Cesar Avila

The aims of this study were to determine which cognitive domains are evaluated by the Paced Auditory Serial Addition Test (PASAT) and to identify which of them are responsible for the poorer performance displayed by multiple sclerosis (MS) patients in this task. A total of 30 healthy controls and 30 MS patients completed the PASAT task as well as the different tests contained in the Brief Repeatable Battery of Neuropsychological Tests (BRB-N), some Wechsler Adult Intelligence Scale (WAIS-III) subtests, the Spanish version of the Chicago Multiscale Depression Inventory (CMDI), and a new PASAT-based task (ADD1) that was specifically designed for this study. Analysis of covariance and regression-based analyses were performed to identify the predictors that are most strongly associated with the PASAT scores and the between-groups differences in the performance of this task. PASAT execution was associated with scores of the Digit Backward test, Symbol Digit Modality Test (SDMT), and measures of working memory and information-processing speed. On the other hand, differences between healthy volunteers and MS patients were mainly associated with the SDMT scores. MS patients also exhibited poorer execution than controls in the ADD1 task. Our results suggest that reduced information-processing speed (and not working memory) is the primary alteration underlying the lower scores in the PASAT task (and probably other cognitive deficits) that characterize MS patients. Based on these results, we suggest that tests that capitalize the role of information-processing speed may be of special relevance in the neuropsychological assessment of this clinical population.

Background/Rationale:  Impulsivity has been associated with alcohol dependence, but impulsivity in alcohol-dependent subjects with a Cluster-B personality disorder (PD) has not been well characterized. Using a variety of laboratory measures of impulsivity, we assessed whether alcohol-dependent patients (ADP) with borderline personality disorder (BPD) exhibited the same pattern of behavioral impulsivity than ADP with antisocial personality disorder (AntPD). Also, differences between ADP without PDs and healthy controls were assessed.Methods:  A cross-sectional patient survey with a community comparison group. Diagnoses were made using the Structured Interview for DSM-IV. Sustained attention and rapid-response impulsivity were assessed using the continuous performance test. Inhibitory control was measured by the stop-signal task. Ability to delay reward task was assessed using differential reinforcement for low-rate responding (DRLR). A final sample of 247 males with alcohol-dependence recruited from 2 alcoholism treatment centers was compared with a matched nonsubstance-abusing comparison group (n = 96).Results:  Alcohol-dependent patients with BPD made more omission errors than ADP with AntPD, but individuals with AntPD exhibited the poorest efficiency in DRLR. ADPs with a Cluster-B PD displayed more impairment across all behavioral measures than ADP without PD and than controls. In contrast, with respect to controls ADP without a Cluster-B PD showed more impairment only in DRLR.Conclusions:  Our findings support the suggestion of 2 paradigms in alcohol dependence. The first, based on inability to delay gratification, might be a vulnerability marker for alcohol dependence. The second was related to inhibitory control and might be specific for AntPD and BPDs.

Recent fMRI studies have suggested that multiple sclerosis (MS) patients show adaptive cortical changes (i.e., compensatory mechanisms) during motor and cognitive tasks to limit the clinical impact of tissue injury. In this study, we investigated the activation pattern during the auditory n-back working memory (WM) paradigm in a group of 17 MS patients and 10 healthy controls with preserved performance in WM tasks. Compared with healthy controls, MS patients showed significantly greater bilateral activation in prefrontal cortex (BA 44), and the insula. These findings were similar to those obtained in previous studies showing that compensatory mechanisms during WM tasks in MS may be based on the use of prefrontal areas adjacent to those involved in the task. Hum. Brain Mapp, 2007. © 2006 Wiley-Liss, Inc.

To describe a syndrome of posterior segment intraocular inflammation that causes visual loss in patients with acquired immunodeficiency syndrome and cytomegalovirus retinitis. This syndrome was associated with immune recovery mediated by combination antiretroviral treatment including protease inhibitors. A case-control study at 2 university medical centers. One hundred thirty patients with acquired immunodeficiency syndrome and cytomegalovirus retinitis were examined at 2 medical centers for 15 months. In addition, the medical records of 509 patients examined at 1 center for 11 years before the initiation of protease inhibitor therapy were analyzed retrospectively. Five patients with symptomatic vitritis and papillitis with cystoid macular edema or epiretinal membrane formation were documented. In each patient there was inactive cytomegalovirus retinitis that had not caused visual decrease before the onset of inflammation. All patients had elevated CD4+ T lymphocyte levels (median increase, 86x10(6)/L [86 cells/mm3]) after combination treatment including protease inhibitors. Two patients with cystoid macular edema were treated with corticosteroids and had resolution of the cystoid macular edema and an increase in visual acuity without reactivation of the retinitis. Retrospective analysis failed to disclose similar patients with intraocular inflammation in the era before the introduction of protease inhibitors. This newly described syndrome of posterior segment inflammation related to cytomegalovirus retinitis is a cause of visual morbidity in patients with acquired immunodeficiency syndrome. It is associated with increased immune competence as a result of combined antiretroviral treatment with protease inhibitors and may be amenable to corticosteroid therapy without reactivation of retinitis.

Pathological gambling (PG) has been associated to both impulsiveness and attention deficit/hyperactivity disorder (ADHD) in different studies. Our objective was to compare different impulsivity and sustained attention variables, using both behavioural tasks and self-administered questionnaires, in a group of pathological gamblers with a history of childhood ADHD (PG-ADHD; n = 16), a group of pathological gamblers without this history (PG-non-ADHD; n = 39), and a control group (n = 40). As instruments of measure, we used the stop signal task (to evaluate inhibitory control/impulsivity), the differential reinforcement of Low Rate Responding Task (delay of gratification/impulsivity) and the Continuous Performance Test (sustained attention). The Barratt Impulsivity Scale (BIS-11) was used as a self-administered questionnaire to measure impulsiveness. Our results show that patients in the PG-ADHD group exhibit a significantly lower capacity to delay gratification than those in the PG-non-ADHD and control groups, and less inhibitory control than patients in the PG-non-ADHD group. On self-administered questionnaires such as the BIS-11 the PG-ADHD group obtained higher scores than the PG-non-ADHD and control groups. However, no differences were found with respect to sustained attention using the CPT. Our results suggest a possible selective implication of the prefrontal cortex in PG, which would be especially evident in those with a childhood history of ADHD.