Professional Workshops

John N. Demos, MA, LCMHC is a BCIA accredited Neurofeedback Instructor. "Interactive" live-webcast workshops are for health care professionals. Contact us at 802-732-8060 or email:

2015 Dates


"Interactive" Live webcast: Getting Started with Neurofeedback. Next workshop starts April 17, 2015! Accredited by the Biofeedback Certification International Alliance ( Workshop is free with equipment purchase ( John N Demos, MA, LCMHC, BCN, author of "Getting Started with Neurofeedback," is the instructor.
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"Interactive" Live webcast: Getting Started with BrainMaster's Microtesla. Next workshop is April 10, 2015! Workshop is free with equipment purchase ( Microtesla or pulsed electro-magnetic field (pEMF) training promotes cellular healing. Pulsing can be EEG contingent (driven) or set for randomization.
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Symptom check lists: (1) Jewel for BrainAvatar (2) QEEG analysis for NeuroGuide Deluxe. Both Software options provide users with symptom check lists, protocol suggestions, network analysis and many other educational and practical features for neurofeedback providers; including software guided z-score training selections.
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Getting started with Neurofeedback can be very challenging without a mentor. If you have already taken BCIA didactic training (e.g., The live-webcast training offered on this website) then likely you have many questions. Mentoring can provide answers to assessment, training and equipment issues that always face new providers.
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ADHD Meds May Double Cardiovascular Event Risk in Kids

Medscape Medical News >Nancy A. Melville>July 02, 2014

The use of psychostimulants in children and adolescents is associated with nearly twice the risk for a cardiovascular event compared with nonuse of the drugs, and the risk is even higher when the drugs are used for the treatment of attention-deficit/hyperactivity disorder (ADHD), new research suggests. However, some experts are questioning whether these findings are clinically meaningful.

“In this large nationwide cohort study, we found that stimulant treatment increased the risk of cardiovascular events both in the total national population and in a population-based sample of children and adolescents with ADHD,” investigators, led by Søren Dalsgaard, MD, PhD, of Aarhus University, in Denmark, write.

The study was published online  June 23 in the Journal of Child and Adolescent Psychopharmacology.

Longest Study to Date

The study, which included more than 700,000 Danish children born between 1990 and 1999, had a mean follow-up of 9.5 years, making it the longest prospective observational study of its kind examining ADHD and stimulant use to date, according to the authors.

Overall, the use of stimulants in the population of 714,258 was associated with a nearly 2-fold risk for a cardiovascular event (adjusted hazard ratio [HR], 1.83; 95% confidence interval [CI], 1.10 – 3.04).

A total of 5734 individuals in the entire cohort, representing 6,767,982 person-years, experienced a cardiovascular event, representing 84 events per 100,000 person-years.

Among children with ADHD (n = 8300), there were 111 cardiovascular events, or 170 events per 100,000 person-years, and those with ADHD who were treated with stimulants had twice the risk for cardiovascular events (HR, 2.34; 95% CI, 1.15 – 4.75) compared with their counterparts who did not use stimulants.

The most common cardiovascular events included arrhythmias (23%), hypertension (8%), ischemic heart disease (2%), pulmonary heart disease (<1%), cardiac arrest (<1%), heart failure (2%), heart disease caused by rheumatic fever (2%), heart disease not otherwise specified (14%), cerebrovascular disease (9%), and cardiovascular disease not otherwise specified (40%).

The study also showed an important, complex dose-response relationship, with ADHD children who were treated with high doses of stimulants (>30 mg methylphenidate) 12 months prior to the cardiovascular event showing a significantly higher risk (HR, 2.24) for cardiovascular events compared with those treated with lower doses (< 15 mg methylphenidate; HR, 1.43, compared with no stimulant use) 12 months before the event.

Potential Mechanism

The authors pointed out that an inverse dose-response relationship was seen when looking at the dosage of stimulants at the time of the cardiovascular event: Among patients with ADHD who used stimulants and who experienced a cardiovascular event, more than half (57%) had reductions in their stimulant dose in the 12 months prior to the event.

Among stimulant users who did not have cardiovascular events, the rate of dose reduction in the previous 12 months was lower ― only 30% (P = .01).

“Our data suggest that high doses of methylphenidate followed by a lower dose may contribute to an increased long-term risk of adverse cardiovascular events,” the authors note.

“A possible biological mechanism for the time-dose-response relationship in our study may involve alterations to cardiac sympathetic function via altered striatal dopamine transporter levels in the brain, mediated through treatment and discontinuation of treatment with stimulants,” they write.

Key limitations of the study include the possibility that cardiovascular symptoms may have been more likely to have been identified in children receiving pharmacologic treatment and that minor cardiovascular symptoms may have led to a reduction in stimulant dose.

With previous studies linking stimulant use among ADHD patients with increases in blood pressure and heart rate, concern about the ever-expanding use of the drugs has grown in recent years.

A recent review of 10 population-based observational studies on cardiovascular risks with psychostimulant medications (Westover and Halm et al, BMC Cardiovasc Disord.2012;12:41 ) showed an increased risk in 1 of 7 studies in children and adolescents and in 2 of 3 studies involving adults.

Dr. Dalsgaard and colleagues report that although their new findings are consistent with the 1 study in the review showing an increased risk (Winterstein et al. 2007), their observation period was significantly longer (9.5 vs 2.3 years), which likely explains the finding of a higher risk (HR, 2.2 vs 1.2).

Clinically Meaningful?

