Multiple deficits in ADHD : executive dysfunction, delay aversion, reaction time variability, and emotional deficits
01 Jun 2013-Journal of Child Psychology and Psychiatry (John Wiley & Sons, Ltd)-Vol. 54, Iss: 6, pp 619-627
TL;DR: The current study supports the view of ADHD as a heterogeneous disorder related to multiple neuropsychological deficits and emotional functioning appears to be an area of importance for ADHD that needs to be incorporated into future theoretical models.
Abstract: Background: The notion that ADHD constitutes a heterogeneous disorder is well accepted. However, this study contributes with new important knowledge by examining independent effects of a large rang ...
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TL;DR: Three models are considered to explain the overlap between emotion dys regulation and ADHD: emotion dysregulation and ADHD are correlated but distinct dimensions; the combination constitutes a nosological entity distinct from both ADHD and emotion Dysregulation alone.
Abstract: Emotion dysregulation, a major contributor to impairment throughout life, is common in ADHD and may arise from deficits in orienting toward and processing emotional stimuli, implicating dysfunction within the prefrontal cortical network. Understanding the nature of the overlap between emotional dysregulation and ADHD can stimulate novel treatment approaches.
759 citations
Cites background from "Multiple deficits in ADHD : executi..."
...Yuill (31) Corbett (30) Malisza (29) Da Fonseca (28) Boakes (21) Cadesky (12) Seymour (32) Shin (27) Rapport (23) Dyck (25) Pelc (26) Downs (33) Greenbaum (34) Sjöwall (boys) (35) Sjöwall (girls) (35) Sinzig (22) Miller (inattentive) (36) Herpertz (24) Miller (combined) (36)...
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...(35) Clinic based; ADHD, N=102; controls, N=102 Parent report of child’s ability to regulate specific emotions Not given ADHD showed significant impairment compared with controls in regulating all emotions...
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...Similarly, modest correlations have been reported between deficits in emotional processes— such as deficits in emotion recognition and frustration tolerance—and the executive dysfunction often held to be a core feature of the disorder (35, 37)....
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...79), albeit with considerable heterogeneity in results (35, 37) (Figure 1C)....
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...Plichta (38) Kuntsi (44) Marx (adult) (46) Solanto (48) Dalen (42) Marco (child) (45) Antrop (39) Marx (child) (46) Vloet (49) Bitsakou (child) (41) Marco (adolescent) (45) Marx (adolescent) (46) Yang (50) Banaschewski (37) Karalunas (43) Sjöwall (boys) (35) Bitsakou (adolescent) (41) Bidwell (40) Solanto (inattentive) (47) Solanto (combined) (47) Sjöwall (girls) (35)...
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659 citations
TL;DR: The need for future non-pharmacological interventions to be more specifically targeted for ADHD symptoms and its commonly associated functioning deficits in order to ensure the best long-term outcomes for children with ADHD is addressed.
Abstract: Attention-deficit hyperactivity disorder (ADHD) is a complex disorder that can affect individuals across the lifespan. It is associated with substantial heterogeneity in terms of aetiology, clinical presentation and treatment outcome and is the subject of extensive research. Because of this, it can be difficult for clinicians to stay up to date with the most relevant findings and know how best to respond to parents' questions and concerns about the disorder and interventions. This is a narrative review that aims to summarize key findings from recent research into ADHD and its treatment that clinicians can share with families in order to increase their knowledge about ADHD and intervention options. ADHD develops as a result of complex interplay between interdependent genetic and non-genetic factors. The disorder is associated with substantial impairments in functioning and poor long-term outcomes. Pharmacological and non-pharmacological treatment options are available for symptom management and to improve function, but functioning outcomes often fail to normalize in children with ADHD. Despite extensive advances in understanding this complex disorder, it is clear that there is still a long way to go. In particular, we address the need for future non-pharmacological interventions to be more specifically targeted for ADHD symptoms and its commonly associated functioning deficits in order to ensure the best long-term outcomes for children with ADHD.
199 citations
Cites background from "Multiple deficits in ADHD : executi..."
...This follows evidence that some children show deficits in emotion functioning yet remain unimpaired on measures of neuropsychological functioning including executive function and delay aversion (Sjowall et al. 2013)....
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...They may also display impairments during emotion recognition tasks (Da Fonseca et al. 2009; Sjowall et al. 2013)....
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TL;DR: A meta-analysis of 77 studies revealed that youth with ADHD have the greatest impairment on ERNL, followed by EREG followed by ECUT, and the association between ADHD and ECUT was significantly weaker among studies that controlled for co-occurring conduct problems.
191 citations
TL;DR: Performance of individuals with ADHD on social cognition lies intermediate between ASD and healthy controls, however, developmental trajectories of social cognition probably differ between ADHD and ASD as social cognitive deficits in ADHD might be improving with age in most individuals.
