For the past two years or so, I have been doing Decrease Deltatraining on children and adults with attention problems. I have found that if the training objective is to increase SMR or Beta, teaching Delta to downtrend at Cz or Pz will generally be more effective than attempting to reward the increase of SMR or Beta.


Übersichtsarbeit: NFB bei Kindern mit ADD



=

Training under Task=
My training objective then is not to decrease Delta or Theta per se. The objective is to teach Delta to downtrend under a performance challenge such as the Game Boy" strategy game Tetris". Once the "decrease under task" goal is achieved, Decrease training is considered complete. The next training as specified in my clinical strategy protocol is then begun.



Snyder 2006



Meta-analytic results of 9 DSM-IV studies and the results of 29 pre–DSM-IV studies support that a theta/beta ratio increase is a commonly observed trait in ADHD relative to controls (normal children, adolescents, and adults). By statistical extrapolation, the effect size of 3.08 predicts a sensitivity and specificity of 94%, which is similar to values predicted by retrospective studies examining ADHD and normal controls in group comparisons. The QEEG trait also follows age-related changes in ADHD symptom presentation. Because it is known that this trait may arise with other conditions, we recommend a prospective study covering differential diagnosis to examine generalizability to clinical applications.




Spectral analysis of the electrophysiological output at a single, midline prefrontal location (the vertex) was conducted in 482 individuals, ages 6-30 years old, to test the hypothesis that cortical slowing in the prefrontal region can serve as a basis for differentiating patients with attention deficit hyperactivity disorder (ADHD) from nonclinical control groups. Participants were classified into 3 groups (ADHD, inattentive; ADHD, combined; and control) on the basis of the results of a standardized clinical interview, behavioral rating scales, and a continuousperformance test. Quantitative electroencephalographic (QEEG) findings indicated significant maturational effects in cortical arousal in the prefrontal cortex as well as evidence of cortical slowing in both ADHD groups, regardless of age or sex. Sensitivity of the QEEG-derived attentional index was 86%; specificity was 98%. These findings constituted a positive initial test of a QEEG-based neurometric test for use in the assessment of ADHD.


The Effectiveness of Neurofeedback and Stimulant Drugs
in Treating AD/HD: Part I. Review of Methodological Issues, Thomas Rossiter
1
Therefore, Fuchs et al. (2003), Monastra et al. (2002), Rossiter (2003), and Rossiter
and La Vaque (1995) do provide evidence that neurofeedback is an effective treatment
for AD/HD. Collectively, they warrant the conclusion that patient outcomes obtained with
neurofeedback are comparable (equivalent, noninferior, not significantly different) to those
obtained with stimulant drug therapy


Neurofeedback Treatment for Attention-Deficit/Hyperactivity Disorder in Children: A Comparison With Methylphenidate ,Thomas Fuchs, 1 Niels Birbaumer,1;2 Werner Lutzenberger, John H. Gruzelier, and Jochen Kaiser1
Clinical trials have suggested that neurofeedback may be efficient in treating attentiondeficit/hyperactivity disorder (ADHD). We compared the effects of a 3-month electroencephalographic feedback program providing reinforcement contingent on the production of cortical sensorimotor rhythm (12–15 Hz) and beta1 activity (15–18 Hz) with stimulant medication. Participants were N D34 children aged 8–12 years, 22 of which were assigned to the neurofeedback group and 12 to the methylphenidate group according to their parents’preference. Both neurofeedback and methylphenidate were associated with improvements on all subscales of the Test of Variables of Attention, and on the speed and accuracy measures of the d2 Attention Endurance Test. Furthermore, behaviors related to the disorder were rated as significantly reduced in both groups by both teachers and parents on the IOWA-Conners Behavior Rating Scale. These findings suggest that neurofeedback was efficient in improving some of the behavioral concomitants of ADHD in children whose parents favored a nonpharmacological treatment.