Commenting on the study’s findings for Medscape Medical News, Arthur N. Westover, MD, of the Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, and lead author on the 10-study review, suggested that another explanation for the higher risk could be the inclusion of a broad scope of cardiovascular events.

“The investigators used a very broad outcome, essentially any kind of cardiovascular event, whether serious or not,” he said.

“When you broaden the outcome to include any kind of cardiovascular event, you are more likely to find a signal, but less able to determine whether it is clinically meaningful,” he said.

“For example, in the study, 40% of the cases were ‘cardiovascular disease not otherwise specified,’ ” he noted. “For a clinician or patient, it may be hard to interpret what that means.”

In contrast, he noted, another prominent study that looked at only serious cardiovascular events, including stroke, heart attack, and sudden death (Cooper, et al, N Engl J Med. 2011;365:1896-1904 ), which was reported by Medscape Medical News, did not find an increased risk.

Likewise, the new study also did not show an increased risk for death or serious cardiovascular events among stimulant users, Dr. Westover pointed out.

Mark Olfson, MD, MPH, professor of psychiatry at Columbia University Medical Center in New York City, and lead author on another of the studies included in Dr. Westover’s review ( J Am Acad Child Adolesc Psychiatry. 2012;51:147-56 ), added that an important limitation of the new study is a lack of information on other therapies that patients received.

“In contrast to most pharmacoepidemiological studies on this topic, the new study finds an association between stimulant treatment and a wide range of cardiovascular events,” he told Medscape Medical News.

“However, without more information on the other medications that the patients were receiving, such as corticosteroids, erythromycin, and oral contraceptives, and the distribution of known disease risk factors, such as prothrombotic states, hyperlipidemia, asthma, and obesity, it is difficult to evaluate the clinical significance of the current findings.”

Among the key challenges in any of the efforts to evaluate cardiovascular risk associated with ADHD psychostimulants is the simple fact that such events, though serious when they do occur, are still highly uncommon, Dr. Olfson added.

“Cardiovascular events in ostensibly healthy young people with ADHD are thankfully quite rare,” he said.

“The [events’] uncommonness has made it exceptionally difficult to determine who is at risk for these potentially catastrophic events.”

The authors and Dr. Olfson report no relevant financial relationships. Dr. Westover reports that he is the recipient of a National Institutes of Health grant for research into ADHD drug risks.

J Child Adolesc Psychopharmacol. Published online June 23, 2014. Full text

Regional Homogeneity within the Default Mode Network in Bipolar Depression: A Resting-State Functional Magnetic Resonance Imaging Study

  • Summary: the following discussion/research presents the likely connection between the Default Modular Network (DMN) and the symptoms related to Bipolar disorder.

    • Chun-Hong Liu, PLOS: 
      • Published: November 02, 2012
      • DOI: 10.1371/journal.pone.0048181
    • thumbnail
    • Here, using BOLD resting-state fMRI and the ReHo analytical method, we found abnormal brain activity in the BD group relative to the HC group in several brain regions within the DMN. Significantly increased ReHo in the BD group was mainly found in the left medial frontal gyrus and the left inferior parietal lobe. To our knowledge, this is the first study of the DMN in bipolar depression using the ReHo method.It is worthwhile to analyze the local connectivity of the time series within a functional cluster, and ReHo reflects intrinsic coherent neuronal activity within spatially organized brain regions[27]. Increased ReHo may be relevant to reflect neural hyperactivity in a regional brain area and vice versa [24]. The medial frontal gyrus, the hub of the DMN, is important for the ability of the affective value of reinforcers, decision making, and expectation [40]. In the current study, ReHo was significantly increased in the left medial frontal gyrus in the resting-state in BD patients, which reflects the enhancement of the local synchronization of spontaneous neural activities in this region. ReHo abnormalities observed in this region may be relevant to high ability in bipolar disorder [41] and support our understanding of the findings of prefrontal overactivity in bipolar disorder during up- and down-regulation of negative affect [42]. Conversely, several previous resting-state functional neuroimaging studies have found decreased ReHo in the medial frontal gyrus in other psychiatric disorders, including social anxiety disorder [43], heroin-dependent individuals [44], major depressive disorder [33], and schizophrenia [39]. Moreover, Lai et al. (2011) demonstrated that first-episode drug-naïve major depressive disorder with panic disorder patients displayed increased ReHo in the medial frontal cortex after short-term duloxetine therapy [45]. This suggests that ReHo differences in the medial frontal gyrus regions may demonstrate differences in the neurobiological substrates between bipolar disorder and other psychiatric disorders or secondary to medication. Future studies examining first-episode drug-naïve and different mood state bipolar disorder participants will aid in the clarification of the mechanisms behind increased homogeneity in bipolar patients.

      The medial frontal gyrus is involved in both emotion perception and cognitive regulation functions [4][21][46][47], and overactivity in this region may be responsible for the cognitive-emotional interference seen in BD. The abnormality of the medial frontal gyrus in BD patients has been reported in studies employing both emotional and cognitive tasks [4][48][49][50]. Fusar-Poli et al. (2012) performed a meta-analysis of different tasks used in fMRI studies of individuals at enhanced genetic risk for bipolar disorder and found that an increased neural response exists for several regions, including the left superior frontal gyrus, medial frontal gyrus, and left insula [47]. In the current study, we found increased ReHo in the left medial frontal gyrus in the BD group, which indicates that there is baseline brain activity impairment in BD patients, supplementing the existing knowledge revealed by various cognitive and emotional tasks. Moreover, Osuch et al. (2000) find a direct correlation between depression severity and regional cerebral metabolism in the bilateral medial frontal gyrus in mood disorders, including bipolar patients [51]. In this study, we found the left medial frontal gyrus was marginally related to the number of depressive episodes. However, we did not find correlations between ReHo values and HAMD scores in this brain region, but this negative finding may be due to the narrow range of depression scores in our subjects. This suggests that the abnormal ReHo in the left medial frontal gyrus may be a biomarker, either trait or state marker, which is related to the depression episode of bipolar disorder. Further studies are required to verify this speculation.

