852 resultados para Attention Deficit with Hyperactivity Disorder
Resumo:
Baerg, S., Cairney, J., Hay, J., Rempel, L. and Faught, B.E. (2009). Physical Activity of Children with Developmental Coordination Disorder in the Presence of Attention Deficit Hyperactivity Disorder: Does Gender Matter? Brock University, St. Catharines, Ontario, CANADA. Children with Developmental Coordination Disorder (DCD) have difficulties in motor coordination. Attention-deficit hyperactive disorder (ADHD) is considered the condition most co-morbid with DCD at approximately 50%. Children with DCD are generally less physically active (PA) than their peers, while children with ADHD are often considered more physically active. It is not known if the physical activity patterns of children with DCD-ADHD resemble those of children with primarily DCD or that of their healthy peers. The primary objective of this research was to contrast physical activity patterns between children with DCD, DCD-ADHD, and healthy controls. Since boys are generally reported as more physically active than girls, a secondary objective was to determine if gender moderated the association between groups and physical activity. A sample of males (n=66) and females (n=44) were recruited from the Physical Health Activity Study Team (PHAST) longitudinal study. The Movement Assessment Battery for Children (2nd Ed.) was used to identify probable cases of DCD, and Connor's Revised Parent Rating Scale- Short Version to identify ADHD. Subjects (mean age=12.8±.4 yrs) were allocated to three groups; DCD (n=32), DCD-ADHD (n=30) and control (n=48). Physical activity was monitored for seven days with the Actical® accelerometer (activity count, step count and energy expenditure). Children completed the Participation Questionnaire (PQ) during the in-school session of data collection for the PHAST study. Height, weight and body mass index (BMI) were also determined. Analysis of variance showed significant group differences for activity count (F(2,56)=5.36, p=.007) and PQ (F(2,44 )=6. 71, p=.003) in males, while a significant group difference for step count (F(2,37)=3.55, p=.04) was found in females. Post hoc comparison tests (Tukey) identified significantly lower PQ and activity count between males with OCD and controls (p=.004) and males with DCD-ADHD and controls (p=.003). Conversely, females with DCD-ADHD had significantly more step counts than their controls (p=.01). Analysis of covariance demonstrated a gender by DCD groups negative interaction for males (activity count) (F(2,92):;:3.11, p=.049) and a positive interaction for females (step count) (F(1,92)=4.92, p=.009). Hyperactivity in females with DCD-ADHD appears to contribute to more physical activity, whereas DCD may contribute to decreased activity in males with DCD and DCDADHD. Further research is needed to examine gender differences in physical activity within the context of DCD and ADHD.
Resumo:
We argue that impulsiveness is characterized by compromised timing functions such as premature motor timing, decreased tolerance to delays, poor temporal foresight and steeper temporal discounting. A model illustration for the association between impulsiveness and timing deficits is the impulsiveness disorder of attention-deficit hyperactivity disorder (ADHD). Children with ADHD have deficits in timing processes of several temporal domains and the neural substrates of these compromised timing functions are strikingly similar to the neuropathology of ADHD. We review our published and present novel functional magnetic resonance imaging data to demonstrate that ADHD children show dysfunctions in key timing regions of prefrontal, cingulate, striatal and cerebellar location during temporal processes of several time domains including time discrimination of milliseconds, motor timing to seconds and temporal discounting of longer time intervals. Given that impulsiveness, timing abnormalities and more specifically ADHD have been related to dopamine dysregulation, we tested for and demonstrated a normalization effect of all brain dysfunctions in ADHD children during time discrimination with the dopamine agonist and treatment of choice, methylphenidate. This review together with the new empirical findings demonstrates that neurocognitive dysfunctions in temporal processes are crucial to the impulsiveness disorder of ADHD and provides first evidence for normalization with a dopamine reuptake inhibitor.
