Cromwell, S.E., Beauchaine, T.P., Gatzke-Kopp, L., Sylvers, P., Mead, H., & Chipman-Chacon, J. (2006). Autonomic Correlates of Attention-Defecit/Hyperactivity Disorder and Oppositional Defiant Disorder in Preschool Children. Journal of Abnormal Psychology, Volume 115, Number 1, 174-178.
Conduct disorder in adolescence and antisocial behavior in adults has been shown to be marked by autonomic underarousal. This study attempted to see if much younger, at-risk pre-schoolers are autonomically similar to older externalizing children and adults. Firstly, the study found that pre-school children with ADHD and ODD showed attenuated EDR, a measure of sympathetic nervous system (SNS). Decreased SNS activity is thought to be a marker of disinhibition. Secondly, the study found ADHD and ODD pre-schoolers have attenuated SNS-linked cardiac activity, which serves as a marker of reward sensitivity. Children with underactive reward systems may engage in reward-seeking behavior to compensate for a chronically suppressed dopaminergic subsystem. Finally, as compared with controls, the paper showed no substantial differences in these ADHD/ODD groups in RSA, a marker of parasympathetic nervous system (PNS) activity, and more generally, emotional regulation. The results support the hypothesis that even very young ADHD and ODD children are similar in autonomic biology to older antisocial groups. However, these preschool years may represent a critical period during which noradrenergic, serotonergic, and dopaminergic systems that govern behavioral control are most vulnerable to long-term changes, and importantly, emotional dysregulation, a hallmark of most psychological disorders, may be positively affected through early detection and intervention during this timeframe.
Showing posts with label ADHD. Show all posts
Showing posts with label ADHD. Show all posts
Friday, February 1, 2008
Thursday, January 3, 2008
Bored?
Gosline, A. (December 2007.) Bored?, Scientific American Mind.
This article suggests boredom is not merely the result of circumstance. Instead, it may also be affected by emotional factors, personality traits, and attention. It may also come in many varieties, ranging from situational boredom to pathological boredom. People who are predisposed to boredom are more likely to suffer from ills such as depression and drug addiction; they also tend to be socially awkward and poor performers at school or work. A Boredom Proneness Scale (BPS), developed by Richard Farmer at the University of Oregon, may help clinicians to identify boredom as a component of other ailments.
Boredom is complicated, but what we have learned from research suggests low arousal and insufficient motivation both play critical roles in this cognitive state. Men are more likely to be bothered by boredom than women. "Men are more likely to say, ‘There is not enough stuff coming through the environment, and that’s why I am bored.’" Similarly, extroverts seem to be more susceptible, requiring a constant and changing supply of stimulation to achieve optimal arousal levels.
Boredom may also be related to the struggle to maintain attention, a pathological inability to focus. Scores on the BPS were correlated with measures for adult ADHD. A chronic inability to focus on activities may render them effectively meaningless. Psychologist Al Cheyne goes so far as to say, "Attention is the common link between lack of meaning, depression and boredom." Others describe boredom as the antithesis of 'flow' (when a person's skills match the challenge presented by the environment). Tasks that are too easy are quickly boring.
Emotional factors may also play a part. Obsessive mood monitoring seems to detract from intense concentration and thus full engagement in the activity at hand. And boredom can arise from an inability to identify activities that will lead to personal happiness and fulfillment. An inability to know what will make you happy can lead to a more profound existential ennui arising from a pervasive sense of meaninglessness. Existential boredom might also occur when a person abandons important drives, desires, and life goals. Thus, being bored is a form of disengagement from the world.
The article suggests methods of combating boredom on all of these axes. Changing jobs or the complexity of tasks, beginning new hobbies and interests, developing inner skills for stimulation, and being more mindful of the beauty of self and surroundings may all help.
This article suggests boredom is not merely the result of circumstance. Instead, it may also be affected by emotional factors, personality traits, and attention. It may also come in many varieties, ranging from situational boredom to pathological boredom. People who are predisposed to boredom are more likely to suffer from ills such as depression and drug addiction; they also tend to be socially awkward and poor performers at school or work. A Boredom Proneness Scale (BPS), developed by Richard Farmer at the University of Oregon, may help clinicians to identify boredom as a component of other ailments.
Boredom is complicated, but what we have learned from research suggests low arousal and insufficient motivation both play critical roles in this cognitive state. Men are more likely to be bothered by boredom than women. "Men are more likely to say, ‘There is not enough stuff coming through the environment, and that’s why I am bored.’" Similarly, extroverts seem to be more susceptible, requiring a constant and changing supply of stimulation to achieve optimal arousal levels.
Boredom may also be related to the struggle to maintain attention, a pathological inability to focus. Scores on the BPS were correlated with measures for adult ADHD. A chronic inability to focus on activities may render them effectively meaningless. Psychologist Al Cheyne goes so far as to say, "Attention is the common link between lack of meaning, depression and boredom." Others describe boredom as the antithesis of 'flow' (when a person's skills match the challenge presented by the environment). Tasks that are too easy are quickly boring.
