Mahoney James J, Kalechstein Ari D, De Marco Anthony P, Newton Thomas F, De La Garza Richard
Department of Behavioral Medicine and Psychiatry, West Virginia University School of Medicine.
Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine.
Neuropsychology. 2017 Mar;31(3):311-318. doi: 10.1037/neu0000344. Epub 2017 Jan 5.
To determine whether premorbid IQ mediates performance on neurocognitive tests in individuals diagnosed with cocaine use disorder (CUD).
Recently abstinent cocaine users (N = 113) completed measures sensitive to the effects of cocaine on cognition: Conners' Continuous Performance Task-II (CPT-II), n-back working memory test, and Hopkins Verbal Learning Task-Revised (HVLT-R). Premorbid IQ was calculated using the Oklahoma Premorbid Intelligence Estimate, which integrates scores from the Wechsler Adult Intelligence Scale-III and demographic variables. Participants were grouped according to their premorbid IQ using commonly accepted classifications of ability level (above average [>110], average [90-109], and below average [<90]) and comparisons in neurocognitive performance were performed using one-way analysis of variance.
Significant differences were detected between groups on the HVLT-R including Trial 1 (p = .002), total word recall across the 3 list-learning trials (p < .001), and recall following a delay (p < .001). Significant differences were also detected on the N-back, including auditory and visual accuracy (p = .022 and p < .001, respectively) and mean and maximum block length (p < .001). Although significant differences were observed between the above average and average groups (mean effect size = .418 [Cohen's d]), the magnitude of group differences was greatest between the average and below average groups (mean effect size = .716).
These results raise questions as to whether the neurocognitive impairment observed in individuals diagnosed with CUD predated the onset of cocaine use or whether the impairments were caused by cocaine use. Because these impairments are potential risk factors for poor treatment outcomes, it is important to consider the need to modify treatment programs to account for lower premorbid IQ. (PsycINFO Database Record
确定病前智商是否介导被诊断为可卡因使用障碍（CUD）个体的神经认知测试表现。
近期戒毒的可卡因使用者（N = 113）完成了对可卡因认知效应敏感的测量：康纳斯连续操作任务-II（CPT-II）、n-back工作记忆测试和修订版霍普金斯言语学习任务（HVLT-R）。使用俄克拉荷马病前智力评估计算病前智商，该评估整合了韦氏成人智力量表-III的分数和人口统计学变量。根据病前智商，使用公认的能力水平分类（高于平均水平[>110]、平均水平[90 - 109]和低于平均水平[<90]）对参与者进行分组，并使用单因素方差分析对神经认知表现进行比较。
在HVLT-R上，各小组之间检测到显著差异，包括第1次试验（p = .002）、3次列表学习试验中的总单词回忆（p < .001）以及延迟后的回忆（p < .001）。在n-back测试中也检测到显著差异，包括听觉和视觉准确性（分别为p = .022和p < .001）以及平均和最大组块长度（p < .001）。虽然在高于平均水平组和平均水平组之间观察到显著差异（平均效应量 = .418[科恩d值]），但平均水平组和低于平均水平组之间的组间差异幅度最大（平均效应量 = .716）。
这些结果引发了关于在被诊断为CUD的个体中观察到的神经认知损害是在可卡因使用开始之前就已存在，还是由可卡因使用导致的问题。由于这些损害是治疗效果不佳的潜在风险因素，因此考虑修改治疗方案以适应较低的病前智商很重要。（PsycINFO数据库记录