Resumo:
Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD) are often comorbid and share behavioural-cognitive abnormalities in sustained attention. A key question is whether this shared cognitive phenotype is based on common or different underlying pathophysiologies. To elucidate this question, we compared 20 boys with ADHD to 20 age and IQ matched ASD and 20 healthy boys using functional magnetic resonance imaging (fMRI) during a parametrically modulated vigilance task with a progressively increasing load of sustained attention. ADHD and ASD boys had significantly reduced activation relative to controls in bilateral striato–thalamic regions, left dorsolateral prefrontal cortex (DLPFC) and superior parietal cortex. Both groups also displayed significantly increased precuneus activation relative to controls. Precuneus was negatively correlated with the DLPFC activation, and progressively more deactivated with increasing attention load in controls, but not patients, suggesting problems with deactivation of a task-related default mode network in both disorders. However, left DLPFC underactivation was significantly more pronounced in ADHD relative to ASD boys, which furthermore was associated with sustained performance measures that were only impaired in ADHD patients. ASD boys, on the other hand, had disorder-specific enhanced cerebellar activation relative to both ADHD and control boys, presumably reflecting compensation. The findings show that ADHD and ASD boys have both shared and disorder-specific abnormalities in brain function during sustained attention. Shared deficits were in fronto–striato–parietal activation and default mode suppression. Differences were a more severe DLPFC dysfunction in ADHD and a disorder-specific fronto–striato–cerebellar dysregulation in ASD.
Resumo:
Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD) are often comorbid and share cognitive abnormalities in temporal foresight. A key question is whether shared cognitive phenotypes are based on common or different underlying pathophysiologies and whether comorbid patients have additive neurofunctional deficits, resemble one of the disorders or have a different pathophysiology. We compared age- and IQ-matched boys with non-comorbid ADHD (18), non-comorbid ASD (15), comorbid ADHD and ASD (13) and healthy controls (18) using functional magnetic resonance imaging (fMRI) during a temporal discounting task. Only the ASD and the comorbid groups discounted delayed rewards more steeply. The fMRI data showed both shared and disorder-specific abnormalities in the three groups relative to controls in their brain-behaviour associations. The comorbid group showed both unique and more severe brain-discounting associations than controls and the non-comorbid patient groups in temporal discounting areas of ventromedial and lateral prefrontal cortex, ventral striatum and anterior cingulate, suggesting that comorbidity is neither an endophenocopy of the two pure disorders nor an additive pathology.
Resumo:
Three-dimensional kinematic analysis of line of gaze, arm and ball was used to describe the visual and motor behaviour of male adolescents diagnosed with attention deficit hyperactivity disorder (ADHD). The ADHD participants were tested when both on (ADHD-On) and off (ADHD-Off) their medication and compared to age-matched normal controls in a modified table tennis task that required tracking the ball and hitting to cued right and left targets. Long-duration information was provided by a pre-cue, in which the target was illuminated approximately 2 s before the serve, and short-duration information by an early-cue illuminated about 350 ms after the serve, leaving -500 ms to select the target and perform the action. The ADHD groups differed significantly from the control group in both the pre-cue and early-cue conditions in being less accurate, in having a later onset and duration of pursuit tracking, and a higher frequency of gaze on and off the ball. The use of medication significantly reduced the gaze frequency of the ADHD participants, but surprisingly this did not lead to an increase in pursuit tracking, suggesting a barrier was reached beyond which ball flight information could not be processed. The control and ADHD groups did not differ in arm movement onset, duration and velocity in the short-duration early-cue condition; in the long-duration pre-cue condition, however, the ADHD group's movement time onset and arm velocity differed significantly from controls. The results show that the ADHD groups were able to process short-duration information without experiencing adverse effects on their motor behaviour; however, long-duration information contributed to irregular movement control.