Abstract: Background Impairment in social cognition is an established finding in autism spectrum disorders (ASD). Emerging evidence suggests that attention-deficit/hyperactivity disorder (ADHD) might be also associated with deficits in theory of mind (ToM) and emotion recognition. However, there are inconsistent findings, and it has been debatable whether such deficits persist beyond childhood and how similar social cognitive deficits are in ADHD v. ASD. Method We conducted a meta-analysis of social cognition, including emotion recognition and ToM, studies in ADHD compared with healthy controls and ASD. The current meta-analysis involved 44 studies comparing ADHD (n = 1999) with healthy controls (n = 1725) and 17 studies comparing ADHD (n = 772) with ASD (n = 710). Results Facial and vocal emotion recognition (d = 0.40–0.44) and ToM (d = 0.43) abilities were significantly impaired in ADHD. The most robust facial emotion recognition deficits were evident in anger and fear. Social cognitive deficits were either very subtle (emotion recognition) or non-significant (ToM) in adults with ADHD. Deficits in social cognition, especially ToM, were significantly more pronounced in ASD compared with ADHD. General cognitive impairment has contributed to social cognitive deficits in ADHD. Conclusions Performance of individuals with ADHD on social cognition lies intermediate between ASD and healthy controls. However, developmental trajectories of social cognition probably differ between ADHD and ASD as social cognitive deficits in ADHD might be improving with age in most individuals. There is a need for studies investigating a potential subtype of ADHD with persistent social cognitive deficits and exploring longitudinal changes in social cognition during development.
187 citations
Cites background from "Multiple deficits in ADHD : executi..."
...Pantelis Sjöwall et al. (2013) 102 ADHD, 102 HC Face emotion NimStim 71 C, 27 I, 4 H/I 10 took medication last 24 h CD or ODD 46% Anxiety disorder 8% MR excluded Impaired in all but disgust Sodian & Hülsken (2005) 32 ADHD, 101 HC FB2, Happé stories Epistemic state attribution task Age (ADHD) = 8.9…...
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01 Dec 1969TL;DR: The concepts of power analysis are discussed in this paper, where Chi-square Tests for Goodness of Fit and Contingency Tables, t-Test for Means, and Sign Test are used.
Abstract: Contents: Prefaces. The Concepts of Power Analysis. The t-Test for Means. The Significance of a Product Moment rs (subscript s). Differences Between Correlation Coefficients. The Test That a Proportion is .50 and the Sign Test. Differences Between Proportions. Chi-Square Tests for Goodness of Fit and Contingency Tables. The Analysis of Variance and Covariance. Multiple Regression and Correlation Analysis. Set Correlation and Multivariate Methods. Some Issues in Power Analysis. Computational Procedures.
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...Effect sizes were calculated using g2 (Cohen, 1988)....
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11 Jun 2013
113,134 citations
TL;DR: An issue concerning the criteria for tic disorders is highlighted, and how this might affect classification of dyskinesias in psychotic spectrum disorders.
Abstract: Given the recent attention to movement abnormalities in psychosis spectrum disorders (e.g., prodromal/high-risk syndromes, schizophrenia) (Mittal et al., 2008; Pappa and Dazzan, 2009), and an ongoing discussion pertaining to revisions of the Diagnostic and Statistical Manuel of Mental Disorders (DSM) for the upcoming 5th edition, we would like to take this opportunity to highlight an issue concerning the criteria for tic disorders, and how this might affect classification of dyskinesias in psychotic spectrum disorders.
Rapid, non-rhythmic, abnormal movements can appear in psychosis spectrum disorders, as well as in a host of commonly co-occurring conditions, including Tourette’s Syndrome and Transient Tic Disorder (Kerbeshian et al., 2009). Confusion can arise when it becomes necessary to determine whether an observed movement (e.g., a sudden head jerk) represents a spontaneous dyskinesia (i.e., spontaneous transient chorea, athetosis, dystonia, ballismus involving muscle groups of the arms, legs, trunk, face, and/or neck) or a tic (i.e., stereotypic or patterned movements defined by the relationship to voluntary movement, acute and chronic time course, and sensory urges). Indeed, dyskinetic movements such as dystonia (i.e., sustained muscle contractions, usually producing twisting and repetitive movements or abnormal postures or positions) closely resemble tics in a patterned appearance, and may only be visually discernable by attending to timing differences (Gilbert, 2006).
When turning to the current DSM-IV TR for clarification, the description reads: “Tic Disorders must be distinguished from other types of abnormal movements that may accompany general medical conditions (e.g., Huntington’s disease, stroke, Lesch-Nyhan syndrome, Wilson’s disease, Sydenham’s chorea, multiple sclerosis, postviral encephalitis, head injury) and from abnormal movements that are due to the direct effects of a substance (e.g., a neuroleptic medication)”. However, as it is written, it is unclear if psychosis falls under one such exclusionary medical disorder. The “direct effects of a substance” criteria, referencing neuroleptic medications, further contributes to the uncertainty around this issue. As a result, ruling-out or differentiating tics in psychosis spectrum disorders is at best, a murky endeavor.
