OBJECTIVEThis review aims to illustrate the relationship between clinical features and the prognosis of patients with limb-shaking transient ischemic attack (LS-TIA).

DATA SOURCESRelevant articles published in two main Chinese medical periodical databases (China National Knowledge Infrastructure and China Science Periodical Database) from 1986 to June 2013 were identified with keywords "limb shaking" and "transient ischemic attack".

STUDY SELECTIONOriginal articles and case reports about LS-TIA were selected.

RESULTSA total of 63 cases collected from 19 articles were included in the pooled analysis. LS-TIA presented in two cerebrovascular diseases, of which atherosclerotic high-grade stenosis or occlusion in carotid artery system and moyamoya disease formed 95.2% and 4.8%, respectively. Of 63 patients, 11 (17.5%) were once misdiagnosed as epileptic and prescribed useless antiepilepsy drugs. The multivariable Logistic regression model showed a significant protective effect of patients with revascularization therapy on prognosis, compared with patients treated with drugs (odds ratio 0.20, 95% CI 0.05-0.74, P = 0.016).

CONCLUSIONSChronic carotid artery system hypoperfusion can induce limb(s) shaking, followed by high possibility of ischemic stroke in the same brain territorial. Revascularization of the responsible artery may work better than conservative drug-based therapy.

Aged ; Extremities ; physiopathology ; Female ; Humans ; Ischemic Attack, Transient ; pathology ; physiopathology ; Male ; Middle Aged ; Prognosis

OBJECTIVETo investigate changes of brain mast cells after transient global ischemia in rats.

METHODSTransient global ischemia damage was induced by four-vessel occlusion. After 1 h to 14 days of ischemia, rats were perfused intracardially by 4% paraformaldehyde. The brains were dissected to serial sections using freeze microtome, and then stained with toluidine blue. Brain mast cell was observed under microscope.

RESULTMost brain mast cells were located in thalamus. The number of mast cells in thalamus markedly decreased during reperfusion after transient global ischemia. However, the degranulation rate of thalamus mast cells showed reverse change after ischemia.

CONCLUSIONBrain mast cells markedly degranulate after transient global ischemia, which may be involved in the pathological process after ischemia.

Animals ; Brain ; pathology ; Cell Degranulation ; Ischemic Attack, Transient ; pathology ; Male ; Mast Cells ; pathology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; pathology

BACKGROUND: Endothelial dysfunction, the initial pathogenic factor in atherosclerosis, can be alleviated via transient limb ischemia. We observed the effects of regular transient limb ischemia (RTLI) on atherosclerosis in hypercholesterolemic rabbits. METHODS: Twenty-eight rabbits were randomized to control, cholesterol, sham, ischemia groups (n = 7 each) between October 2010 and March 2011. They were fed a normal diet in the control group and hypercholesterolemic diet in other groups for 12 weeks. Six cycles of RTLI were performed once per day on the ischemia group. Serum samples were prepared to measure the total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) before the experiment (W0), at the end of weeks 4, 8, 12 (W4, W8, W12). The whole aorta was harvested at W12 and stained using Sudan IV to identify the plaque. The plaque area was measured using Image J. Results were analyzed by analysis of variance or rank sum test. RESULTS: Concentrations of TC in the cholesterol group were higher than those in the control group at W4 (29.60 [23.75, 39.30] vs. 1.00 [0.80, 1.55], Z = -2.745, P = 0.006), W8 (41.78 [28.08, 47.37] vs. 0.35 [0.10, 0.68], Z = -2.739, P = 0.006), W12 (48.32 [40.04, 48.95] vs. 0.61 [0.50, 0.86], Z = -2.739, P = 0.006). Similar results were obtained for HDL-C and LDL-C. Serum concentrations of TC, HDL-C, and LDL-C in the hypercholesterolemic groups had no differences (all P > 0.05). The percentage of plaque area in the cholesterol group was higher than that in the control group (47.22 ± 23.89% vs. 0, Z = -2.986, P = 0.003). Square root of the percentage of plaque area was smaller in the ischemia group than that in the cholesterol (0.44 ± 0.13 vs. 0.67 ± 0.18, P = 0.014) or sham groups (0.44 ± 0.13 vs. 0.61 ± 0.12, P = 0.049). CONCLUSION In hypercholesterolemic rabbits, RTLI might prevent atherosclerosis progression by reducing the percentage of plaque area.
Animals ; Atherosclerosis ; blood ; prevention & control ; Cholesterol ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Extremities ; pathology ; Hypercholesterolemia ; blood ; Ischemic Attack, Transient ; blood ; Ischemic Postconditioning ; methods ; Male ; Rabbits ; Triglycerides ; blood

AIMTo investigate whether the selective AT1 receptor antagonist irbesartan exerts neuroprotective effect on focal cerebral ischemia in normotensive rats.

METHODSCerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 90 min followed by reperfusion, with the monitoring of laser Doppler flowmetry. To avoid the interaction with peripheral AT1 receptors, irbesartan was infused intracerebroventricularly (ICV) at a dose which effectively inhibited brain- but not vascular AT1 receptors. Neurological status was evaluated daily after MCAO. Rats were killed and brain samples were collected for the measurement of infarct size and immunohistochemical evaluation of apoptosis by deoxynucleotidyltransferase-mediated biotinylated UTP nick end labeling (TUNEL) and expression of activated Caspase-3 and the cleavage fragment of poly (ADP-ribose) polymerase (PARP).

RESULTSTreatment with irbesartan improved significantly the neurobehavioral functions after cerebral ischemia. The infarct size was reduced about 42% on day 7 after MCAO (P < 0.05). Meanwhile,irbesartan treatment significantly decreased the number of TUNEL-positive cells in the penumbra. The expression of activated Caspase-3 and the downstream cleavage fragment of poly (ADP-ribose) polymerase in the penumbra were also inhibited by irbesartan therapy on day 3 after transient cerebral ischemia.

CONCLUSIONAngiotensin AT1 receptor antagonist exhibits neuroprotection against transient cerebral ischemia in the brain. The neuroprotective effects in ischemic tissue may be associated with its inhibition of apoptotic cell death in the penumbra.

Angiotensin Receptor Antagonists ; pharmacology ; Animals ; Biphenyl Compounds ; pharmacology ; Cerebral Infarction ; pathology ; Ischemic Attack, Transient ; drug therapy ; pathology ; Lateral Ventricles ; Male ; Neuroprotective Agents ; pharmacology ; Rats ; Rats, Wistar ; Tetrazoles ; pharmacology

OBJECTIVETo investigate the characteristics of cerebral artery lesions in patients with limb-shaking transient ischemic attacks (LS-TIA) and its treatment.

METHODSWe retrospectively analyzed the clinical data of 20 patients with LS-TIA who received treatment in Peking Union Medical College Hospital from 2005 to 2008.

RESULTSCritical stenosis or occlusion of contralateral arteries were found in the siphonic part of internal carotid artery (ICA) in 6 patients, terminal ICA or proximal middle cerebral artery (MCA) in 6 patients, and distal MCA in 1 patient. Seven patients had proximal ICA occlusion. The brain MRI showed typical watershed cerebral infarctions in 8 patients. EEG studies failed to show epileptiform activity associated with LS-TIA, but found focal frontotemporal lobe slow activity in 6 patients, which was consistent with hypoperfusion area in CT perfusion. Six patients received surgical revascularization and no one recurred.

CONCLUSIONIntracranial artery including the siphonic part of ICA, terminal ICA and proximal MCA stenosis is the main underlying cause of LS-TIA in Chinese, and surgical revascularization may be effective in abolishing the attacks.

Adult ; Aged ; Aged, 80 and over ; Cerebral Arteries ; pathology ; Female ; Humans ; Ischemic Attack, Transient ; complications ; pathology ; therapy ; Male ; Middle Aged ; Retrospective Studies ; Tremor ; etiology

The involvement of apoptosis in mitochondrial toxin 3-nitropropionic acid (3-NPA)-induced ischemic tolerance to transient focal cerebral ischemia in rats and the mechanism was investigated. 3-NPA at a dose of 20 mg/kg or vehicle control was intraperitoneally into the rats. Three days later, rats were exposed to 2 h of middle cerebral artery occlusion followed by 24 h of reperfusion. Infarct volumes were assessed by 2,3,5-triphenyltetrazolinm chloride (TTC) staining 24 h after reperfusion. Neural cell apoptosis in cerebral ischemic penumbra was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) and flow cytometry methods (FCM). The results showed that as compared to the vehicle-treated group, pretreatment with 3-NPA could reduce the infarct volume by 23.3% and decrease the number of TUNEL-positive neural cells and apoptotic percentage by 47% (P<0.05) and 44.9% (P<0.01), respectively. It was concluded that the development of 3-NPA-induced ischemic tolerance in brain might be related to the decreases in neural cell apoptosis.
Animals ; Apoptosis ; drug effects ; Cerebral Cortex ; blood supply ; Cerebrovascular Circulation ; DNA Damage ; Infarction, Middle Cerebral Artery ; pathology ; Ischemic Attack, Transient ; chemically induced ; pathology ; Ischemic Preconditioning ; Male ; Middle Cerebral Artery ; pathology ; Nitro Compounds ; Propionates ; Rats ; Reperfusion Injury ; pathology

Neurogenesis can be induced by pathological conditions such as cerebral ischemia. However the molecular mechanisms or modulating reagents of the reactive neurogenesis after the cerebral ischemia are poorly characterized. Retinoic acid (RA) has been shown to increase neurogenesis by enhancing the proliferation and neuronal differentiation of forebrain neuroblasts. Here, we examined whether RA can modulate the reactive neurogenesis after the cerebral ischemia. In contrast to our expectation, RA treatment decreased the reactive neurogenesis in subventricular zone (SVZ), subgranular zone (SGZ) and penumbral region. Furthermore, RA treatment also decreased the angiogenesis and gliosis in penumbral region.
Animals ; Brain/blood supply ; Cell Differentiation ; Cell Proliferation ; Ischemic Attack, Transient/metabolism/*pathology ; Male ; Neovascularization, Pathologic ; Neuroglia/pathology/physiology ; Neurons/pathology/*physiology ; Rats ; Rats, Sprague-Dawley ; Tretinoin/*pharmacology/physiology

