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

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

BACKGROUND & OBJECTIVE: Recent studies suggest that anticoagulation, or antiplatelet therapy is safe and effective for the prevention of cardiogenic embolic stroke. However it has not been studied in Korea how the patients with cardioembolic source were managed in practice for the prevention of stroke. This study was done to assess the current status of primary and secondary prevention of cardioembolic stroke. METHODS: Retrospective study was undertaken in 124 patients with cardiogenic embolic stroke, following items were examined, previous anticoagulation or antiplatelet therapy, previous stroke, Insight of the heart disease, and International Normalize Ratio(INR) value on arrival at the hospital. RESULTS: In 124 patients cardioembolic sources were constituted of non-valvular atrial fibrillation (NVAF) in 54, rheumatic heart disease In 40, prosthetic cardiac valve In 14, dilated cardiomyopathy(D-CMP) in 6, left ventricular akinetic segment in 7(including 3 cases of LV thrombi), recent myocardial infarction in 3. In 93 patients with no previous stroke, 44 patients had regular medical follow-up because of his/her cardiac problems and primary prevention of stroke was made only in 12 (27%) patients (8 on anticoagulation and 4 on antiplatelet therapy). The rate of primary prevention varied according to the type of cardioembolic source; 100% with mechanical prosthetic valve, 33.3% with valvular atrial fibrillation, 6.7% with NVAF, and none with D-CMP and bioprosthetic valve. Previous stroke was found in 31 patients, among whom 24 had been followed regularly. Twenty patients(83%) were under secondary prevention of cardioembolic stroke (anticoagulation in 11 and antiplatelet agents in 9). Among 19 patients who developed stroke in spite of anticoagulation, INR values were lower than 1.5 in 12(63%), between 1.5 and 2.0 in 5(26%), and above 2.0 in 2(11%). CONCLUSION: Our results suggest that cardioembolic strokes have not been prevented properly. Many physicians seem to be reluctant to anticoagulate their patients with cardioembolic source, and even with anticoaguation the dosage is frequently insufficient to prevent stroke.
Atrial Fibrillation ; Follow-Up Studies ; Heart Diseases ; Heart Valves ; Humans ; International Normalized Ratio ; Korea ; Myocardial Infarction ; Platelet Aggregation Inhibitors ; Primary Prevention ; Retrospective Studies ; Rheumatic Heart Disease ; Secondary Prevention ; Stroke*

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

No abstract available.
Gait* ; Humans ; Spinal Cord Diseases*

We retrospectively analyzed 29 patients with caudate hemorrhage, and evaluated the prognosis and the predictors of short-term and long-term outcomes. P With caudate hemorrhage showed better short-term outcome compared to those with intracerebral hemorrhages in general. However, the ciance re -ing was Rebleedmg, which had interval of less than 1 year in most cases, occurred mainly in patients with previous stroke. And this worsened the patients' outcome. Management of risk factors is critical. The prognostic factor influencing on the short-term outcome was the initial consciousness level and the long-term outcome could be anticipated through the evaluation of the neurologic status on the 30th day; subsequent improvement was expected in patients with mild abnormality, but not in those with moderate to severe disability.
Cerebral Hemorrhage ; Consciousness ; Hemorrhage* ; Humans ; Prognosis* ; Retrospective Studies ; Risk Factors ; Stroke

BACKGROUND: Transient global ischemia causes delayed neuronal death (DND) in the CA1 area, of which the mecha-nism is controversial. Induction of apoptosis-regulating proteins during the process of DND has been reported, howev-er ,the exact role of Bcl-2/Bax is not well understood. We tried to reveal the pattern of the Bax/Bcl-2 expression modi-fied by the duration of ischemia and hypothermia. METHODS: Global ischemia was induced in Mongolian gerbils for 2, 5, and 10 minutes under the temperature of 36 degrees C and 32 degrees C. Hippocampal sections were evaluated 48 hours after ischemia with H&E and immunohistochemical staining to Bcl-2/Bax. Viable neuronal density and semi-quantitative grading were compared. RESULTS: In the CA1 area, neurons were intact in 2 min ischemia, while partial or significant ischemic changes were observed in 5-10 min ischemia of 36 degrees C setting, which were less severe in 32 degrees C . Bcl-2 was posi-tive in 2 min ischemia, while negative in 5~10 min ischemia of 36 degrees C . Bax was negative in 2 and 10 min ischemia, while positive in 5 min ischemia. In 32 degrees C setting, Bcl-2 was also positive in 2 min ischemia and partially positive in 5- 10 min ischemia, although Bax expression was not different from 36 degrees C. CONCLUSIONS: The complex mechanism of DND, which is in the spectrum of apoptosis and necrosis, seems to be determined by the severity of ischemia. The bal-ance between Bcl-2 and Bax may determine the survival of neurons in mild to moderate ischemia. Further evidence remains to be determined by morphological and molecular biological methods.
Apoptosis ; Body Temperature* ; Gerbillinae ; Hypothermia ; Ischemia* ; Necrosis ; Neurons

