Recent advances in the management of transient ischemic attacks

Abstract

Transient ischemic attack (TIA) constitutes an important clinical condition, indicating the presence of considerable risk for a subsequent ischemic stroke. Its prompt diagnosis and management have the potential for reducing the risk of neurologic disability, highlighting the critical need to prioritize the care of patients with TIA. The risk of ischemic stroke following a TIA is directly related to its etiopathogenesis, and recognizable causes are commonly categorized within one of three domains: cerebrovascular pathology, cardiac dysfunction, and hematologic disorders. Therefore, the clinical approach to patients suspected of having suffered a TIA demands a comprehensive evaluation, including testing of possible etiologic conditions in all three of these domains, best carried out in an expedited fashion since the stroke risk is greatest in the hours and days that follow the index event. The present is a review of the existing literature addressing the diagnosis, evaluation, prioritization, and management strategies available to clinicians who provide care to patients with TIA.

TRPM2-mediated Ca2+ signaling as a potential therapeutic target in cancer treatment: an updated review of its role in survival and proliferation of cancer cells

“…Ischemic stroke is caused by interruption of cerebral blood flow due to an obstruction and the main risk factors for ischemic, hemorrhagic and transient stroke are due to the sedentary lifestyle that generates overweight, the chronic consumption of alcohol or narcotics (cocaine, methamphetamines). Pathologies that favor the occurrence of transient ischemic, ischemic or hemorrhagic accidents are represented by heart diseases (heart failure, congenital heart malformations, heart infections, heart rhythm disorders), obstructive sleep apnea syndrome [ 83 ]. Recent studies showed the involvement of TRPM2 in pathogenesis factors of ischemic stroke as follows: by reducing oxidative stress in cardiomyocytes, TRPM2 reduces inflammation and stimulates the remodeling of the atria; it models endothelial dysfunction by deregulating the influx of calcium ions, mediates the damaging effects of ROS on the endothelium and favors hypertension; induces the death of pancreatic β cells that secrete insulin, thus promoting the development of diabetes; promotes the aggregation of platelets and favors the appearance of vascular thrombus [ 84 – 86 ].…”

Vascular neuro-otology: vestibular transient ischemic attacks and chronic dizziness in the elderly

“…Twenty years later, the NIH defined TIA as temporary focal neurologic deficit of vascular origin, with a rapid onset (between one to five minutes), lasting as long as 24 h. This time frame definition evolved to transient neurologic deficits caused by focal brain, spinal cord or retinal ischemia without acute infarction, and without imaging evidence of infarction, thus, the key modern TIA definition is a tissue-based versus a time-frame diagnosis. In general, the main difficulty clinicians encounter is delayed presentation after symptom resolution [ 1 ].…”