Emotional factors may also play a part. Obsessive mood monitoring seems to detract from intense concentration and thus full engagement in the activity at hand. And boredom can arise from an inability to identify activities that will lead to personal happiness and fulfillment. An inability to know what will make you happy can lead to a more profound existential ennui arising from a pervasive sense of meaninglessness. Existential boredom might also occur when a person abandons important drives, desires, and life goals. Thus, being bored is a form of disengagement from the world.
The article suggests methods of combating boredom on all of these axes. Changing jobs or the complexity of tasks, beginning new hobbies and interests, developing inner skills for stimulation, and being more mindful of the beauty of self and surroundings may all help.
Saturday, December 1, 2007
Selective Effects of Ritalin in ADHD
Vaidya, C.J., Austin, G., Kirkorian, G., Ridlehuber, H.W., Desmond, J.E., Glover, G.H., & Gabrieli, J.D.E. (November 1998). Selective effects of methylphenidate in attention deficit hyperactivity disorder: A functional magnetic resonance study, Neurobiology, 95, 14494-14499.
ADHD is the most common developmental disorder of childhood and has been associated with such adverse life outcomes as lower educational and occupational achievement, as well as increased risk for various disorders in adulthood. Evidence suggests that ADHD is characterized by dysfunction in transmission of dopamine to the frontal lobes and striatal (basal ganglia) structures of the brain since ADHD symptoms typically respond favorably to stimulant medications (e.g. methylphenidate) that release and inhibit reuptake of dopamine in these regions. However, prior to this study, there was no direct evidence to indicate differences in dopaminergic modulation between ADHD and normal children. Therefore, the purpose of this study was to see: (a) how performance in response inhibition tasks differs between ADHD children and normal children, (b) how administration of methylphenidate improved performance in response inhibition tasks in ADHD children in comparison with normal children, (c) how baseline frontal-striatal function differ in ADHD and control children, and (d) how methylphenidate modulates frontal-striatal function differently in ADHD and control children. Since inhibition of motor responses is known to depend on the integrity of both frontal and striatal structures, functional magnetic resonance imaging (fMRI) was used to image the frontal lobes, as well as the head of the caudate nucleus and the anterior portion of the putamen during response inhibition tasks to assess the four aforementioned points.
Each subject in the study was presented with various computer-generated stimuli and instructed to respond with a button-press on a hand-held joystick. In one block, they were told to respond to all stimuli presented. In another block, they were told to respond to all stimuli except for one (inhibition). Their behavioral performance was measured by the percentage of errors committed during the task. At the same time, activation of certain brain regions was gathered during the trials via fMRI. With the different independent variables and levels, the overall design looks something like the following table for the "stimulus-controlled" task (for brevity, I will neglect to mention the "response-controlled" task and results):
The results can be condensed as follows: (a) The ADHD group made more errors than the control group on the response inhibition task. (b) Both the ADHD and the control groups showed significant improvements on the task with the administration of MPH. (c) Baseline striatal activation was shown to be lower in ADHD subjects than in the control group. (d) Administration of MPH increased striatal activation in ADHD subjects but decreased striatal activation in control subjects.
The results support the hypothesis that there are indeed differences between ADHD children and normal children, both in performance on response inhibition tasks and in their striatal activation in the absence of stimulant medication. And further, when administered stimulant medication, ADHD children showed different functional reactions to the medication in the striatum than their control group counterparts. These are important findings, especially given the neural specificity of the results.
ADHD is the most common developmental disorder of childhood and has been associated with such adverse life outcomes as lower educational and occupational achievement, as well as increased risk for various disorders in adulthood. Evidence suggests that ADHD is characterized by dysfunction in transmission of dopamine to the frontal lobes and striatal (basal ganglia) structures of the brain since ADHD symptoms typically respond favorably to stimulant medications (e.g. methylphenidate) that release and inhibit reuptake of dopamine in these regions. However, prior to this study, there was no direct evidence to indicate differences in dopaminergic modulation between ADHD and normal children. Therefore, the purpose of this study was to see: (a) how performance in response inhibition tasks differs between ADHD children and normal children, (b) how administration of methylphenidate improved performance in response inhibition tasks in ADHD children in comparison with normal children, (c) how baseline frontal-striatal function differ in ADHD and control children, and (d) how methylphenidate modulates frontal-striatal function differently in ADHD and control children. Since inhibition of motor responses is known to depend on the integrity of both frontal and striatal structures, functional magnetic resonance imaging (fMRI) was used to image the frontal lobes, as well as the head of the caudate nucleus and the anterior portion of the putamen during response inhibition tasks to assess the four aforementioned points.
