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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study examined the construct of attention control, which is an important aspect of effortful control, in a sample of non-clinical children aged between 9 and 13 years. Results demonstrated that attention control was associated with a broad range of psychopathological complaints, including symptoms of anxiety, aggression, depression, and ADHD. As predicted, lower levels of attention control were accompanied by higher levels of these symptoms. Further, attention control was also negatively related to threat perception distortions, which indicates that children who display low levels of this regulative temperament factor are more prone to such cognitive biases. Third, when controlling for neuroticism, attention control remained significantly (negatively) associated with symptoms of anxiety, depression (child report only), and ADHD. The correlations between attention control and threat perception distortions largely disappeared when the influence of neuroticism was partialled out. Only the link between attention control and anxious interpretations of ambiguous vignettes survived this correction. Finally, no evidence was found for the hypothesised mediating role of cognitive distortions on the relation between temperament factors and psychopathological symptoms.
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PMID:Attention control in middle childhood: relations to psychopathological symptoms and threat perception distortions. 1698 96

The study builds on the propositions introduced in a companion paper on the neuropharmacology of cognition and its relation to key findings in psychiatry. Cognitive inhibition is often invoked to explain performance in psychiatric illness. Yet it remains only a general conceptual model of executive dysfunction. Premotor theory proposes both neuroanatomical and neuropharmacological equivalents of conscious and unconscious processes. The interaction between monoaminergic and cholinergic neurotransmission is stated to have an inverse effect on these two fundamental psychological processes. If one conceives of cognitive inhibition as a failure to voluntarily suppress unconscious prepotent responses, then a deficit in monoaminergic antagonism of cholinergic facilitated prepotent responses accounts for the observed behavioural phenotypes. The plasticity of behaviour is further hypothesized to have an equivalent in intracellular signalling leading to plastic changes in neural networks. Apart from inhibition of prepotent responses it permits the formulation of new behavioural phenotypes. At the receptor level Gi-Gq/11 transduction coupling is proposed to mediate this effect. A hypofunctioning monoaminergic system is thought to underlie the clinical pictures of major depression and ADHD. The neurocognitive deficits of depression include memory loss, poor concentration and rumination. ADHD is characterized by inattention, impulsivity and hyperactivity. Both these syndromes effectively respond to raising serotonin and dopamine levels, respectively. The core symptoms can usefully be attributed to an imbalance between the neuromodulatory effects of monoamines and ACh. Taking the model of monoaminergic-muscarinic receptor interactions presented previously and extended here, a new hypothesis is proposed for the core symptoms of ADHD. Accordingly, impulsivity and hyperactivity result from impaired dopaminergic inhibition and remodelling of muscarinic mediated prepotent responses. The model also predicts memory impairment in major depression by proposing that low serotonin levels in the neocortex is linked to focal hippocampal dysfunction. Hippocampal theta is proposed to trigger phasic monoaminergic activation involved in encoding of cortical traces and plasticity of propotent networks. It proposes a hypothesis for the enhancement of mood and behaviour induced by antidepressants is partly a response to plasticity of neural networks, that is, remodelling of cholinergic-mediated negative habitual behaviours.
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PMID:Neurocognitive deficits in major depression and a new theory of ADHD: a model of impaired antagonism of cholinergic-mediated prepotent behaviours in monoamine depleted individuals. 1699 97

CNS Vital Signs (CNSVS) is a computerized neurocognitive test battery that was developed as a routine clinical screening instrument. It is comprised of seven tests: verbal and visual memory, finger tapping, symbol digit coding, the Stroop Test, a test of shifting attention and the continuous performance test. Because CNSVS is a battery of well-known neuropsychological tests, one should expect its psychometric properties to resemble those of the conventional tests upon which it is based. 1069 subjects age 7-90 participated in the normative database for CNSVS. Test-retest reliability (TRT) was evaluated in 99 Ss who took the battery on two separate occasions, separated, on the average, by 62 days; the results were comparable to those achieved by equivalent conventional and computerized tests. Concurrent validity studies in 180 subjects, normals and neuropsychiatric patients, indicate correlations that are comparable to the concurrent validity of similar tests. Discriminant validity is supported by studies of patients with mild cognitive impairment and dementia, post-concussion syndrome and severe traumatic brain injury, ADHD (treated and untreated) and depression (treated and untreated). The tests in CNSVS are also sensitive to malingerers and patients with conversion disorders. The psychometric characteristics of the tests in the CNSVS battery are very similar to the characteristics of the conventional neuropsychological tests upon which they are based. CNSVS is suitable for use as a screening instrument, or as a serial assessment measure. But it is not a substitute for formal neuropsychological testing, it is not diagnostic, and it will have only a limited role in the medical setting, absent the active participation of consulting neuropsychologists.
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PMID:Reliability and validity of a computerized neurocognitive test battery, CNS Vital Signs. 1701 81

