Prior investigations have shown that individuals with attention deficit hyperactivity disorder (ADHD) have impaired neuropsychological functions. This study had two aims, first to investigate weakened cognitive functions in adult ADHD (aADHD), and second, to investigate difference between persisters (those having persistently ongoing ADHD diagnosis in adulthood), and remitters (those having ADHD diagnosis only in childhood and not in adulthood), in terms of cognitive deficits. We evaluated performance on a comprehensive neuropsychological battery in three groups including 34 persisters, 35 remitters, and 35 healthy control group (absence of childhood and adulthood ADHD diagnosis). Our findings showed that adults with ADHD have inefficient attention, interference control and set-shifting functions, which may be revealed on neuropsychological tests that require greater cognitive demand. Given the finding that interference control deficit exists across the lifespan in people with ADHD, we suggest that interference control-associated functional weakness may be a core deficit for ADHD. (JINS, 2012, 18, 1–8)

The present study examined neuropsychological (NP) functioning and associated medical, neurological, brain magnetic resonance imaging (MRI), and psychiatric findings in 389 nondemented males infected with Human Immunodeficiency Virus-Type 1 (HIV-1), and in 111 uninfected controls. Using a comprehensive NP test battery, we found increased rates of impairment at each successive stage of HIV infection. HIV-related NP impairment was generally mild, especially in the medically asymptomatic stage of infection, and most often affected attention, speed of information processing, and learning efficiency; this pattern is consistent with earliest involvement of subcortical or frontostriatal brain systems. NP impairment could not be explained on the bases of mood disturbance, recreational drug or alcohol use, or constitutional symptoms; by contrast, impairment in HIV-infected subjects was related to central brain atrophy on MRI, as well as to evidence of cellular immune activation and neurological abnormalities linked to the central nervous system. (JINS, 1995, 1, 231–251.)

Treatment with interferon-alpha (IFN-α) has been shown to adversely affect cognitive functioning in patients with a variety of medical disorders, but information about the effects of IFN-α on cognitive functioning in patients with chronic hepatitis C (CHC) is limited. The purpose of this study was to examine the effects of IFN-α on neuropsychological test performance in CHC patients. Participants were 30 patients with CHC, 11 who underwent IFN-α therapy and 19 who did not. All participants were tested at baseline (i.e., pretreatment) and approximately 6 months later with the Symbol Digit Modalities Test and Trail Making Test. Results revealed that the treatment group performed significantly worse than untreated CHC patients on Part B of the Trail Making Test after approximately 6 months of treatment. No significant group differences were found on Part A of the Trail Making Test or Symbol Digit Modalities Test. Findings suggest that CHC patients undergoing treatment with IFN-α may experience reduced abilities to benefit from practice but suffer no decrements in performance after 6 months of treatment. Additional research is needed to replicate these findings and to explore risk factors for susceptibility to IFN-α-induced effects. (JINS, 2005, 11, 16–22.)

Hepatitis C virus (HCV) infection is a major public-health-care problem, with over 170 million infected worldwide. Patients with chronic HCV infection often complain of various cognitive problems as well as symptoms of depression, anxiety, and fatigue. Relatively little is known, however, about the specific cognitive deficits that are common among HCV patients, and the influence of psychiatric symptomatology on cognitive functioning. In the current study of 21 chronically infected HCV patients, we assessed subjective cognitive dysfunction, depression, anxiety, and fatigue and compared these symptom areas to cognitive tests assessing visuoconstruction, learning, memory, visual attention, psychomotor speed, and mental flexibility. Results revealed that cognitive impairment ranged from 9% of patients on a visuoconstruction task to 38% of patients on a measure of complex attention, visual scanning and tracking, and psychomotor speed, and greater HCV disease severity as indicated by liver fibrosis was associated with greater cognitive dysfunction. Objective cognitive impairment was not related to subjective cognitive complaints or psychiatric symptomatology. These findings suggest that a significant portion of patients with chronic HCV experience cognitive difficulties that may interfere with activities of daily living and quality of life. Future research using cognitive measures with HCV-infected patients may assist researchers in identifying if there is a direct effect of HCV infection on the brain and which patients may be more likely to progress to cirrhosis and hepatic encephalopathy. (JINS, 2003, 9, 847–854.)

HIV infection often results in neuropsychological (NP) impairment. In order to assess the impact that HIV-related NP deficits may have on automobile driving, we evaluated 68 HIV-seropositive drivers using an NP battery and two PC-based driving simulations. Thirty-two participants were classified as NP impaired; most (72%) evidenced only mild impairment, and none met criteria for HIV-associated dementia. After controlling for degree of immunosuppression and disease stage, NP-impaired participants failed a previously validated driving simulation at a much higher rate than cognitively intact participants [OR = 5.3, 95% CI (1.7, 17.0), p = .006]. Similarly, on a simulation of city driving, NP impaired participants were more likely to fail based upon the number of accidents [OR = 6.1, 95% CI (1.5, 24.6), p = .01]. Simulator performance was predicted by functioning in a number of NP domains, with NP tests accounting for 13–30% of the variance on the simulations. Although it would be premature to extrapolate these findings to impairment in on-the-road driving, they do argue for greater attention to the impact that even mild HIV-related NP deficits may have on driving skills. (JINS, 1999, 5, 579–592.)

This study sought to determine if human immunodeficiency virus–type 1 (HIV-1) infected depressed men were more likely to be neuropsychologically impaired than their nondepressed counterparts. Subjects were 47 HIV-1 infected men who met DSM–III–R criteria for current major depressive disorder (MDD) and 47 HIV-1 infected nondepressed male controls (M age = 34.2 years) equated on HIV-1 disease severity, demographics, and drug use. The psychiatric interview included the Structured Clinical Inventory for the DSM–III–R, and Hamilton Rating Scale for Depression. The neuropsychological battery included tests covering 8 functional domains based on an expanded Halstead-Reitan Battery. The medical assessment included a history and physical examination, immunologic staging, and evaluation of prescription and recreational drug use. Prevalence of global neuropsychological impairment in the two groups (depressed vs. control) did not differ [53% vs. 38% respectively; χ2(1, N = 94) = 2.11, p > .05]. While syndromically depressed patients performed less well than nondepressed individuals on memory tests [delayed retention portions of the Story Memory Test: F(1,91) = 5.34, p < .05; and Figure Memory Test: F(1,90) = 4.16, p < .05], the majority of depressed participants (64%) did not have clinically impaired memory. No relationship between neuropsychological impairment and severity of depression was observed. The results suggest that, while HIV-1 infected men with major depression may perform more poorly than nondepressed men on some aspects of memory tasks, they are not more likely to evidence clinically significant neurocognitive impairment. (JINS, 1997, 3, 457–463.)