This study replicated T. R. Rossiter and T. J. La Vaque (1995) with a larger sample, expanded age range, and improved statistical analysis. Thirty-one AD/HD patients who chose stimulant drug (MED) treatment were matched with 31 patients who chose a neurofeedback (EEG) treatment program. EEG patients received either office (n = 14) or home (n =17) neurofeedback. Stimulants for MED patients were titrated using the Test of Variables of Attention (TOVA). EEG (effect size [ES] = 1.01–1.71) and MED (ES = 0.80–1.80) groups showed statistically and clinically significant improvement on TOVA measures of attention, impulse control, processing speed, and variability in attention. The EEG group demonstrated statistically and clinically significant improvement on behavioral measures (Behavior Assessment System for Children, ES = 1.16–1.78, and Brown Attention Deficit Disorder Scales, ES = 1.59). TOVA gain scores for the EEG and MED groups were not significantly different. More importantly, confidence interval and nonequivalence null hypothesis testing confirmed that the neurofeedback program produced patient outcomes equivalent to those obtained with stimulant drugs. An effectiveness research design places some limitations on the conclusions that can be drawn.
















Abstract

Studies examining the efficacy, safety and mechanisms of action of agents for the treatment of attentiondeficit/hyperactivity disorder (ADHD) are reviewed, with an emphasis on newer agents such as the long acting stimulants and atomoxetine. Recent studies of medications are characterized by large, rigorously diagnosed samples of children, adolescents and adults with ADHD, use of standardized rating scales and extensive safety data. These studies confirm a robust treatment effect for the Food and Drug Administration approved agents ranging from 0.7 to 1.5. The most common short term side effects to the most commonly used agents include insomnia, loss of appetite, and headaches. Despite public controversy and labeling changes to warn of extremely rare cardiovascular and psychiatric side effects, the evidence does not support the hypothesis that medication for ADHD increases risk for sudden death, mania or psychosis. A wide variety of neuroimaging techniques including electrocephalogram (EEG) power, event related potentials (ERP), functional magnetic resonance imaging (fMRI), and positron emission tomography (PET) are beginning to examine the mechanisms of action of medications for ADHD, and implicating the catecholamines and prefrontal and anterior cingulate cortices as prime sites of actions for these agents.


The objective was to investigate the effectiveness of rating scales and electroencephalography (EEG) in detecting the presence of attention-deficit/hyperactivity disorder (ADHD) within a diverse clinical sample. A standard psychiatric evaluation was used to assess 26 children/adolescents who presented to a clinic because a parent suspected the presence of ADHD. EEG data was collected in a blinded protocol, and rating scales were collected as well. Although all subjects had presented with ADHD-like symptoms, only 62% were diagnosed with ADHD, while the remaining 38% had other disorders or no diagnosis. Rating scales readily classified inattentive, impulsive, and/or hyperactive symptoms as being due to ADHD, regardless of the actual underlying disorder, leading to a sensitivity of 81% and a specificity of 22%. Previous studies have observed that there is an EEG marker that identifies ADHD vs. controls, and this marker was present in 15 out of 16 of the ADHD subjects (sensitivity=94%) and in none of the subjects with ADHD-like symptoms due to other disorders (specificity=100%). In the detection of ADHD in a diverse clinical sample, rating scales and EEG were both sensitive markers, whereas only EEG was specific. These results may have important implications to ADHD differential diagnosis.


Primary evidence-based treatment approaches for ADHD involve pharmacological and behavioral treatments. However, there
continue to be investigations of cognitive-behavioral, cognitive, and neural-based intervention approaches that are not considered
evidence-based practice. These particular treatments are summarized, as they all involve training in cognitive skills or cognitive
strategies. We identified 26 studies (six cognitive-behavioral, six cognitive, and 14 neural-based), and calculated effect sizes where
appropriate. Overall, our analysis suggests that further research is needed to determine the efficacy of these approaches on both
cognitive and behavioral outcome measures, but that some of these methods show promise for treating ADHD. We discuss some
important conceptual and methodological issues that need to be taken into account for future research in order to evaluate the
clinical efficacy of these approaches.