      Chepenik et al. (2010) demonstrated a decreased negative correlation between the activity of the left ventral prefrontal cortex and the amygdala in bipolar disorder subjects [22]. A noticeable difference between our current findings, e.g., in the left inferior parietal lobe, and those reported by Chepenik et al., (2010) concerns the amygdala. The medial frontal gyrus area is a functional hub that is closely connected to the ventral lateral prefrontal cortex and subcortical networks (e.g., limbic systems including the amygdala and frontoparietal networks) [21][52], and converging neuroimaging evidence demonstrates the critical role of the medial frontal gyrus in emotional recognition and cognitive control [53][54][55]. Because local and global functional connectivity reveals the functional links (usually revealed by correlations) between a pair of regions within a region and the whole brain, respectively, we speculate that the impaired functional connectivity within the amygdala and inferior parietal lobe may due to dysfunction in the ventral prefrontal gyrus, especially the medial frontal gyrus, as found in the current study. Therefore, our findings do not conflict with or replicate existing functional connectivity studies. Instead, combining previous functional connectivity data and ReHo may increase our understanding of the impaired prefrontal limbic-related network underlying the neurobiology of bipolar disorder.

      There are several limitations of the current study. First, the evaluation of the effects of medication is problematic in fMRI studies of medicated bipolar patients because the complete lifetime medication data (e.g., dose and duration) of the patients were difficult to obtain. Moreover, medications were not withdrawn at the time of the study due to ethical reasons [56]. Second, comparing BD patients with healthy controls cannot disentangle the differences between depressed and euthymic subjects from the differences between subjects with bipolar disorder and unaffected individuals. Given these limitations, future studies that include larger numbers of non-medicated subjects who are better balanced for age and take all of the above factors into account are warranted. In addition, to further clarify whether the ReHo abnormalities are shared by bipolar disorder patients in both depressed and euthymic episodes, future studies can compare patients in different episodes of BD with healthy controls.

      In summary, we adopted ReHo to investigate the differences in resting-state brain activity between BD patients and healthy control subjects within the DMN. Our findings support a model of BD that involves dysfunction within prefrontal-limbic circuits, which may shed light on the pathophysiological mechanisms underlying BD.

Neurofeedback Treatment for Traumatic Brain Injury

International Brain Injury Association: December 06th, 2012 10:26 AM
By: D. Corydon Hammond, Ph.D., ECNS, QEEG-D, BCIA-EEG

Following acute TBI rehabilitation there have been a limited number of strategies that have been used in the treatment of cognitive disorders. These methods have included restorative cognitive rehabilitation procedures that utilize stimulation and practice (e.g., of vigilance with a computer intervention); strategy cognitive rehabilitation (e.g., utilizing visualization, creating associations), compensatory cognitive rehabilitation strategies; and medications (e.g., cognitive enhancing medications directed at arousal, attention and/or memory). All of these methodologies provide at best modest improvements, but it is still common for patients with TBI to be told that after a year and a half they have obtained about all of the improvement that they can expect, and that, therefore, they must simply adjust to the current state of affairs.

There is, however, another rehabilitation strategy that is commonly underutilized, but which holds definite potential to provide further assistance in cognitive rehabilitation. This method is neurofeedback (EEG biofeedback).

What is Neurofeedback?

Neurofeedback training is brainwave biofeedback. The process consists of placing an electrode or two on the scalp and reference and ground electrodes on the earlobes. Ordinarily we cannot reliably influence brainwave activity because we lack awareness of that activity. However, when EEG biofeedback equipment allows us to see a representation of our brainwave activity a few thousands of a second after it occurs, it allows us to influence this activity. A computer display may be as simple as two bar graphs, with one representing slow, inefficient activity, and another efficient beta brainwave activity. When the patient concentrates on the display and through this concentration decreases slow (e.g., theta or alpha) activity and slightly increases efficient activity, they receive both visual and auditory feedback (for instance, a bell may ring after they have held these improvements for one-half a second). Change occurs through a process of operant conditioning, gradually reconditioning and retraining how the brain is functioning.

Problems that Neurofeedback Can Address

There are several problem areas that are not uncommonly seen in TBI patients that neurofeedback has been used to improve. These difficulties include problems with attention, impulse and emotional control, seizures, memory, anxiety, insomnia, depression, and physical balance.

Research on neurofeedback began about 40 years ago. The initial research focused on reduction of anxiety and on the treatment of drug-resistant, uncontrolled epilepsy. Sterman (2000) reviewed this literature, which included blinded, placebo-controlled cross-over studies, on the use of neurofeedback with uncontrolled epilepsy. Out of a total of 174 medically intractible patients in these studies it was found that in 82% of cases there were significant improvements in the seizure rate, and there were no reports of an increase in seizures. Some of these studies evaluated pre- and post-treatment sleep EEG’s, finding that following treatment even when the patient was asleep, their EEG showed less epileptiform activity, thus demonstrating that conditioned changes in brain function.

