OBJECTIVETo establish a convenient method for preparing rabbit models of ischemic cerebral infarction using autologous clot embolism.

METHODSIschemic cerebral infarction was induced in rabbits by embolizing the middle cerebral artery using autologous clot emboli. Clinical and histological observations were carried out to evaluate the validity of the animal model.

RESULTSHemiplegia of different severities was observed in the rabbits after the operation. TTC and HE staining of the brain sections confirmed ischemic cerebral infarction 6 h after obstructing the middle cerebral artery with the autologous clot emboli.

CONCLUSIONEmbolizing the middle cerebral artery using the autologous emboli is convenient to induce focal ischemic cerebral infarction in rabbits. This model has practical value in the study on the mechanism of ischemic cerebrovascular disease and in developing new strategies for prevention and treatment of the relevant diseases in human.

Animals ; Cerebral Infarction ; etiology ; Disease Models, Animal ; Infarction, Middle Cerebral Artery ; etiology ; Male ; Rabbits ; Random Allocation

Brain Ischemia ; Cerebral Infarction ; Humans ; Subarachnoid Hemorrhage ; Vasospasm, Intracranial/etiology*

Central nervous system is often involved by herpes zoster but it is very rarely seen that contralateral hemiparesis or hemiplegia developed after herpes zoster ophthalmicus. We report a case of herpes zoster ophthalmicus followed by the delayed contralateral hemiparesis. A 33-year-old man developed acute cerebral infarction and resultant right hemiparesis 44 days after herpes zoster ophthalmicus in the left side. Brain CT disclosed hypodense area in the left basal ganglia. Cerebral angiography revealed segmental narrowing of M1 portion of the right middle cerebral artery.
Adult ; Cerebral Angiography ; Cerebral Arteries/pathology ; Cerebral Infarction/*etiology/radiography ; Dominance, Cerebral ; Hemiplegia/*etiology ; Herpes Zoster Ophthalmicus/*complications ; Humans ; Male ; Tomography, X-Ray Computed ; Vasculitis/etiology

Acupuncture Therapy ; Cerebral Hemorrhage ; complications ; Cerebral Infarction ; etiology ; therapy ; Humans ; Male ; Middle Aged

BACKGROUND: Single subcortical infarction (SSI) is caused by two main etiological subtypes, which are branch atheromatous disease (BAD) and cerebral small vessel disease (CSVD)-related SSI. We applied the Beijing version of the Montreal Cognitive Assessment (MoCA-BJ), the Shape Trail Test (STT), and the Stroop Color and Word Test (SCWT) to investigate the differences in cognitive performance between these two subtypes of SSI. METHODS: Patients with acute SSIs were prospectively enrolled. The differences of MoCA-BJ, STT, and SCWT between the BAD group and CSVD-related SSI group were analyzed. A generalized linear model was used to analyze the associations between SSI patients with different etiological mechanisms and cognitive function. We investigated the correlations between MoCA-BJ, STT, and SCWT using Spearman's correlation analysis and established cut-off scores for Shape Trail Test A (STT-A) and STT-B to identify cognitive impairment in patients with SSI. RESULTS: This study enrolled a total of 106 patients, including 49 and 57 patients with BAD and CSVD-related SSI, respectively. The BAD group performances were worse than those of the CSVD-related SSI group for STT-A (83 [60.5-120.0] vs. 68 [49.0-86.5], P = 0.01), STT-B (204 [151.5-294.5] vs. 153 [126.5-212.5], P = 0.015), and the number of correct answers on Stroop-C (46 [41-49] vs. 49 [45-50], P = 0.035). After adjusting for age, years of education, National Institutes of Health Stroke Scale and lesion location, the performance of SSI patients with different etiological mechanisms still differed significantly for STT-A and STT-B. CONCLUSIONS BAD patients were more likely to perform worse than CSVD-related SSI patients in the domains of language, attention, executive function, and memory. The mechanism of cognitive impairment after BAD remains unclear.
Cerebral Infarction ; Cerebral Small Vessel Diseases ; Cognitive Dysfunction/etiology* ; Executive Function ; Humans ; Mental Status and Dementia Tests

Cerebral Infarction ; complications ; Cerebral Veins ; pathology ; Humans ; Thrombosis ; Venous Thrombosis ; etiology

Cerebral Infarction ; etiology ; Dextrocardia ; etiology ; Female ; Humans ; Infant ; Spleen ; abnormalities ; Syndrome

Adult ; Cerebral Infarction ; etiology ; Humans ; Intraoperative Complications ; etiology ; Lung Neoplasms ; pathology ; surgery ; Male

OBJECTIVETo investigate the impact of obstructive sleep apnea-hypopnea syndrome (OSAHS) on cerebral microbleeds (CMBs) in patients with cerebral infarction.

