Sport-related concussion affects athletes at every level of participation. The short and long-term effects of concussions that occur during childhood and adolescence are not fully understood. The purpose of this review is to describe the current burden of disease, current practice patterns and current recommendations for the assessment and management of sport-related concussions sustained by United States high school athletes. Millions of high school students participate in organized sports in the United States. Current estimates suggest that, across all sports, approximately 2.5 concussions occur for every 10 000 athletic exposures, in which an athletic exposure is defined as one athlete participating in one game or practice. At schools that employ at least one athletic trainer, most high school athletes who sustain sport-related concussions will be cared for by athletic trainers and primary care physicians. Approximately 40% will undergo computerized neurocognitive assessment. The number of high school athletes being diagnosed with sport-related concussions is rising. American football has the highest number of concussions in high school with girls' soccer having the second highest total number. Fortunately, coaches are becoming increasingly aware of these injuries and return-to-play guidelines are being implemented.

Summary: Objective: To identify factors associated with in‐hospital mortality in neonates and children undergoing continuous electroencephalography (cEEG) monitoring in the intensive care unit (ICU).Methods: We performed a retrospective observational study in patients from birth to 21 years of age who underwent clinically indicated cEEG in the ICU from 2011 to 2013. The main outcome measure was in‐hospital mortality.Results: Six‐hundred and twenty‐five patients (54.2% male) met eligibility criteria, of whom 211 were neonates (55% male, 24.8% premature) and 414 were pediatric patients (53.9% male). Electrographic seizures occurred in 176 patients (28.2%) and status epilepticus (SE) occurred in 20 (11.4%). The time from ICU admission to cEEG initiation was 16.7 (5.1–94.4) h. Eighty‐nine patients (14.2%) (30 [14.2%] neonates, and 59 [14.3%] pediatric patients) died in the hospital. In neonates—after controlling for gender and prematurity—independent factors associated with mortality were prematurity (odds ratio [OR] 2.63. 95% confidence interval [CI] 1.06–6.5, p = 0.037), presence of status epilepticus (SE); OR 8.82, 95% CI 1.74–44.57, p = 0.008), and time from ICU admission to initiation of cEEG (OR 1.002, 95% CI 1.001–1.004 per hour, p = 0.008]. In pediatric patients—after controlling for gender and age—independent factors associated with mortality were the absence of seizures factors associated with mortality were absence of seizures (OR = 4.3, (95% CI: 1.5–12.4), p = 0.007), the presence of SE (OR 7.76, 95% CI 1.47–40.91, p = 0.016), and the time from ICU admission to initiation of cEEG (OR 1.001, 95% CI 1.0002–1.001, per hour, p = 0.005].Significance: Both presence of electrographic SE and time from ICU admission to cEEG initiation were independent factors associated with mortality in neonates and pediatric patients with cEEG in the ICU.

L-type Ca²⁺channels (LTCCs) play an important role in chronic psychostimulant-induced behaviors. However, the Ca²⁺second messenger pathways activated by LTCCs after acute and recurrent psychostimulant administration that contribute to drug-induced molecular adaptations are poorly understood. Using a chronic amphetamine treatment paradigm in rats, we have examined the role of LTCCs in activating the mitogen-activated protein (MAP) kinase pathway in the ventral tegmental area (VTA), a primary target for the reinforcing properties of psychostimulants. Using immunoblot and immunohistochemical analyses, we find that in chronic saline-treated rats a challenge injection of amphetamine increases phosphorylation of MAP [extracellular signal-regulated kinase 1/2 (ERK1/2)] kinase in the VTA that is independent of LTCCs. However, in chronic amphetamine-treated rats there is no increase in amphetamine-mediated ERK1/2 phosphorylation unless LTCCs are blocked, in which case there is robust phosphorylation in VTA dopamine neurons. Examination of the expression of phosphatases reveals an increase in calcineurin [protein phosphatase 2B (PP2B)] and MAP kinase phosphatase-1 (MKP-1) in the VTA. Usingin situhybridization histochemistry and immunoblot analyses, we further examined the mRNA and protein expression of the LTCC subtypes Ca_v1.2 and Ca_v1.3 in VTA dopamine neurons in drug-naive animals and in rats after chronic amphetamine treatment. We found an increase in Ca_v1.2 mRNA and protein levels, with no change in Ca_v1.3. Together, our results suggest that one aspect of LTCC-induced changes in second messenger pathways after chronic amphetamine exposure involves activation of the MAP kinase phosphatase pathway by upregulation of Ca_v1.2 in VTA dopaminergic neurons.