Studies with ADD/ADHD have likewise documented improvements equivalent to (e.g., Fuchs et al., 2003) or superior (Monastra et al., 2002) to those produced by methylphenidate on 1 year follow-up, and follow-ups have continued for as long at 10 years demonstrating the maintenance of improvements. This is significant since the average stimulant medication follow-up study is only 3 weeks long, Symptomatic changes have occurred in concentration/attention, academic performance, mood stability, impulsiveness, hyperactivity, and sleep. Along with behavioral changes, various studies have also shown post-treatment improvements in brain function on EEG measures, and a recent study (Levesque, Beauregard, & Mensour, 2006) established with fMRI that not only did neurofeedback improve behavior in ADHD children compared with a no-treatment control group, but that positive changes in both subcortical and cortical functioning also occurred.. Overall, close to 80% of ADD/ADHD patients show significant improvement. Placebo-controlled research with learning disabilities (Fernandez et al., 2003) has also demonstrated the effectiveness of neurofeedback.

Some recent studies with normal individuals also have implications for TBI treatment. Vernon et al. (2003) documented in a control group study that only 8 sessions of neurofeedback could improve memory recall, and a recent placebo controlled study (Hoedlmoser et al., 2008) of neurofeedback validated that only 10 sessions improved sleep onset latency and subsequent declarative learning in normal subjects. Other reviews have been published on the use of neurofeedback in the treatment of depression and anxiety (Hammond, 2005a), for improving physical balance (Hammond, 2005b), and in the treatment of obsessive-compulsive disorder (Hammond, 2003).

Although better and more well controlled research is needed preliminary neurofeedback treatment outcome studies of closed and open brain injuries too numerous to cite have been published. For example, Schoenberger et al (2001) compared treatment (25 sessions) with the Low Energy Neurofeedback System (LENS) of 9 mild and 3 moderate TBI patients with a wait-list control group. They found significant improvement in measures of attention and recall. Thornton and Carmody (2005) found 186% improvement in memory scores in TBI patients treated with neurofeedback compared to a control group with no TBI history. When Thornton and Carmody (2008) compared neurocognitive rehabilitation strategies, medication treatment, and neurofeedback treatment in an effect size analysis, neurofeedback appeared more efficacious than other treatment strategies. Ayers (1999) has even brought many patients out of coma using neurofeedback.

Successful Neurofeedback Treatment of Post-Traumatic Anosmia

In an acceleration-deceleration, coup-contrecoup injury damage can be done to cranial nerve I as the brain moves within the anterior cranial fossa. This can result in either focal or diffuse injury in the orbitofrontal, and less frequently temporal areas, producing posttraumatic anosmia. This symptom is most likely to occur in patients with posttraumatic amnesia lasting for 5 or more minutes Subsequent improvements in smell have only been found in 36% of patients (Doty, Yousem, Pham, Kreshak, Geckle, & Lee, 1997), usually in the first 6-12 months (while 18% of cases worsen in this time period), and usually such injuries are regarded as permanent with no more than 10% of patients improving more than 2 years post-injury (Costanzo & Becker, 1986). Posttraumatic anosmia has proven resistant to treatment with medication (Hirsch, Doughtery, Aranda, Vanderbilt, & Weclaw, 1996). Reviews have found that anosmia has a very severe negative effect on quality of life, safety and interpersonal relations, as well as eating habits and nutritional intake. However, I (Hammond, 2007) reported a case study of a 29 year old male in which neurofeedback was used to treat a patient nine and one-half years following a a moderate level TBI which had resulted in loss of consciousness for 10-15 minutes and resulted in a week long hospitalization. The accident resulted in a change in personality, increased irritability, difficulties concentrating, explosiveness, problems with short-term memory, insomnia, anxiety, and mood swings. The only medication he was taking was testosterone. After his 13th treatment session utilizing the Low Energy Neurofeedback System (LENS) the patient spontaneously reported being able to smell sagebrush. The author had been unaware of his anosmia until that time. After 22 sessions the patient’s mean rating (on a 0-10 scale) on the symptoms identified above had decreased from 9 to 3.75 and he indicated that his sense of smell and taste seemed completely normal.

Conclusions & Recommendations

Neurofeedback research has documented its value in the treatment of a variety of symptoms relevant to a brain injury population, including seizures, memory, concentration and attention, unstable mood, impulsiveness, anxiety, depression, sleep issues, and even anosmia and physical balance. Preliminary research on neurofeedback treatment of TBI is very encouraging, but certainly more rigorous research is needed. The accumulating work on neurofeedback led Frank H. Duffy, M.D., a Professor and Pediatric Neurologist at Harvard Medical School, to state in an editorial in the January 2000 issue of the journal Clinical Electroencephalography that scholarly literature now suggests that neurofeedback “should play a major therapeutic role in many difficult areas. In my opinion, if any medication had demonstrated such a wide spectrum of efficacy it would be universally accepted and widely used: (p. v). “It is a field to be taken seriously by all” (p. vii).

I find it unfortunate when physicians including those involved with TBI neurorehabilitation tell patients that after 18 months they have obtained all the return they can expect and will have to learn to adapt to their remaining deficits. I have often seen neurofeedback produce significant improvements years after the original injury.

There is one cautionary note, however. It has been documented (Hammond & Kirk, 2008) that neurofeedback in unskilled hands can occasionally result in side effects and less frequently in adverse effects. We are seeing an increasing number of lay persons (as well as untrained “professionals”) inappropriately obtaining neurofeedback equipment in violation of FDA regulations. Some of these individuals are then presuming that they are qualified to put electrodes on someone’s head and to seek to alter the brain functioning of persons with serious medical and psychological conditions. As part of consumer protection it is incumbent upon professionals to report such unlicensed lay practitioners to state regulatory bodies as practicing psychology and medicine without a license when they are found to be offering services for medical, psychiatric and psychological conditions.

