How Prosecutors and Defense Attorneys Differ in Their Use of Neuroscience Evidence

Much of the public debate surrounding the intersection of neuroscience and criminal law is based on assumptions about how prosecutors and defense attorneys differ in their use of neuroscience evidence. For example, according to some commentators, the defense’s use of neuroscience evidence will abdicate criminals of all responsibility for their offenses. In contrast, the prosecution’s use of that same evidence will unfairly punish the most vulnerable defendants as unfixable future dangers to society. This “double- edged sword” view of neuroscience evidence is important for flagging concerns about the law’s construction of criminal responsibility and punishment: it demonstrates that the same information about the defendant can either be mitigating or aggravating depending on who is raising it. Yet empirical assessments of legal decisions reveal a far more nuanced reality, showing that public beliefs about the impact of neuroscience on the criminal law can often be wrong. This Article takes an evidence-based and multidisciplinary approach to examining how courts respond to neuroscience evidence in capital cases when the defense presents it to argue that the defendant’s mental state at the time of the crime was below the given legal requisite due to some neurologic or cognitive deficiency

Shunt lock therapy with micafungin to treat shunt-associated Candida albicans meningitis in an infant

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High-Dose Micafungin for Preterm Neonates and Infants with Invasive and Central Nervous System Candidiasis

High doses of micafungin are advocated in neonates with systemic candidiasis but limited pharmacokinetic (PK) and safety data are available to support their use. Eighteen preterm neonates and infants with systemic candidiasis, 3 with meningitis, were treated for at least 14 days with 8 to 15 mg/kg/day of intravenous micafungin. Plasma concentrations (4 measurements) were determined after the third dose and cerebrospinal-fluid (CSF) concentrations were also obtained in three patients. Population PK analyses were used to identify the optimal model and further validated using external data (n=5). The safety of micafungin was assessed through liver and kidney function biomarkers. The mean (standard deviation) age and weight at administration was 2.33 (1.98) months and 3.24 (1.61) kg, respectively. The optimal PK model was one that scaled plasma clearance to weight and the transaminase ratio. The CSF was sampled in three patients with observed concentrations between 0.80-1.80 mg/L. The model predicted mean (SD) micafungin AUC24 values is 336 (165) h•mg/L with a 10 mg/kg/day dosage. Eighteen of the 23 subjects (78.2%) had clinical resolution of their infection but five had neurologic impairments. Among transaminases, alkaline phosphatase measurements were significantly higher post-treatment with a geometric mean ratio [90% confidence interval] of 1.17 [1.01, 1.37]. Furthermore, marked elevations in gamma-glutamyl transferase (GGT) was observed in three patients treated with 10-15 mg/kg/day doses and improvement in GGT was noted after dose reduction. Higher weight-based doses of micafungin are generally well tolerated in neonates and infants and achieve pharmacokinetic profiles predictive of effect