Stroke pathophysiology, treatments and outcomes are an active field of interest. Copy number variants, specific genetic polymorphisms, toll-like receptors, inflammatory citochines, and chemokines represent factors of susceptibility for stroke [1–6].… Click to show full abstract
Stroke pathophysiology, treatments and outcomes are an active field of interest. Copy number variants, specific genetic polymorphisms, toll-like receptors, inflammatory citochines, and chemokines represent factors of susceptibility for stroke [1–6]. Moreover, microRNAs appear to play a role in post-stroke excitotoxicity [7], while Brainderived neurotrophic factor Val66Met polymorphism is associated with functional and cognitive outcomes of stroke [8]. A specific ACE gene polymorphism has been reported to predispose to hemorrhagic stroke [9]. Acid uric and antioxidants act as a neuroprotective agent for the ischemic stroke [10]. Granulocyte-colony stimulating factor (G-CSF) combined with repetitive transcranial magnetic stimulation (rTMS), administered in the early subacute phase of ischemic stroke, may exert a hazardous effect on functional recovery, possibly due to impaired angiogenic mechanism, decreased cell survival, and increased inflammation [11]. Single small subcortical infarction has been reported associated to early neurological deterioration [12]. Investigations on the influence of cognition changes during post-stroke rehabilitation is relevant [13], associated to post stroke depression and to the degree of neurological deficit [14], while long-term mortality after stroke is higher than after myocardial infarction [15]. Several articles discuss epidemiology and diagnosis. The incidence of hemorrhagic stroke in Japan has been reported higher than in the western countries [16]. Glial fibrillary acidic protein test is a promising technique for diagnosis of intracerebral hemorrhage from ischemic stroke and prediction of short-term functional outcomes [17]. In mice, lithium treatment exerted a neuroprotective effect on learning and memory by potentiating the Akt/GSK3b cell-signaling pathway [18]. Antiplatelet treatment is useful both in primary and secondary prevention, but poor response to aspirin or clopidogrel is a not rare condition [19, 20]. A public education campaign or health-related applications (app) could potentially reduce pre-hospital delay for ischemic stroke patients [21], and also a web-based telemedicine system for thrombolysis could give a growing number of patients access to treatment [22]. Stroke awareness in general population could improve public behavior in terms of prevention, symptom recognition, and timely response [23]. Creation of hospital-based registers may help to ameliorate stroke management [24]. Endovascular treatment (ET) has shown to be safe in acute stroke, but its superiority over intravenous thrombolysis is debated [25]. In murine models, the adenosine A2A receptor antagonist, administered soon after ischemia, has been shown to protect from neurological deficit in the first days but not later [26]. A. Federico: Editor in Chief Neurological Sciences.
               
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