Health care professionals who are licensed for independent practice may learn more about neurofeedback training and certification, or identified certified individuals, through consulting the Biofeedback Certification Institute of America (, the International Society for Neurofeedback and Research ( or the Association for Applied Psychophysiology and Biofeedback ( The ISNR website also includes a comprehensive bibliography of outcome literature on neurofeedback which is periodically updated.


  • Ayers, M. E. (1999). Assessing and treating open head trauma, coma, and stroke using real-time digital EEG neurofeedback. In J. R. Evans & A. Abarbanel (Eds.), Introduction to quantitative EEG and neurofeedback. (pp. 203-222). New York: Academic Press.
  • Costanzo, R. M., & Becker, D. P. (1986). Smell and taste disorders in head injury and neurosurgery patients. In H. L. Meiselman & R. S. Rivlin (Eds.), Clinical measurements of taste and smell. New York: MacMillan, pp. 565-578.
  • Doty, R. L., Yousem, D. M., Pham, L. T., Kreshak, A. A., Geckle, R., & Lee, W. W. (1997). Olfactory dysfunction in patients with head trauma. Archives of Neurology54, 1131-1140.
  • Fernandez, T., Herrera, W., Harmony, T., Diaz-Comas, L., Santiago, E., Sanchez, L., Bosch, J., Fernandez-Bouzas, A., Otero, G., Ricardo-Garcell, J., Barraza, C., Aubert, E., Galan, L., & Valdes, P. (2003). EEG and behavioral changes following neurofeedback treatment in learning disabled children. Clinical Electroencephalography34(3), 145-150.
  • Fuchs, T., Birbaumer, N., Lutzenberger, W., Gruzelier, J. H., & Kaiser, J. (2003). Neurofeedback treatment for attention deficit/hyperactivity disorder in children: A comparison with methylphenidate. Applied Psychophysiology and Biofeedback28, 1-12.
  • Hammond, D. C. (2003). QEEG-guided neurofeedback in the treatment of obsessive compulsive disorder.Journal of Neurotherapy7(2), 25-52.
  • Hammond, D. C. (2005a). Neurofeedback with anxiety and affective disorders. Child & Adolescent Psychiatric Clinics of North America14(1), 105-123.
  • Hammond, D. C. (2005b). Neurofeedback to improve physical balance, incontinence, and swallowing.Journal of Neurotherapy9(1), 27-36.
  • Hammond, D. C. (2007). Can LENS neurofeedback treat anosmia resulting from a head injury? Journal of Neurotherapy11(1), 57-62.
  • Hammond, D. C., & Kirk, L. (2008). First, do no harm: Adverse effects and the need for practice standards in neurofeedback. Journal of Neurotherapy12(1), 79-88.
  • Hirsch, A. R., & Johnston, L. H. (1996). Odors and learning. Journal of Neurological & Orthopedic Medicine & Surgery17, 119-124.
  • Hoedlmoser, K., Pecherstorfer, T., Gruber, E., Anderer, P., Doppelmayr, M., Klimesch, W., & Schabus, M. (2008). Instrumental conditioning of human sensorimotor rhythm (12-15 Hz) and its impact on sleep as well as declarative learning. Sleep31(10), 1401-1408.
  • Levesque, J., Beauregard, M., & Mensour, B. (2006). Effect of neurofeedback training on the neural substrates of selective attention in children with attention-deficit/hyperactivity disorder: a functional magnetic resonance imaging study. Neuroscience Letters394(3), 216-221.
  • Monastra, V. J., Monastra, D. M., & George, S. (2002). The effects of stimulant therapy, EEG biofeedback, and parenting style on the primary symptoms of attention-deficit/hyperactivity disorder. Applied Psychophysiology and Biofeedback27(4), 231-249.
  • Schoenberger, N. E., Shif, S. C., Esty, M. L., Ochs, L., & Matheis, R. J. (2001). Flexyx neurotherapy system in the treatment of traumatic brain injury: an initial evaluation. Journal of Head Trauma Rehabilitation,16(3), 260-31.
  • Sterman, M. B. (2000). Basic concepts and clinical findings in the treatment of seizure disorders with EEG operant conditioning. Clinical Electroencephalography31(1), 45-55.
  • Thornton, K. E., & Carmody, D. P. (2005). Electroencephalogram biofeedback for reading disability and traumatic brain injury. Child & Adolescent Psychiatric Clinics of North America14(1), 137-162.
  • Thornton, K. E., & Carmody, D. P. (2008). Efficacy of traumatic brain injury rehabilitation: Interventions of QEEG-guided biofeedback, computers, strategies, and medications. Applied Psychophysiology & Biofeedback33, 101-124.
  • Vernon, D., Egner, T., Cooper, N., Compton, T., Neilands, C., Sheri, A., & Gruzelier, J. (2003). The effect of training distinct neurofeedback protocols on aspects of cognitive performance. International Journal of Psychophysiology47, 75-85.


“Salience network” dysfunction hypothesis in autism

The following is brief review of the Article that has been edited for this website:

Japanese Psychological Research
2013, Volume 55, No. 2, 175–185
Special issue: Developmental disorders and cognitive science Review

Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental disorder charac-
terized by impaired social interaction and communication, as well as repetitive and
stereotyped patterns of behavior. Although most patients with ASD show sensory
abnormalities such as hyperesthesia and hypoesthesia, its relation to social cognition
has not been well studied. Recently, a salience network (SN) dysfunction hypothesis
of ASD has been proposed. This neuroscientific hypothesis might explain how a
SN integrating external sensory stimuli with internal states mediates interactions
between large-scale networks involved in externally and internally oriented cognitive
processing. In the brain of patients with ASD, areas of the SN, including the anterior
insula, become dysfunctional, which results in difficulty in operating social cognition
and self-referential processing.