Each subject in the study was presented with various computer-generated stimuli and instructed to respond with a button-press on a hand-held joystick. In one block, they were told to respond to all stimuli presented. In another block, they were told to respond to all stimuli except for one (inhibition). Their behavioral performance was measured by the percentage of errors committed during the task. At the same time, activation of certain brain regions was gathered during the trials via fMRI. With the different independent variables and levels, the overall design looks something like the following table for the "stimulus-controlled" task (for brevity, I will neglect to mention the "response-controlled" task and results):
The results can be condensed as follows: (a) The ADHD group made more errors than the control group on the response inhibition task. (b) Both the ADHD and the control groups showed significant improvements on the task with the administration of MPH. (c) Baseline striatal activation was shown to be lower in ADHD subjects than in the control group. (d) Administration of MPH increased striatal activation in ADHD subjects but decreased striatal activation in control subjects.
The results support the hypothesis that there are indeed differences between ADHD children and normal children, both in performance on response inhibition tasks and in their striatal activation in the absence of stimulant medication. And further, when administered stimulant medication, ADHD children showed different functional reactions to the medication in the striatum than their control group counterparts. These are important findings, especially given the neural specificity of the results.
Neuroscience of ADHD
Castellanos, F. X. (August 2002). Neuroscience of Attention-Deficit/Hyperactivity Disorder: The Search for Endophenotypes, Nature Reviews. Volume 3.
An endophenotype is an heritable quantitative trait that can be used to index and predict a person's risk of developing a given disease. Research into ADHD has traditionally been hampered by confusion over fuzzy operational definitions and diagnostic criteria. Towards development of an objective diagnostic test, the authors of this article propose three categories of endophenotypes, each grounded in neuroscience.
Abnormality in the reward-related circuitry that leads to shortened delay gradients. Delay aversion tasks can assess a person's intolerance for waiting that can lead to selection of an immediate reward over a larger, delayed reward. Sonuga-Barke argues that fundamental abnormalities in the reward mechanisms of ADHD subjects translate into a faster decline in the effectiveness of reinforcement as the delay between behavior and reward increases.
Deficits in temporal processing. People with ADHD appear to exhibit deficits in time-estimation and time-production, especially time estimation tasks between 2-60 seconds which require cortical mediation and rehearsal in working memory (as opposed to smaller durations which are dependent on the basal ganglia and cerebellum), but not wholesale -- instead, they exhibit variability in performance. This article suggests that this variability itself is a characteristic of the disorder and can be used as a rating.
Deficits in working memory. Working memory controls attention and guides decision-making and behavior. It is mediated by the prefrontal cortex and modulated by the catecholamines dopamine and noradrenaline. Catecholaminergic dysregulation and prefrontal dysfunction are central to the pathophysiology of ADHD. A P300 Component, derived from EEG analysis, provides an index of the attentional and working memory demands of a task and may be fitting for use as an endophenotype. (See also Coherence wave patterns.)
Other candidate endophenotypes were ruled out due to incompleteness of data, potential confounds, or the multiplicity of operational definitions. These include genetic factors, locomotor hyperactivity, and general response inhibition.
An endophenotype is an heritable quantitative trait that can be used to index and predict a person's risk of developing a given disease. Research into ADHD has traditionally been hampered by confusion over fuzzy operational definitions and diagnostic criteria. Towards development of an objective diagnostic test, the authors of this article propose three categories of endophenotypes, each grounded in neuroscience.
Abnormality in the reward-related circuitry that leads to shortened delay gradients. Delay aversion tasks can assess a person's intolerance for waiting that can lead to selection of an immediate reward over a larger, delayed reward. Sonuga-Barke argues that fundamental abnormalities in the reward mechanisms of ADHD subjects translate into a faster decline in the effectiveness of reinforcement as the delay between behavior and reward increases.
Deficits in temporal processing. People with ADHD appear to exhibit deficits in time-estimation and time-production, especially time estimation tasks between 2-60 seconds which require cortical mediation and rehearsal in working memory (as opposed to smaller durations which are dependent on the basal ganglia and cerebellum), but not wholesale -- instead, they exhibit variability in performance. This article suggests that this variability itself is a characteristic of the disorder and can be used as a rating.
Deficits in working memory. Working memory controls attention and guides decision-making and behavior. It is mediated by the prefrontal cortex and modulated by the catecholamines dopamine and noradrenaline. Catecholaminergic dysregulation and prefrontal dysfunction are central to the pathophysiology of ADHD. A P300 Component, derived from EEG analysis, provides an index of the attentional and working memory demands of a task and may be fitting for use as an endophenotype. (See also Coherence wave patterns.)
Other candidate endophenotypes were ruled out due to incompleteness of data, potential confounds, or the multiplicity of operational definitions. These include genetic factors, locomotor hyperactivity, and general response inhibition.
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