To evaluate the difference in prognosis between hypertensive (HTN) and normotensive (NTN) cerebellar hemorrhages, we compared 20 HTN with 7 NTN patients with cerebellar hemorrhage. A series of 27 cerebellar hemorrhages diagnosed by CT scan in Seoul National University Hospital were divided into two groups: hypertensive(HTN) and normotensive (NTN). We analyzed two groups about clinical and radiological findings including outcome. We also evlauated the factors that had an effect on the prognosis of cerebellar hemorrhage. The etiologies of NTN were AVM in four, tumor in two and one unknown cause. The prognostic factors in both groups were initial consciousness level, degree of hydrocephalus, quadrigeminal cisternal obliteration, hematoma size and volume while the differences between HTN and NTN were age, hematoma size and volume, quadrigeminal obliteration and outcome. Therefore, the hematoma size. Volume and quadrigeminal cisternal obliteration might lead to poorer outcome in HTN group. We concluded that hypertensive cerebellar hemorrhages revealed poorer progonsis than normotensive cerebellar hemorrhage and hypertension should be considered as an underlying factor determining the prognosis of cerebellar hemorrhages.
Consciousness ; Hematoma ; Hemorrhage* ; Humans ; Hydrocephalus ; Hypertension ; Prognosis* ; Seoul ; Tomography, X-Ray Computed

It has recently been known that the temperature of the brain during a period of transient cerebral ischemia can critically influence neuropathologic outcome in experimental animals. Thus the severity of brain edema may be thought to be changed according to body temperature during acute stage of cerebral ischemia. We investigated the effects of hypothermia and hyperthermia on the acute brain edema during the transient global ischemia in Mongolian gerbils. During 20 miuntes of global ischemia, body temperatures were maintained at 35* in the hypothermic group (n=10). 37* in the normothermic group (n=10). 39* in the hyperthermic group (n=10). Respectively. During the period of reperfusion. Body temperatures were maintained at 37* in each group. Two hours after reperfusion. The animals were decapitated and the waler content of the brain was determined by oven dry method. The uater content were high in (1) the hyperthermic group (79.5+0.3%). (2) the normothermic group (79.2+0.2%). (3) the hypothermic group (79.0+0.2%) the control group (78.6+0.3%) in order of amount. Also there were significant differences of the water content among four groups according to the changes of intraischemic body temperature (p<0.05). At the same time we carried out another experiment for comparing the survival rates in each group. The survival rate of the hypothermic group was sillgificantly higher than that of the normothermic or the hyperthermic groups (p<0.005).
Animals ; Body Temperature* ; Brain Edema* ; Brain Ischemia ; Brain* ; Fever ; Gerbillinae* ; Hypothermia ; Ischemia* ; Ischemic Attack, Transient ; Reperfusion ; Survival Rate* ; Water

BACKGROUND: In experimental cerebral ischemia, hypothermia protects the brain, while hyperglycemia aggravates ischemic damage. Clinical studies have also reported worse outcomes in ischemic stroke patients with hyperglycemia or fever and improved outcomes with hypothermic therapy. However, it is not well known what will happen if these opposite effects exist together. METHODS: Sixty male Sprague-Dawley rats were used. Focal cerebral ischemia was induced for 2 hours by an intraluminal thread followed by reperfusion for 4 hours. Rats were divided into 4 groups; 1) normo-glycemic normothermic (NGNT), 2) normoglycemic hypothermic (low temperature) (NGLT), 3) hyperglycemic normothermic (HGNT), and 4) hyperglycemic hypothermic (HGLT) groups (n=15 for each group). Hyperglycemia wasmade by intraperitoneal injection of streptozotocin (60 mg/kg) 3 days before ischemia. The body temperature was maintained at 37+/-1 degrees C in normothermic animals, while lowered at 32+/-1 degrees C in hypothermic animals during the ischemic period. Following reperfusion, 2-mm thick coronal slices were obtained and stained by triphenyltetrazolium chloride. The infarct volume was measured using an image analyzer. RESULTS: Mean glucose levels (mean+/-SD in mg/dl) were 77.9+/-9.3 in NGNT, 77.7+/-11.5 in NGLT, 311.0+/-69.2 in HGNT, and 355.3+/-57.7 in HGLT. Mean infarct volumes (mean+/-SD in mm 3) were 168.2+/-44.2 in NGNT, 66.2+/-24.2 in NGLT, 417.6+/-123.2 in HGNT, and 337.2+/-89.3 in HGLT. The protective effect of hypothermia was less evident in hyperglycemic rats and the aggravating effect of hyper-glycemia was more evident in hypothermic rats. Infarct volume of HGLT was 2-fold bigger than that of NGNT (p<0.05). CONCLUSIONS: Our results suggest that the detrimental effect of hyperglycemia may override the protective effect of hypothermia in transient focal cerebral ischemia.
Animals ; Body Temperature ; Brain ; Brain Ischemia* ; Fever ; Glucose ; Humans ; Hyperglycemia* ; Hypothermia* ; Injections, Intraperitoneal ; Ischemia ; Male ; Rats* ; Rats, Sprague-Dawley ; Reperfusion ; Streptozocin ; Stroke