Here we discuss the controversial points and future directions of this hypothesis. Thus, the activity of the Anterior Insula (AI) itself partially contributes to social difficulty in individuals with ASD, and the neural network (SN), including the AI, dynamically affects various aspects of social cognition. There is a strong expectation that hypoactivity of the AI contributes to difficulties in emotion recognition such as alexithymia, which is not an autistic trait, andthe subsequent SN dysfunction induces a comprehensive autistic clinical representation due to a dysregulated Central Executive Network (ECN) and/or Default Modular Network (DMN). From a psychological perspective, the SN dysfunction hypothesis may support hierarchical processes for emotion recognition.

A role for the precuneus in thought–action fusion: Evidence from participants with significant obsessive–compulsive symptoms

Rhiannon Jones and Joydeep Bhattacharya

Neuroimage Clin 2014;4:112-121


Likelihood thought–action fusion (TAF-L) refers to a cognitive bias in which individuals believe that the mere thought of a negative event increases its likelihood of occurring in reality. TAF-L is most commonly associated with obsessive–compulsive disorder (OCD) but is also present in depression, generalized anxiety disorder and psychosis. We induced TAF-L in individuals with high (High-OC, N = 23) and low (Low-OC, N = 24) levels of OC traits, and used low resolution electromagnetic tomography (LORETA) to localise the accompanying electrical brain activity patterns. The results showed greater TAF-L in the High-OC than in the Low-OC group (p < .005), which was accompanied by significantly greater upper beta frequency (19–30 Hz) activity in the precuneus (p < .05). Further, the precuneus activity was positively correlated with self-reported magnitude of TAF-L (p < .01), suggesting a specific role of this region in this cognitive bias. Results are discussed with reference to self-referential processing and the default-mode network.

Keywords: Thought–action fusion, Electroencephalography, Precuneus, Default mode network, Obsessive–compulsive disorder
The precuneus in OCD, schizophrenia, anxiety and depression

While rarely mentioned in the models of OCD or discussed in detail in meta-analyses, a large proportion of neuroimaging studies have found abnormalities in precuneus structure and function in OCD populations. For example, reductions in precuneus grey matter have been found in OCD patients compared with controls in both adult (Soriano-Mas et al., 2007) and paediatric samples (Carmona et al., 2007), while Van den Heuvel et al. (2009) found positive correlations between the left precuneus grey matter and the harm/checking symptoms. Rotge et al.’s meta-analysis of 8 fMRI OCD symptom provocation studies found significant activation of the left precuneus (Rotge et al., 2008). Similarly, Menzies et al. (2008) found significant activation of the left precuneus of schizophrenic patient groups during attribution tasks, suggested to reflect automatic self-reflection, and to accompany delusions of reference (Menon et al., 2011). Delusions of reference refers to the endorsement, normally found in schizophrenic patients, that generic stimuli are related to themselves. As previously mentioned, parallels have been drawn between TAF and delusions of reference (Starcevic and Berle, 2006), both of which involve misattributions of personal significance, so it is interesting to see that precuneus activity has been found to accompany this phenomenon.

In GAD, abnormal connectivity has been observed between the posterior cingulate and precuneus and prefrontal cortices (Strawn et al., 2012), and significantly greater right precuneus volume has been found in adolescents with GAD compared with healthy controls (Strawn et al., 2013). Further, in young adults a positive relationship has been found between cortical thickness of the precuneus/PCC and depression/anxiety symptoms (Ducharme et al., 2013).

Moreover, in addition to specific involvement of the precuneus in psychopathology, there is considerable evidence of a link between psychopathology and abnormal DMN function (see Broyd et al., 2009 for a review).

Brain differences between persistent and remitted attention deficit hyperactivity disorder

NEW YORK (Reuters Health) – Brains of adults whose childhood attention deficit hyperactivity disorder (ADHD) has remitted are structurally different from brains of adults whose childhood ADHD persists, a new longitudinal study suggests.

“These findings suggest that indeed there is a biological brain basis underlying the distinction between ADHD remission and persistence,” wrote first author Dr. Aaron T. Mattfeld of the Massachusetts Institute of Technology in Cambridge, in an email to Reuters Health.

“The first and possibly most important finding is that participants diagnosed with ADHD in childhood but who no longer meet the diagnostic criteria for full or subthreshold ADHD as adults look just like participants who never had ADHD when we examine the correlations in functional magnetic resonance imaging (fMRI) activations between two important regions of the default mode network, the medial prefrontal cortex and the posterior cingulate cortex,” he wrote.

“The second finding suggests that people who have ever been diagnosed with ADHD don’t entirely resemble those who have never had ADHD. The typical negative relationship between the medial prefrontal cortex and the dorsolateral prefrontal cortex – a region important for working memory and attention – is reduced in anyone who has ever been diagnosed with ADHD compared with people who have never had ADHD. This may be related to deficits in executive functions that are common in ADHD but do not define it,” he added.

To characterize the brain differences and similarities between adults with persistent vs remitted ADHD, Dr. Mattfeld and his colleagues performed resting state fMRI 16 years after their subjects’ baseline assessment. They reported their results online June 10 in Brain.

