Alcohol-impaired driving in US counties, 2002–2012

Abstract Background Excessive alcohol consumption and alcohol-impaired driving remain significant public health problems, leading to considerable morbidity and mortality, particularly among younger populations. Methods Using data from the Behavioral Risk Factor Surveillance System (BRFSS), we employed a small areas modeling strategy to estimate the county-level annual prevalence of alcohol-impaired driving in every United States county for the years 2002 through 2012, the latest year in which county identifiers were publicly available. Results Alcohol-impaired driving episodes declined from 157.0 million in 2002 (prevalence 3.8%: 95% uncertainty interval [UI], 3.7%–4.0%) to 129.7 million in 2012 (prevalence 3.7%: 95% UI, 3.5%–3.8%), a 17.4% decline. There is considerable variation in the prevalence of alcohol-impaired driving at the county level, ranging from 2.0% in the Sitka City Borough of Alaska to 9.3% in Nance County, Nebraska. Clusters of increased alcohol-impaired driving were observed in Northern Wisconsin (Marinette, Florence, Forest, Vilas, Oneida, Iron counties), North Dakota (Cavalier, Pembina, Walsh, Ramsey, Nelson, Benson, Eddy counties) and Montana (Sheridan, Daniels, Roosevelt, Valley, Phillips, Petroleum, Garfield counties). Conclusions This study showed guarded progress with respect to the occurrence of alcohol-impaired driving episodes in the US from 2002 to 2012. Because these data rely on self-report, this likely represents an underestimate of the true prevalence of alcohol-impaired driving in the US. As the US continues to have several million episodes of alcohol-impaired driving each month, renewed efforts are needed to mitigate this high-risk health behavior

Impairment of specific episodic memory processes by sub-psychotic doses of ketamine: The effects of levels of processing at encoding and of the subsequent retrieval task

Rationale: The precise nature of the impact of the N-methyl-d-aspartate antagonist, ketamine, upon human episodic memory, has yet to be elucidated fully. Objectives: This study sought to assess the effects of ketamine on the sub-processes facilitating memory encoding and retrieval. Methods: We evaluated the effects of the drug on a series of memory performance measures depending upon whether it was administered at the encoding or retrieval stage and on the nature of the encoding task used. Twelve healthy volunteers participated in a double-blind, placebo-controlled, randomized, within-subjects study. Intravenous infusions of placebo, 50 ng/ml ketamine or 100 ng/ml ketamine were administered. We investigated the effects of ketamine on three key aspects of episodic memory: encoding vs retrieval processes, source memory, and depth of processing. Data were analysed using both multinomial modelling and standard measures of item discrimination and response bias. Results: Deleterious effects of ketamine on episodic memory were primarily attributable to its effects on encoding, rather than retrieval processes. Recognition memory was impaired for items encoded at an intermediate level of processing, but preserved for shallowly and deeply encoded items. Increased source guessing bias was also observed when encoding took place under ketamine. Conclusions: The effects of ketamine upon episodic memory seem, therefore, to predominate at encoding. Furthermore, our results are also consistent with a specific impairment of encoding processes that result in subsequent recollective, as opposed to familiarity-based, retrieval. The observed effects are compatible with memory deficits seen in schizophrenia and thus provide some support for the ketamine model of the disease. © Springer-Verlag 2005