METHODSConsecutive patients with acute cerebral infarction who had cerebral microbleeds shown by susceptibility-weighted imaging (SWI) were enrolled to undergo polysomnography (PSG). The patients were divided into two groups, namely non-OSAHS group with apnea-hypopnea index (AHI) less than 5 and OSAHS group with greater AHI, and the clinical and radiological features of cerebral microbleeds were compared between them.

RESULTSForty-nine patients were enrolled in this study, including 27 (55.1%) with both cerebral infarction and OSAHS and 22 (44.9%) with cerebral infarction but not OSAHS. A comparison of the risk factors showed that hypertension, a smoking history, and a history of stroke were more prevalent in patients with OSAHS than in those without OSAHS (P<0.05). The incidences of subclinical stroke in OSAHS and non-OSAHS patients were 37.0% (10/27) and 9.0% (2/22) (P<0.05), respectively. Neurological imaging revealed a greater number of cerebral microbleeds in OSAHS group than in non-OSAHS group (P<0.05). In OSAHS patients, 77.8% of the microbleeds were distributed in cortical-subcortical areas, 55.6% in the basal ganglia area, and 25.9% in the infratentorial area, as compared to the percentages of 50.0%, 40.9% and 50.0% in non-OSAHS patients, respectively (P<0.05). In OSAHS patients, 40.7% also had leukoaraiosis, and 48.1% had two or more causes, as compared to the percentages of 13.6% and 18.2% in non-OSAHS patients, respectively (P<0.05).

CONCLUSIONSOSAHS can be a risk factor for cerebral microbleeds. Patients with both cerebral infarction and OSAHS tend to have greater and more extensive lesions of cerebral microbleeds, more complicated cause of the disease, and a grater likeliness of stroke recurrence.

Aged ; Cerebral Hemorrhage ; etiology ; pathology ; Cerebral Infarction ; pathology ; Female ; Humans ; Male ; Middle Aged ; Risk Factors ; Sleep Apnea, Obstructive ; complications ; pathology

OBJECTIVETo study the plasma HCII activity and antigen level variations and their relationship with arterial and deep venous thrombotic diseases.

METHODSSeventy-five patients with brain infarction (BI), 50 myocardial infarction (MI), 36 deep venous thromboembolic disease (DVT) and 50 healthy controls were entered in this study. Plasma HCII activity was measured with chromogenic substrate method and the HCII antigen level by Western blotting assay. Plasma antithrombin (AT) activity was detected for the HCII deficiency individuals with DVT using chromogenic substrate method.

RESULTSThere was no significant difference in the mean plasma HCII activity and antigen levels between BI group [(99.97 +/- 21.14)% and 0.96 +/- 0.24], MI group [(98.18 +/- 29.35)% and 0.95 +/- 0.20] and healthy controls [(96.80 +/- 20.11)% and 0.93 +/- 0.19]. The plasma HCII activity and antigen concentrations in patients with DVT [(89.57 +/- 17.12)% and 0.87 +/- 10.18] tended to be decreased as compared with healthy controls, but they were not significant. No significant difference was found for the prevalence of HCII deficiency between patient groups and control group. The HCII deficiency individuals with DVT had normal AT activity and fibrinogen concentration.

CONCLUSIONSPlasma HCII deficiency may not be the risk factor for arterial thrombosis in the Han population of Hunan Chinese. It is needed to further confirm if decreased plasma HCII is correlated with venous thrombosis.

Adult ; Aged ; Blotting, Western ; Cerebral Infarction ; blood ; etiology ; Female ; Heparin Cofactor II ; analysis ; deficiency ; immunology ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; blood ; etiology ; Venous Thrombosis ; blood ; etiology