They measured intrinsic functional brain organization in 13 patients whose childhood diagnosis persisted into adulthood, 22 patients who were diagnosed in childhood but not in adulthood, and 17 controls who’d never had ADHD. All groups were clinically and demographically well matched.

A positive functional correlation between posterior cingulate and medial prefrontal cortices was reduced only in patients whose diagnosis persisted into adulthood (p<0.05); and a negative functional correlation between medial and dorsolateral prefrontal cortices was reduced in both persistent and remitted patients (p<0.05).

“This work represents some of the most exciting scientific work that I have been involved in, a 20-year study of a group of boys and girls with ADHD, whose average age is now close to 30 years, whom we have followed from childhood into adult life,” co-author Dr. Joseph Biederman of Massachusetts General Hospital in Boston, said in a phone interview.

The research team based its study on prior data from other research in adults that showed that adults with ADHD by definition have active symptoms of ADHD; and the team examined whether, in a longitudinal sample, it could capture findings similar to those of the earlier researchers.

“Adult ADHD is diagnosed retrospectively,” Dr. Biederman said. “Because the disorder is defined by having symptoms that began in the formative years, we ask patients to recall childhood symptoms.”

“Now, for the first time we have the convergence of data from prior retrospective studies of adults and our prospective data from children followed into adulthood, which gives us an important argument for the continuity of ADHD from childhood into adulthood,” he said.

“We found that people who remitted by definition no longer had ADHD, so it is very reassuring that the networks in the brain that are impaired in people who have it are no longer impaired, that they are truly normalized or remitters,” he said.

“ADHD is a brain disorder of genetic etiology. The clinical implications of this are vast. We are documenting that this is a highly persistent condition associated with network disturbances in the brain that can be captured with imaging. ADHD is not a fabrication, as some have suggested,” Dr. Biederman said.

According to Dr. Mattfeld, surprisingly little research has investigated brain differences between remitted and persistent ADHD.

“Our study was the first resting-state study, we believe, to directly compare the two groups to each other, and thus these data really add to the literature in that respect,” he wrote.

“Right now we have very static understandings of very dynamic systems,” he wrote, and he called for further research, “longitudinal studies, with multiple scanning time points, and larger samples – to look at the evolution of these disorders over time and aid in the diagnosis and assessment of the efficacy of different treatments.



For Immediate Release: July 15, 2013

Media Inquiries: Synim Rivers, 301-796-8729,
Consumer Inquiries: 888-INFO-FDA

FDA permits marketing of first brain wave test to help assess children and teens for ADHD

The U.S. Food and Drug Administration today allowed marketing of the first medical device based on brain function to help assess attention-deficit/hyperactivity disorder (ADHD) in children and adolescents 6 to 17 years old. When used as part of a complete medical and psychological examination, the device can help confirm an ADHD diagnosis or a clinician’s decision that further diagnostic testing should focus on ADHD or other medical or behavioral conditions that produce symptoms similar to ADHD.
The device, the Neuropsychiatric EEG-Based Assessment Aid (NEBA) System, is based on electroencephalogram (EEG) technology, which records different kinds of electrical impulses (waves) given off by neurons (nerve cells) in the brain and the number of times (frequency) the impulses are given off each second.
The NEBA System is a 15- to 20-minute non-invasive test that calculates the ratio of two standard brain wave frequencies, known as theta and beta waves. The theta/beta ratio has been shown to be higher in children and adolescents with ADHD than in children without it.
“Diagnosing ADHD is a multistep process based on a complete medical and psychiatric exam,” said Christy Foreman, director of the Office of Device Evaluation at the FDA’s Center for Devices and Radiological Health. “The NEBA System along with other clinical information may help health care providers more accurately determine if ADHD is the cause of a behavioral problem.”
ADHD is one of the most common neurobehavioral disorders in childhood. According to the American Psychiatric Association, 9 percent of U.S. adolescents have ADHD and the average age of diagnosis is 7 years old. Children with ADHD have difficulty with attention, hyperactivity, impulsivity and behavioral problems.
The FDA reviewed the NEBA System through the de novo classification process, a regulatory pathway for some low- to moderate-risk medical devices that are not substantially equivalent to an already legally marketed device.
In support of the de novo petition, the manufacturer submitted data including a clinical study that evaluated 275 children and adolescents ranging from 6 to 17 years old with attention or behavioral concerns. Clinicians evaluated all 275 patients using the NEBA System and using standard diagnostic protocols, including the Diagnostic and Statistical Manual of Mental Disorders IV Text Revision(DSM-IV-TR) criteria, behavioral questionnaires, behavioral and IQ testing, and physical exams to determine if the patient had ADHD. An independent group of ADHD experts reviewed these data and arrived at a consensus diagnosis regarding whether the research subject met clinical criteria for ADHD or another condition. The study results showed that the use of the NEBA System aided clinicians in making a more accurate diagnosis of ADHD when used in conjunction with a clinical assessment for ADHD, compared with doing the clinical assessment alone.
NEBA Health of Augusta, Ga., manufactures the NEBA System.
For more information:
The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.
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Brain Connectivity in Autism

Front. Hum. Neurosci., 02 June 2014 | doi: 10.3389/fnhum.2014.00349
Topic Editors:

Rajesh K. KanaUniversity of Alabama at Birmingham, AL., USA
Lucina Q. UddinUniversity of Miami, USA
Tal KenetMassachusetts General Hospital, USA
Diane ChuganiWayne State University, USA
Ralph-Axel MüllerSan Diego State University, USA