Research indicates that cannabis continues to be a popular illegal drug internationally. Furthermore, adolescent rates of use appear to be significant. Whilst the non-acute effect of cannabis use on adult cognition has been extensively researched, there has been less examination of adolescents. This study aimed to investigate the non-acute relationship between cannabis and cognitive function in a sample of adolescents with a continuum of cannabis use, taking into account additional predictor variables (psychiatric functioning, general functioning, demographics and other drug use). Seventy adolescents were recruited from clinical and community sources as well as through newspaper advertisements. After 12 hours abstinence from cannabis, adolescents completed a two-hour interview covering: demographics; alcohol and drug use history; drug use in the past 28 days; depression; further psychiatric functioning (including ADHD and Conduct Disorder); and cognitive functioning as measured by computerised tasks (CANTAB) and traditional pen and paper tests. Adolescents who were regular cannabis users (more than once a week) had a significantly poorer performance on four measures of cognitive function reflecting attention, spatial working memory and learning. Cannabis use remained an independent predictor of performance on the working memory and strategy measures after additional predictor variables were included in a multivariate regression analysis. The results suggest that aspects of adolescent cognitive function are independently related to the frequency of cannabis use beyond acute intoxication.
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PMID:The relationship between non-acute adolescent cannabis use and cognition. 1745 21

Co-occurring psychiatric disorders have been associated with poor prognosis among substance-dependent patients, but few studies have examined this association among patients with cocaine dependence (CD). We compared baseline characteristics and treatment outcome between cocaine-dependent patients with major depressive disorder (MDD; n = 66), those with attention-deficit/hyperactivity disorder (ADHD; n = 53), and those with CD without comorbid disorders (CD alone; n = 48) who had been randomized to the placebo arms of clinical trials with venlafaxine, methylphenidate, and gabapentin, respectively. The three groups differed significantly in racial makeup, with more Caucasians and Hispanics among patients with MDD and those with ADHD but more African Americans among those with CD alone. The groups did not differ significantly in treatment retention, with retention rates ranging from 42% to 47%; neither did they differ in the rates of achieving 2 consecutive weeks of urinalysis-confirmed abstinence, with rates ranging from 40% to 50%. Using logistic regression for repeated measures with general estimating equations, modeling the likelihood of a cocaine-positive week over time in treatment, we found the diagnostic group to interact with the baseline level of cocaine use and time. Among cocaine-dependent patients who achieved abstinence at baseline, those with MDD and those with ADHD had better outcome over time as compared with patients with CD alone. However, among patients with cocaine-positive urine specimens at baseline, those with MDD and those with ADHD were associated with poor outcome as compared with patients with CD alone. The findings suggest that diagnosis and treatment of co-occurring disorders such as depression and ADHD may be important components of treatment planning for CD and that the baseline level of cocaine use should be included as a covariate in studies evaluating the impact of such treatment.
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PMID:Effects of major depressive disorder and attention-deficit/hyperactivity disorder on the outcome of treatment for cocaine dependence. 1757 96