Historically, the advent of antipsychotic medication in the 1950s has contributed to the confusion about movement signs in psychiatric populations. Because neuroleptic medications produce characteristic movement disorder in some patients (i.e. extrapyramidal side effects), drug-induced movement disturbances have been the focus of research attention in psychotic disorders. However, accumulating data have documented that spontaneous dyskinesias, including choreoathetodic movements, can occur in medication naive adults with schizophrenia spectrum disorders (Pappa and Dazzan, 2009), as well as healthy first-degree relatives of chronically ill schizophrenia patients (McCreadie et al., 2003). Taken together, this suggests that movement abnormalities may reflect pathogenic processes underlying some psychotic disorders (Mittal et al., 2008; Pappa and Dazzan, 2009).
More specifically, because spontaneous hyperkinetic movements are believed to reflect abnormal striatal dopamine activity (DeLong and Wichmann, 2007), and dysfunction in this same circuit is also proposed to contribute to psychosis, it is possible that spontaneous dyskinesias serve as an outward manifestation of circuit dysfunction underlying some schizophrenia-spectrum symptoms (Walker, 1994). Further, because these movements precede the clinical onset of psychotic symptoms, sometimes occurring in early childhood (Walker, 1994), and may steadily increase during adolescence among populations at high-risk for schizophrenia (Mittal et al., 2008), observable dyskinesias could reflect a susceptibility that later interacts with environmental and neurodevelopmental factors, in the genesis of psychosis.
In adolescents who meet criteria for a prodromal syndrome (i.e., the period preceding formal onset of psychotic disorders characterized by subtle attenuated positive symptoms coupled with a decline in functioning), there is sometimes a history of childhood conditions which are also characterized by suppressible tics or tic like movements (Niendam et al., 2009). On the other hand, differentiating between tics and dyskinesias has also complicated research on childhood disorders such as Tourette syndrome (Kompoliti and Goetz, 1998; Gilbert, 2006).
We propose consideration of more explicit and operationalized criteria for differentiating tics and dyskinesias, based on empirically derived understanding of neural mechanisms. Further, revisions of the DSM should allow for the possibility that movement abnormalities might reflect neuropathologic processes underlying the etiology of psychosis for a subgroup of patients. Psychotic disorders might also be included among the medical disorders that are considered a rule-out for tics.
Related to this, the reliability of movement assessment needs to be improved, and this may require more training for mental health professionals in movement symptoms. Although standardized assessment of movement and neurological abnormalities is common in research settings, it has been proposed that an examination of neuromotor signs should figure in the assessment of any patient, and be as much a part of the patient assessment as the mental state examination (Picchioni and Dazzan, 2009).
To this end it is important for researchers and clinicians to be aware of differentiating characteristics for these two classes of abnormal movement. For example, tics tend to be more complex than myoclonic twitches, and less flowing than choreoathetodic movements (Kompoliti and Goetz, 1998). Patients with tics often describe a sensory premonition or urge to perform a tic, and the ability to postpone tics at the cost of rising inner tension (Gilbert, 2006). For example, one study showed that patients with tic disorders could accurately distinguish tics from other movement abnormalities based on the subjective experience of some voluntary control of tics (Lang, 1991). Another differentiating factor derives from the relationship of the movement in question to other voluntary movements. Tics in one body area rarely occur during purposeful and voluntary movements in that same body area whereas dyskinesia are often exacerbated by voluntary movement (Gilbert, 2006). Finally, it is noteworthy that tics wax and wane in frequency and intensity and migrate in location over time, often becoming more complex and peaking between the ages of 9 and 14 years (Gilbert, 2006). In the case of dyskinesias among youth at-risk for psychosis, there is evidence that the movements tend to increase in severity and frequency as the individual approaches the mean age of conversion to schizophrenia spectrum disorders (Mittal et al., 2008).
As revisions to the DSM are currently underway in preparation for the new edition (DSM V), we encourage greater attention to the important, though often subtle, distinctions among subtypes of movement abnormalities and their association with psychiatric syndromes.
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...Effect sizes were calculated using g2 (Cohen, 1988)....
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...Effect sizes were calculated using g(2) (Cohen, 1988)....
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TL;DR: The results suggest that it is important to recognize both the unity and diversity ofExecutive functions and that latent variable analysis is a useful approach to studying the organization and roles of executive functions.
12,182 citations
"Multiple deficits in ADHD : executi..." refers methods in this paper
...The second task was a Navon-like task used by, for example, Miyake et al. (2000)....
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