The brain’s ability to process information crucially relies on connectivity. Understanding how the brain processes complex information and how such abilities are disrupted in individuals with neuropsychological disorders will require an improved understanding of brain connectivity. Autism is an intriguingly complex neurodevelopmental disorder with multidimensional symptoms and cognitive characteristics. A biological origin for autism spectrum disorders (ASD) had been proposed even in the earliest published accounts (Kanner, 1943; Asperger, 1944). Despite decades of research, a focal neurobiological marker for autism has been elusive. Nevertheless, disruptions in interregional and functional and anatomical connectivity have been a hallmark of neural functioning in ASD. Theoretical accounts of connectivity perceive ASD as a cognitive and neurobiological disorder associated with altered functioning of integrative circuitry. Neuroimaging studies have reported disruptions in functional connectivity (synchronization of activated brain areas) during cognitive tasks and during task-free resting states. While these insights are valuable, they do not address the time-lagged causality and directionality of such correlations. Despite the general promise of the connectivity account of ASD, inconsistencies and methodological differences among studies call for more thorough investigations. A comprehensive neurological account of ASD should incorporate functional, effective, and anatomical connectivity measures and test the diagnostic utility of such measures. In addition, questions pertaining to how cognitive and behavioral intervention can target connection abnormalities in ASD should be addressed. This research topic of the Frontiers in Human Neuroscience will address “Brain Connectivity in Autism” primarily from cognitive neuroscience and neuroimaging perspectives.

Specifically with respect to the wealth of neuroimaging findings, fundamental questions still await definitive answers. Among these are:

• How can the inconsistencies in the fcMRI literature – with abundant evidence of underconnectivity in many functional networks contrasting with some reports of overconnectivity in ASD – be explained and reconciled?
• How do findings for low temporal frequency bands from fcMRI relate to those for higher frequencies, as detected by EEG and MEG?
• What are the underlying pathological changes suggested by DTI findings of reduced fractional anisotropy or increased mean and radial diffusion?
• How does evidence of white matter compromise and abnormal functional connectivity in children and adults relate to evidence of early brain overgrowth in infants that develop ASD?
• What are the links between abnormalities of functional and anatomical connectivity and those of cortical organization, e.g., those affecting cytoarchitecture or regional cortical thickness?
• How can techniques that are not typically applied in connectivity studies (e.g., TMS, MR spectroscopy) contribute to the understanding of connectivity in ASD?
• How do imaging findings inform us about the causation of sociocommunicative and other impairments in ASD? How can we determine whether they provide developmental explanations or simply reflect atypical social interaction in children with ASD?

We welcome contributions addressing one (or several) of the questions above or any other relevant questions related to network connectivity in ASD. Specifically, we welcome not only authors with a track record in ASD connectivity research, but also those in fields not conventionally considered to be related to connectivity (e.g., postmortem cytoarchitectonics, brain volumetrics, computational modeling), who may add valuable ‘outside-the-box’ contributions. The main goal of this venture is to search for a comprehensive and cohesive framework for better conceptualization of connection abnormalities.

Brainwave Neurofeedback for Autism: Can It Help?

Helping children to control their own brainwaves may help autism symptoms

Published on June 12, 2013 by Arshya Vahabzadeh, M.D. in Spectrum Theory

Brainwaves being monitored with EEG machine

Autism is a condition that effects 1 in 88 children according to estimates from the Centers for Disease Control. Treatments for autism remain very limited with many families attempting to try to improve symptoms based on changes in diet, supplements, or other interventions.

What is neurofeedback ?

Several people had recently mentioned the benefits their children had experienced from neurofeedback. Neurofeedback involves being monitored by a machine that monitors your brainwave activities through an electroencephalographic (EEG) machine. These brainwaves can be presented on a computer screen by either lines or graphs, or by simple objects such as a ball. As the child uses neurofeedback, and gets closer to having the “normal” brainwave patterns, they will notice the ball or lines on the screen change. This is essentially a way of teaching a child how to self-regulate their own brainwaves.

As with any activity, practice is essential to improving performance. Very few side effects to neurofeedback have been identified, and in large part no serious concerns have been seen. Some children have noted headaches and muscular tension.

Does it work for autism?

Reports from caregivers of people with autism suggest people have witnessed improvements in a variety of areas including speech and irritability. A few scientific reports have highlighted that a demonstrated increase in social interaction may be seen in child with autism following treatment. One study suggested that parents who noticed an improvement continued to see the benefits for at least a year after neurofeedback. We know from other studies that the brainwaves of children with autism may well be different in many ways to the brainwaves of their non-autistic peers.

Although neurofeedback looks promising as one option for treating some of the symptoms of autism, looking through the scientific literature, it appears that there have been only a very limited number of small studies, with widely varying methods. Some researchers have suggested that the findings supporting the use of neurofeedback in ASD are inconclusive. I think, as several others have commented, that this is likely to be as a result of a lack of research studies into this interesting area.

The story of neurofeedback and another childhood condition, attention-deficit–hyperactivity disorder (ADHD), is different. Neurofeedback has been shown to help children with ADHD by improving hyperactivity, impulsivity, and inattention. Interestingly, we know that many children with autism may also have these symptoms. It has been suggested that 1 in 3 children with autism may also have ADHD.

Future directions

It is clear that we need further research in this area, as we need to explore how the brainwaves of children with autism may be different, and then determine if neurofeedback is an intervention that we should be using more frequently.

Neurofeedback Interest in MicroTesla pEMF

The latest news for BrainMaster the addition of randomizing for Microtesla applications for the brain.  This new feature helps to breakup unwanted EEG patterns.  We are excited to receive results from the use of this new formula