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.

No abstract available.
Diagnosis* ; Encephalitis, Herpes Simplex* ; Herpes Simplex*

We reviewed forty five cases of intracranial arteriovenous malformation (AVM) who were admitted in Seoul National University Hospital within recent 7 years; thirty one patients revealed intracerebral hemorrhage and fourteen patients showed seizure or progressived focal neurologic deficit as an initial presentation. To evaluate the natural history of AVM after initial hemorrhage, out of these 45 cases, we selected 22 cases who were, operated or not, observed naturally for at least 1 year. To know the post operative course, we also selected 18 cases who were operated on. Thses two groups were compared with respect to the mortality, morbidity, frequency of rebleeding or seizure, which were 9%, 27%, 55%, 27%, in the former, and 0%, 17%, 0%, and 28% in the latter. Among the 14 patients whose initial presentation was not intracranial bleeding, 9 had seizure, 5 had progressive focal neurologic deficit, and 4 had both. During the follow-up period (average 5 years), only one patient had intracranial bleeding. Seizures in this group were relatively well controlled by regular antiepileptic regimen. Out of the 2 cases who were operated for seizure control, one had considerable degree of neurologic deficit after operation. From above evidences, we tentatively conclude that the AVM with initial bleeding should be better operated on if accessible, whereas the AVM without initial bleeding should be best managed conservatively. For a more definite conclusion, large, radomized controlled studies should be done again which, however, may meet ethical problems.
Cerebral Hemorrhage ; Follow-Up Studies ; Hemorrhage ; Humans ; Intracranial Arteriovenous Malformations* ; Mortality ; Natural History ; Neurologic Manifestations ; Seizures ; Seoul

BACKGROUND AND PURPOSE: Cerebrovascular reactivity (CVR) can be estimated by measuring the change of cerebral blood flow that occurs during vasostimulation. To estimate the cerebrovascular reactivity, we investigated the change of flow velocity of the internal carotid artery (ICA) and the middle cerebral artery (MCA) during hyperventilation and hypoventilation with the transcranial doppler. So we studied whether the CVR measured by this method could show a significant difference between the normal and the atherosclerotic subjects and whether the CVR may decrease with age in normal gubjects. METHODS: Using transcranial doppler, we measured the mean velocity (Vm), the pulsatility index (P.I.) at the resting state, the end of breath-holding and the end of hyperventilation in 30 normal and 10 atherosclerotic subjects, so we calculated the percentile change of mean velocity (% Vm) and P.I. (% P.I.) after the vasostimulation. We estimated the change of Vm, P.I., % Vm and % P.I. By the age group and compared those parameters between the age-matched normal control and atherosclerotic subjects. RESULTS: The Vm in ICA and MI significantly decreased with age (p<0.01), but there was no significant difference in Vm and P. I. Between normal and atherosclerotic subjects. The % Vm and % P.I. In response to hyperventilation significantly decreased with age in ICA, M1, M2 and there was significant difference in % Vm of ICA and M1 after breath-holding and % Vm of ICA after hyperventilation between the normal and atherosclerotic subjects. CONCLUSION: The breath-holding and hyperventilation tests could be non-invasive and useful methods in estimation of the cerebrovascular reactivity and could be applied in the basal and follow-up evaluation of the cerebrovascular reserve of the ischemic stroke patients.
Carotid Artery, Internal ; Humans ; Hyperventilation ; Hypoventilation ; Middle Cerebral Artery ; 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: 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

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