Genetic factors have a variable impact on Alzheimer's Disease (AD), ranging from familial forms that are transmitted in an autosomal dominant fashion to sporadic AD, where a polygenic component is present. Most genes conferring susceptibility to AD are related to amyloid-beta deposition (APP; PS1; PS2; APOE; Cystatin-C; ubiquilin-1), oxidative stress (NOS2; NOS3) and inflammatory response (IL-1 alpha; IL-1 beta; IL-6; TNF-alpha). Genome-wide analyses, transcriptomics and proteomics approaches have pointed also to proapoptotic genes as increasing AD liability. Depression and psychotic symptoms that occur in a large proportion of AD patients have been associated with monoamine genes coding for metabolic enzymes (COMT), transporters (5-HTTLPR) and receptors (DRD1; DRD3). Genetic testing may be useful to confirm the diagnosis of AD in individuals with clinical signs of dementia, while it is generally not recommended as a predictive testing for AD in asymptomatic individuals. Drugs currently in use to treat AD are effective in only 20% of patients; their therapeutic effect is predominantly under genetic control (CYP26 gene; APOE). Environmental factors have been shown to moderate the effects of genes on psychiatric disorders such as depression, schizophrenia and ADHD. The study of gene-environment interactions in AD, that are still poorly understood, is essential to predict disease-risk in asymptomatic individuals. Genomics will provide a dynamic picture of biological processes in AD and new targets for the forthcoming anti-AD drugs.
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PMID:Genetics of Alzheimer's disease. A rapidly evolving field. 1785 Nov 96

Learning, attention, graphomotor, and processing speed scores were analyzed in 149 typical control children and 886 clinical children with normal intelligence. Nonsignificant differences were found between control children and children with anxiety, depression, and oppositional-defiant disorder. Control children performed better than children with ADHD and autism in all areas. Children with ADHD and autism did not differ, except that children with ADHD had greater learning problems. Attention, graphomotor, and speed weaknesses were likely to coexist, the majority of children with autism and ADHD had weaknesses in all three areas, and these scores contributed significantly to the prediction of academic achievement.
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PMID:Learning, attention, writing, and processing speed in typical children and children with ADHD, autism, anxiety, depression, and oppositional-defiant disorder. 1785 25

The predictive validity of symptom criteria for different subtypes of ADHD among children who were impaired in at least one setting in early childhood was examined. Academic achievement was assessed seven times over 8 years in 125 children who met symptom criteria for ADHD at 4-6 years of age and in 130 demographically-matched non-referred comparison children. When intelligence and other confounds were controlled, children who met modified criteria for the predominantly inattentive subtype of ADHD in wave 1 had lower reading, spelling, and mathematics scores over time than both comparison children and children who met modified criteria for the other subtypes of ADHD. In some analyses, children who met modified criteria for the combined type had somewhat lower mathematics scores than comparison children. The robust academic deficits relative to intelligence in the inattentive group in this age range suggest either that inattention results in academic underachievement or that some children in the inattentive group have learning disabilities that cause secondary symptoms of inattention. Unexpectedly, wave 1 internalizing (anxiety and depression) symptoms independently predicted deficits in academic achievement controlling ADHD, intelligence, and other predictors.
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PMID:Academic achievement over 8 years among children who met modified criteria for attention-deficit/hyperactivity disorder at 4-6 years of age. 1794 Aug 63

Mixed episodes are associated with greater total lifetime costs, increased suicide risk, and increased substance misuse than pure manic episodes and may resemble depressive episodes due to similar quality of life scores, cognitive styles, and likelihood of cycling to depression. Patients with mixed states have an increased potential for abnormally low cholesterol, hypothyroidism, and other medical comorbidities that can slow recovery. In addition, patients with mixed states can have comorbid anxiety disorders and ADHD.
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PMID:Bipolar mixed episodes: characteristics and comorbidities. 1796 Sep 58

Research within the area of paranoid thinking has focused primarily on adults and has only recently looked at the effects during the critical life stage of adolescence, with even less research in the context of the juvenile justice system. This article aims to explore the relationship between antisocial behaviour in adolescence and the development of paranoid thinking, set within wider contexts that surround the juvenile justice system. The information presented is drawn from both the current research and the clinical experiences of those working in adolescent forensic psychiatry services. The relationships with other disorders such as conduct disorder, ADHD, PTSD, and depression are also explored.
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PMID:A developmental approach to violence, hostile attributions, and paranoid thinking in adolescence. 1804 36


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