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

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

Artemisia capillaris Thunberg is a medicinal plant used as a traditional medicine in many cultures. It is an effective remedy for liver problems including hepatitis. Recent pharmacological reports have indicated that Artemisia species can exert various neurological effects. Previously, we reported a memory-enhancing effect of Artemisia species. However, the mechanisms underlying the neuroprotective effect of A. capillaris (AC) are still unknown. In the present study, we investigated the effect of an ethanol extract of AC on ischemic brain injury in a mouse model of transient forebrain ischemia. The mice were treated with AC for seven days, beginning one day before induction of transient forebrain ischemia. Behavioral deficits were investigated using the Y-maze. Nissl and Fluoro-jade B staining were used to indicate the site of injury. To determine the underlying mechanisms for the drug, we measured acetylcholinesterase activity. AC (200 mg·kg) treatment reduced transient forebrain ischemia-induced neuronal cell death in the hippocampal CA1 region. The AC-treated group also showed significant amelioration in the spontaneous alternation of the Y-maze test performance, compared to that in the untreated transient forebrain ischemia group. Moreover, AC treatment showed a concentration-dependent inhibitory effect on acetylcholinesterase activity in vitro. Finally, the effect of AC on forebrain ischemia was blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor antagonist. Our results suggested that in a model of forebrain ischemia, AC protected against neuronal death through the activation of nicotinic acetylcholine receptors.
Acetylcholinesterase ; metabolism ; Animals ; Artemisia ; Cell Death ; drug effects ; Cholinergic Antagonists ; pharmacology ; Disease Models, Animal ; Ethanol ; chemistry ; Hippocampus ; pathology ; physiopathology ; Ischemic Attack, Transient ; drug therapy ; pathology ; physiopathology ; Male ; Mecamylamine ; pharmacology ; Memory ; drug effects ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Neuroprotective Agents ; administration & dosage ; pharmacology ; Phytotherapy ; Plant Components, Aerial ; chemistry ; Plant Extracts ; administration & dosage ; pharmacology ; Receptors, Cholinergic ; metabolism