OBJECTIVE: To investigate the relationship between the clinical features of carotid transient ischemic attacks (TIA) and the intracranial or extracranial angiostenosis. METHODS: Location and degree of stenosis of involved arteries were examined by the digital subtraction angiography in 52 patients with carotid TIA. RESULTS: Intracranial or extracranial vascular lesions of different degrees were revealed in 45 patients (86.5%), and 29 out of 45 (64.4%) had more than one site. Severe stenosis and occlusion occurred more frequently in TIA patients with short duration (less than 1 hour) and multiple attacks (more than twice). CONCLUSION Most patients with TIA of carotid systems have stenosis in intracranial or extracranial arteries. TIA with short duration and multiple attacks always accompany with severe stenosis or occlusion in intracranial or extracranial arteries. Digital subtraction angiography helps to identify the vascular etiology of TIA and provides the instruction of therapeutic regimen.
Adult ; Aged ; Angiography, Digital Subtraction ; Carotid Stenosis ; complications ; diagnostic imaging ; pathology ; Cerebral Angiography ; Cerebrovascular Disorders ; complications ; diagnostic imaging ; pathology ; Female ; Humans ; Ischemic Attack, Transient ; diagnostic imaging ; pathology ; Male ; Middle Aged

OBJECTIVE: We wanted to differentiate between transient ischemic attack (TIA) and minor stroke using fractional anisotropy and three-dimensional (3D) fiber tractography. MATERIALS AND METHODS: The clinical data, conventional magnetic resonance imaging (MRI), diffusion weighted imaging (DWI) and diffusion tensor imaging (DTI) were obtained for 45 TIA patients and 33 minor stroke patients. The fractional anisotrophy ratio (rFA) between the lesion and the mirrored corresponding contralateral normal tissue was calculated and analyzed. The spatial relationship between the lesion and the corticospinal tract (CST) was analyzed and the lesion sizes in the minor stroke patients and TIA patients were compared. RESULTS: Twenty-two of the 45 TIA patients (49%) revealed focal abnormalities following DWI. The rFA was significantly lower (p < 0.05) in the stroke patients (0.71 +/- 0.29) compared to that of the TIA patients (1.05 +/- 0.37). The CST was involved in almost all stroke lesions, but it was not involved in 68% of the TIA lesions. The TIA patients had significantly lower CST injury scores (3.25 +/- 1.75) than did the stroke patients (8.80 +/- 2.39) (p = 0.004). CONCLUSION: Our data indicate that TIA and minor stroke can be identified by analyzing the rFA and the degree of CST involvement, and this may also allow more accurate prediction of a patient's long-term recovery or disability.
Aged ; Anisotropy ; Area Under Curve ; Chi-Square Distribution ; Diagnosis, Differential ; Diffusion Tensor Imaging/*methods ; Female ; Humans ; Image Interpretation, Computer-Assisted ; *Imaging, Three-Dimensional ; Ischemic Attack, Transient/*pathology ; Male ; Middle Aged ; ROC Curve ; Sensitivity and Specificity ; Stroke/*pathology

Blood cells are transported into the brain and are thought to participate in neurodegenerative processes following hypoxic ischemic injury. We examined the possibility that transient forebrain ischemia (TFI) causes the blood-brain barrier (BBB) to become permeable to blood cells, possibly via dysfunction and degeneration of endothelial cells in rats. Extravasation of Evans blue and immunoglobulin G (IgG) was observed in the hippocampal CA1-2 areas within 8 h after TFI, and peaked at 48 h. This extravasation was accompanied by loss of tight junction proteins, occludin, and zonula occludens-1, and degeneration of endothelial cells in the CA1-2 areas. Iron overload and mitochondrial free radical production were evident in the microvessel endothelium of the hippocampus before endothelial cell damage occurred. Administration of deferoxamine (DFO), an iron chelator, or Neu2000, an antioxidant, blocked free radical production and endothelial cell degeneration. Our findings suggest that iron overload and iron-mediated free radical production cause loss of tight junction proteins and degeneration of endothelial cells, opening of the BBB after TFI.
Animals ; Blood-Brain Barrier/*metabolism ; Capillary Permeability ; Endothelial Cells/*metabolism ; Evans Blue/metabolism ; Free Radicals/metabolism ; Hippocampus/*metabolism/pathology ; Iron/*metabolism ; Ischemic Attack, Transient/pathology/*physiopathology ; Male ; Membrane Proteins/metabolism ; Rats ; Rats, Sprague-Dawley