Resumo:
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Resumo:
Abstract Background Attention deficit hyperactivity disorder (ADHD) is a neurobiological condition that affects 3%–7% of the pediatric population and significantly compromises the quality of life (QoL) of these individuals. The aim of the current study was to compare child self-reports and parent proxy reports on the QoL of children with ADHD. Methods Forty-five children with ADHD, combined type, aged 8–12 years without comorbidities, were compared with 43 typically developing children. PedsQL™ 4.0 (Pediatric QoL Inventory™) Generic Core Scales (physical, emotional, social, and school functioning) were completed by families and children self-reporting their health-related QoL. Results Children with ADHD reported themselves significantly lowered their PedsQL™ scores on all dimensions in comparison to typically developing children. Statistically significant differences were observed in social functioning (p = 0.010), school functioning (p <0.001), psychosocial health (p <0.001), and total score (p = 0.002). The physical functioning and emotional functioning dimensions did not differ significantly between groups, with p = 0.841 and p = 0.070, respectively. Parents of children with ADHD also reported lower PedsQL™ scores, with statistically significant differences in all dimensions. The relationship between child self-reports and parent proxy reports indicated that there is greater agreement among children with ADHD, except for the school functioning. Conclusions This suggests that children with the disorder and their parents have a perception of the functional limitations the disorder brings. It is therefore important to undertake studies to verify the QoL in children with ADHD that aim to provide and measure the scope of the well-being of these children.
Resumo:
In contrast to studies of depression and psychosis, the first part of this study showed no major differences in serum levels of cytokines and tryptophan metabolites between healthy children and those with attention-deficit/hyperactivity disorder of the combined type (ADHD). Yet, small decreases of potentially toxic kynurenine metabolites and increases of cytokines were evident in subgroups. Therefore we examined predictions of biochemical associations with the major symptom clusters, measures of attention and response variability.
Resumo:
The heritability of attention deficit hyperactivity disorder (ADHD) is approximately 0.8. Despite several larger scale attempts, genome-wide association studies (GWAS) have not led to the identification of significant results. We performed a GWAS based on 495 German young patients with ADHD (according to DSM-IV criteria; Human660W-Quadv1; Illumina, San Diego, CA) and on 1,300 population-based adult controls (HumanHap550v3; Illumina). Some genes neighboring the single nucleotide polymorphisms (SNPs) with the lowest P-values (best P-value: 8.38 × 10(-7)) have potential relevance for ADHD (e.g., glutamate receptor, metabotropic 5 gene, GRM5). After quality control, the 30 independent SNPs with the lowest P-values (P-values ≤ 7.57 × 10(-5) ) were chosen for confirmation. Genotyping of these SNPs in up to 320 independent German families comprising at least one child with ADHD revealed directionally consistent effect-size point estimates for 19 (10 not consistent) of the SNPs. In silico analyses of the 30 SNPs in the largest meta-analysis so far (2,064 trios, 896 cases, and 2,455 controls) revealed directionally consistent effect-size point estimates for 16 SNPs (11 not consistent). None of the combined analyses revealed a genome-wide significant result. SNPs in previously described autosomal candidate genes did not show significantly lower P-values compared to SNPs within random sets of genes of the same size. We did not find genome-wide significant results in a GWAS of German children with ADHD compared to controls. The second best SNP is located in an intron of GRM5, a gene located within a recently described region with an infrequent copy number variation in patients with ADHD.
Resumo:
Adult Alcohol Use Disorders (AUD) patients with Attention Deficit/Hyperactivity Disorder (ADHD) symptoms may suffer more from craving than patients who only have AUD. However, craving may be even more strongly related to withdrawal and psychiatric symptoms; therefore, the association between craving and ADHD may be misinterpreted. The purpose of this study is to examine the association between craving and ADHD symptoms among AUD patients in more detail.
Resumo:
The aim of the present study was to investigate prefrontal brain function and cognitive response control in patients with personality disorders who either suffered or did not suffer from psychopathology related to attention deficit hyperactivity disorder (ADHD) during childhood. For this purpose, 36 psychiatric out-patients with personality disorders--24 of whom showed ADHD-related psychopathology during childhood assessed by the German short form of the Wender Utah Rating Scale--and 24 healthy controls were investigated electrophysiologically by means of a cued Go-NoGo task (Continuous Performance Test). Topographical analyses were conducted to individually quantify the NoGo anteriorisation (NGA), a neurophysiological correlate of prefrontal response control that has been suggested to reflect activation of the anterior cingulate cortex. ADHD patients exhibited a significantly reduced mean NGA and diminished amplitudes of the Global Field Power, as well as a reduced increase of fronto-central P300 amplitudes, in NoGo-trials compared with the healthy controls, whereas patients with personality disorders alone did not differ from the control group in any of the electrophysiological parameters. The results indicate that ADHD-related psychopathology is associated with prefrontal brain dysfunction, probably related to processes of response inhibition and/or cognitive response control.
