Stimulants have been used throughout human history for a variety of reasons. High levels of stress and the demanding nature of medical school make their usage among medical students particularly common. The most prevalent stimulant used by students is coffee, followed by tea and other forms of caffeine like sugary energy drinks. In addition, amphetamine-based medications for treating attention deficit hyperactivity disorder (ADHD) have been increasing in popularity, which many students take illicitly. Students report taking various forms of stimulants to promote cognitive enhancement, prolong wakefulness and retain focus for long periods of time. Moderate doses of caffeine and amphetamines would lead to enhanced alertness and concentration. However, large increases in dosage or frequency would lead to an increased risk of toxicity and adverse effects. The positive outcomes from stimulant consumption are often overshadowed by the negative side effects and incorrect dosage. Thus, it appears that usage of stimulants should be limited, in favor of a more sustainable approach to cognitive enhancement. This review analyzes the use of stimulants among the medical student community, consequences of misuse and discussed the healthy and organic approaches to lessen the stress and improve academic performance. This article also discusses the mechanisms of action, acceptable doses, additives, ingredients of stimulants commonly used by medical students for cognitive enhancement and the implications of long-term use as the stress of practicing medicine extends well beyond the medical school years.

Carotid artery calcification (CAC) is a well-known marker of atherosclerosis and is linked to a high rate of morbidity and mortality. CAC is divided into two types: intimal and medial calcifications, each with its own set of risk factors. Vascular calcification is now understood to be an active, enzymatically regulated process involving dystrophic calcification and endothelial dysfunction at an early stage. This causes a pathogenic inflammatory response, resulting in calcium phosphate deposition in the form of microcalcifications, which causes plaque formation, ultimately becoming unstable with sequelae of complications. If the inflammation goes away, hydroxyapatite crystal formation takes over, resulting in macro-calcifications that help to keep the plaque stable. As CAC can be asymptomatic, it is critical to identify it early using diagnostic imaging.The carotid artery calcification score is calculated using computed tomography angiography (CTA), which is a confirmatory test that enables the examination of plaque composition and computation of the carotid artery calcification score. Magnetic resonance angiography (MRA), which is sensitive as CTA, duplex ultrasound (DUS), positron emission tomography, and computed tomography (PET-CT) imaging with (18) F-Sodium Fluoride, and Optical Coherence Tomography (OCT) are some of the other diagnostic imaging modalities used. The current therapeutic method starts with the best medical care and is advised for all CAC patients. Carotid endarterectomy and carotid stenting are two treatment options that have mixed results in terms of effectiveness and safety. When patient age and anatomy, operator expertise, and surgical risk are all considered, the agreement is that both techniques are equally beneficial.

No abstract

Acute ischemic strokes (AIS) and hemorrhagic strokes lead to disabling neuropsychiatric and cognitive deficits. A serious and fatal complication of AIS is the occurrence of hemorrhagic transformation (HT). HT is cerebral bleeding that occurs after an ischemic event in the infarcted areas. This review summarises how specific risk factors such as demographic factors like age, gender, and race/ethnicity, comorbidities including essential hypertension, atrial fibrillation, diabetes mellitus, congestive heart failure, and ischemic heart disease along with predictors like higher NIHSS score, larger infarction size, cardioembolic strokes, systolic blood pressure/pulse pressure variability, higher plasma glucose levels, and higher body temperature during ischemic event, lower low-density lipoprotein and total cholesterol, early ischemic changes on imaging modalities, and some rare causes make an individual more susceptible to developing HT. We also discuss few other risk factors such as the role of blood-brain barrier, increased arterial stiffness, and globulin levels in patients postreperfusion using thrombolysis and mechanical thrombectomy. In addition, we discuss the implications of dual antiplatelet therapy and the length of treatment in reference to the incidence of developing HT. Current research into inflammatory mediators and biomarkers such as Cyclooxygenase-2, matrix metalloproteinases, and soluble ST2 and their potential role as treatment options for HT is also briefly discussed. Finally, this review calls for more research into use of dual antiplatelet and the timing of antiplatelet and anticoagulant use in reference to hemorrhagic transformation.

Background and Purpose Environmental enrichment (EE) improves brain function and ameliorates cognitive impairments; however, whether EE can reverse the learning and memory deficits seen following seizures remains unknown. Methods We tested the hypothesis that EE augments neurogenesis and attenuates the learning and memory deficits in rats subjected to kainate-induced seizures in hippocampus, amygdala and motor cortex. EE consisted of daily exposures immediately after KA lesioning (early EE) and after a 60-day period (late EE). Morphometric counting of neuron numbers (NN), dendritic branch-points and intersections (DDBPI) were performed. Spatial learning in a T-maze test was described as percent correct responses and memory in a passive-avoidance test was calculated as time spent in the small compartment where they were previously exposed to an aversive stimulus. Results EE increased NN and DDBPI in the normal control and in the KA-lesioned rats in all brain areas studied, after both early and late exposure to EE. Late EE resulted in significantly fewer surviving neurons than early EE in all brain areas ( p < 0.0001). EE increased the percent correct responses and decreased time spent in the small compartment, after both early and late EE. The timing of EE (early vs. late) had no effect on the behavioral measurements. Conclusions These findings demonstrate that, after temporal lobe and motor cortex epileptic seizures in rats, EE improves neural plasticity in areas of the brain involved with emotional regulation and motor coordination, even if the EE treatment is delayed for 60 days. Future studies should determine whether EE is a useful therapeutic strategy for patients affected by seizures.