Cerebral Infarction ; diagnosis ; Child ; Humans ; Male ; Purpura, Schoenlein-Henoch ; pathology

Astrocytes are the most abundant cells in the central nervous system and play significant roles in normal brain. With cerebral infarction, astrocytes are activated as reactive astrocytes and form glial scars, which play an essential part in brain injury. According to their roles in neuroprotection after cerebral infarction, regulation of scar formation, nerve regeneration, maintenance of blood-brain barrier, promotion of angiogenesis and immune response, scholars have proposed a variety of therapeutic strategies based on targeting astrocytes. This article reviews the research progress on the changes in astrocyte signaling pathways before and after cerebral infarction and the related therapeutic strategies.
Astrocytes ; Cerebral Infarction ; physiopathology ; therapy ; Humans ; Neuroglia ; pathology ; Signal Transduction

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

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

It is known that ischemic cerebrovascular disease is causing enormous harm to human health on account of the resultant high morbidity and disability rate. In this connexion, the anticipated target is to control the size of focal ischemic cerebral infarction, which is also an important method for judgment of therapeutic efficacy. The key question is to survey the size accurately and objectively; at the same time, the quantitative analysis of focal ischemic cerebral infarction is the pivotal question affecting the experiment conclusion and the reliability level. In this paper are introduced and summarized the methods being recently and commonly used in survey and computation, and the studies made on quantitative analysis of focal ischemic cerebral infarction by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining method. Also are summarized the principles of dyeing in TTC method, the preparatory work, and the commonly used method of surveying and computation. It is the intent of this review to provide relevant data and suggestion for research workers.
Animals ; Brain Ischemia ; pathology ; Cerebral Infarction ; pathology ; Coloring Agents ; Humans ; Reperfusion Injury ; pathology ; Tetrazolium Salts

PURPOSE: Patients with superficial middle cerebral artery (MCA) territory infarction may have concomitant lenticulostriate artery (LSA) territory infarction. We investigated the mechanisms thereof and the outcomes of patients with superficial MCA territory infarction according to the presence or absence of LSA involvement. MATERIALS AND METHODS: Consecutive patients with first-ever infarction in the unilateral superficial MCA territory were included in this study. They were divided into the superficial MCA only (SM) group and the superficial MCA plus LSA (SM+L) group. RESULTS: Of the 398 patients, 84 patients (21.1%) had LSA involvement (SM+L group). The SM+L group more frequently had significant stenosis of the proximal MCA or carotid artery and high-risk cardioembolic sources. Stroke severity and outcomes were remarkably different between the groups. The SM+L group showed more severe neurologic deficits (National Institute of Health Stroke Scale score 10.8±7.1 vs. 4.0±5.0, p<0.001) and larger infarct in the superficial MCA territory (40.8±62.6 cm³ vs. 10.8±21.8 cm³, p<0.001) than the SM group. A poor functional outcome (mRS >2) at 3 months was more common in the SM+L group (64.3% vs. 15.9%, p<0.001). During a mean follow-up of 26 months, 67 patients died. All-cause (hazard ratio, 2.246) and stroke (hazard ratio, 9.193) mortalities were higher in the SM+L group than the SM group. In multivariate analyses, LSA involvement was an independent predictor of poor functional outcomes and stroke mortality. CONCLUSION: LSA territory involvement is predictive of poor long-term outcomes in patients with superficial MCA territory infarction.
Carotid Stenosis/mortality/pathology ; Constriction, Pathologic/pathology ; Female ; Humans ; Infarction, Middle Cerebral Artery/mortality/*pathology ; Male ; Middle Cerebral Artery/*pathology ; Multivariate Analysis ; Severity of Illness Index ; Stroke/mortality/pathology

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

Brain ; pathology ; Brain Infarction ; diagnosis ; Cerebral Angiography ; Cerebral Arterial Diseases ; diagnosis ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Posterior Cerebral Artery ; pathology

BACKGROUNDMotor dysfunction is common in stroke patients. Clinical electrophysiological studies suggest that transsynaptic degeneration occurred in the lower motor neurons, while pathological evidence is lacked. This study aimed to combine the electrophysiological and pathological results to prove the existence of transsynaptic degeneration in the motor system after stroke.

METHODSModified neurologic severity score, electrophysiological, and pathological assessments were evaluated in rats before middle cerebral artery occlusion (MCAO), and at 24 hours, 7 days, and 14 days after MCAO. Paired and independent-sample t-tests were applied to assess the changes of electrophysiological and pathological data.

RESULTSCompound motor action potential amplitude in the paretic side was significantly lower than the nonparetic side at both 24 hours (61.9 ± 10.4 vs. 66.6 ± 8.9, P < 0.05) and 7 days (60.9 ± 8.4 vs. 67.3 ± 9.6, P < 0.05) after MCAO. Motor unit number estimation of the paretic side was significantly less than the nonparetic side (379.0 ± 84.6 vs. 445.0 ± 89.5, P < 0.05) at 7 days after MCAO. Until 14 days after stroke, the pathological loss of motor neurons was detected. Motor neurons in 14-day MCAO group were significantly decreased, compared with control group (5.3 ± 0.7 vs. 7.3 ± 1.8, P < 0.05).

CONCLUSIONSBoth electrophysiological and pathological studies showed transsynaptic degeneration after stroke. This study identified the asynchronization in changes of electrophysiology and pathology. The abnormal physiological changes and function impairment can be detected in the early stage and recovered quickly, while the pathological loss of motor neuron can be detected only in a later stage.

Animals ; Electrophysiology ; Infarction, Middle Cerebral Artery ; pathology ; physiopathology ; Male ; Motor Neurons ; pathology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; pathology ; physiopathology

Immunohistochemistry and double immunofluorescent labeling techniques combined with confocal laser scanning microscope analysis were used to investigate the characteristic spatial induction profile of nestin following a transient middle cerebral artery occlusion in adult rat brain. The results showed that nestin was induced in ischemic core at 1 day after reperfusion. In addition to ischemic core, the expression of nestin increased in peri-ischemic I, II and III regions at 3 days and 1 week, then it decreased and narrowed along the rim of ischemic core 2 weeks after reperfusion. Double immunofluorescent labeling showed that nestin positive cells were mostly co-stained with GFAP,a astrocyte marker, in peri-ischemic I region 3 days after reperfusion. At 2 weeks, however nestin cells showed a long process and the cells double stained with nestin and NSE,a neuonal specific marker,increased in the ischemic brain. The results suggest that cerebral ischemia induces nestin expression in damaged neurons which might favor the neuroprotection against ischemic damage.
Animals ; Brain ; metabolism ; pathology ; Brain Ischemia ; metabolism ; pathology ; Immunohistochemistry ; Infarction, Middle Cerebral Artery ; metabolism ; pathology ; Nestin ; metabolism ; Neurons ; metabolism ; Rats