Resumo:
Aims To determine comorbidity patterns in treatment-seeking substance use disorder (SUD) patients with and without adult attention deficit hyperactivity disorder (ADHD), with an emphasis on subgroups defined by ADHD subtype, taking into account differences related to gender and primary substance of abuse. Design Data were obtained from the cross-sectional International ADHD in Substance use disorder Prevalence (IASP) study. Setting Forty-seven centres of SUD treatment in 10 countries. Participants A total of 1205 treatment-seeking SUD patients. Measurements Structured diagnostic assessments were used for all disorders: presence of ADHD was assessed with the Conners' Adult ADHD Diagnostic Interview for DSM-IV (CAADID), the presence of antisocial personality disorder (ASPD), major depression (MD) and (hypo)manic episode (HME) was assessed with the Mini International Neuropsychiatric Interview-Plus (MINI Plus), and the presence of borderline personality disorder (BPD) was assessed with the Structured Clinical Interview for DSM-IV Axis II (SCID II). Findings The prevalence of DSM-IV adult ADHD in this SUD sample was 13.9%. ASPD [odds ratio (OR) = 2.8, 95% confidence interval (CI) = 1.8–4.2], BPD (OR = 7.0, 95% CI = 3.1–15.6 for alcohol; OR = 3.4, 95% CI = 1.8–6.4 for drugs), MD in patients with alcohol as primary substance of abuse (OR = 4.1, 95% CI = 2.1–7.8) and HME (OR = 4.3, 95% CI = 2.1–8.7) were all more prevalent in ADHD+ compared with ADHD− patients (P < 0.001). These results also indicate increased levels of BPD and MD for alcohol compared with drugs as primary substance of abuse. Comorbidity patterns differed between ADHD subtypes with increased MD in the inattentive and combined subtype (P < 0.01), increased HME and ASPD in the hyperactive/impulsive (P < 0.01) and combined subtypes (P < 0.001) and increased BPD in all subtypes (P < 0.001) compared with SUD patients without ADHD. Seventy-five per cent of ADHD patients had at least one additional comorbid disorder compared with 37% of SUD patients without ADHD. Conclusions Treatment-seeking substance use disorder patients with attention deficit hyperactivity disorder are at a very high risk for additional externalizing disorders.
Resumo:
OBJECTIVE: To examine the relationships between physical growth and medications prescribed for symptoms of attention-deficit hyperactivity disorder in children with HIV. METHODS: Analysis of data from children with perinatally acquired HIV (N = 2251; age 3-19 years), with and without prescriptions for stimulant and nonstimulant medications used to treat attention-deficit hyperactivity disorder, in a long-term observational study. Height and weight measurements were transformed to z scores and compared across medication groups. Changes in z scores during a 2-year interval were compared using multiple linear regression models adjusting for selected covariates. RESULTS: Participants with (n = 215) and without (n = 2036) prescriptions were shorter than expected based on US age and gender norms (p < .001). Children without prescriptions weighed less at baseline than children in the general population (p < .001) but gained height and weight at a faster rate (p < .001). Children prescribed stimulants were similar to population norms in baseline weight; their height and weight growth velocities were comparable with the general population and children without prescriptions (for weight, p = .511 and .100, respectively). Children prescribed nonstimulants had the lowest baseline height but were similar to population norms in baseline weight. Their height and weight growth velocities were comparable with the general population but significantly slower than children without prescriptions (p = .01 and .02, respectively). CONCLUSION: The use of stimulants to treat symptoms of attention-deficit hyperactivity disorder does not significantly exacerbate the potential for growth delay in children with HIV and may afford opportunities for interventions that promote physical growth. Prospective studies are needed to confirm these findings.