in 11 patients (65%), while vertebrobasilar in 4(24%) and undetermined in 2. Duration was less than an hour in 10 patients(59%), and attacks were multiple in about half. Time interval between the last attack and infarction was less than one week in 10 cases(59%). Incidence of recent TIA ((1 month) was 22% in large artery disease(LAD), 11% In cardioembolism(CE), 9% in small-artery disease(SAD), and 7% in mixed etiology. Conclusion, TIAs preceding cerebral infarcts are not rare, but seems to be less common in Koreans than in Caucasians. As expected, atherothrombosis of large artery is supposed to be the leading cause of TIAs.
Arteries ; Cerebral Infarction ; Consensus ; Humans ; Incidence ; Infarction ; Ischemic Attack, Transient* ; National Institute of Neurological Disorders and Stroke ; Prospective Studies