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Neurofeedback Los Angeles

Neurofeedback training and therapy Neurofeedback

Neurofeedback for Sleep Disorders and Insomnia

Neurofeedback for Sleep Disorders and Insomnia

Neurofeedback for Sleep Disorders and Insomnia

Neurofeedback for Sleep Disorders and Insomnia

Neurofeedback for Sleep Disorders and Insomnia
Neurofeedback for Sleep Disorders and Insomnia

Neurofeedback for Sleep Disorders and Insomnia

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Devin Lockett Professional Consultant
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Neurofeedback is a powerful tool for regulating sleep. Health professionals around the world report significant improvement in a large percentage of their clients using neurofeedback to treat chronic, long term sleep problems. What are the most commonly reported sleep issues that improve with neurofeedback training? Insomnia - Difficulty falling asleep; difficulty maintaining sleep during the night Difficulty waking from sleep Difficulty getting to bed Not feeling rested after sleep Sleeping too long neurofeedback sleep disorders insomnia over 10 hours neurofeedback sleep disorders insomnia Physically restless sleep Nightmares Bedwetting neurofeedback sleep disorders insomnia Nocturnal enuresis neurofeedback sleep disorders insomnia Sleepwalking Restless leg syndrome - Leg discomfort or sleep causing movement neurofeedback sleep disorders insomnia arousal Bruxism - teeth grinding during sleep Sleep terrors - Abrupt arousal with intense fear, difficult to awaken, no dream recall or memory of event Narcolepsy Dysregulated sleep patterns/cycles neurofeedback sleep disorders insomnia circadian rhythms neurofeedback sleep disorders insomnia Neurofeedback training often helps these problems as it improves brain regulation. These are common reports: A 75 year-old reported recently that she "slept like a baby for the first time in 25 years" after neurofeedback training. Parents of children with Attention Deficit Hyperactivity Disorder neurofeedback sleep disorders insomnia ADHD neurofeedback sleep disorders insomnia often say it's easier to get their kids to sleep. Depressed clients remark they have a much easier time getting going in the morning. The role of the brain and sleep The brain regulates sleep. Neuroscience has established the role of neuromodulator systems in the brainstem that play a role in maintaining awake states and, conversely, help the brain sleep. The EEG neurofeedback sleep disorders insomnia brainwaves neurofeedback sleep disorders insomnia clearly reflects changes in sleep stages.Training brainwaves using neurofeedback to decrease or increase slow brainwave activity, or to increase specific EEG activation patterns appears to help the brain normalize sleep. Based on reports from a large number of licensed health professionals the evidence shows that training the EEG impacts sleep regulatory mechanisms and people sleep better. Since sleep is complex and involves many systems, it is not possible to suggest that sleep problems always improve as a result of neurofeedback. But clinicians say that they routinely expect changes to occur in sleep patterns after appropriate training for a large percentage of their patients. As with any program, a complete sleep assessment is helpful. Sleep hygiene issues neurofeedback sleep disorders insomnia including caffeine, alcohol and other behavioral factors neurofeedback sleep disorders insomnia and other potential contributory factors such as possible sleep apnea also need to be carefully reviewed and corrected in combination with neurofeedback training. What research exists? Sleep is a good example of the research challenge of neurofeedback. There are good neurofeedback studies in ADHD, epilepsy and addiction. The fact that no significant studies exist on sleep and neurofeedback is remarkable. In virtually every study related to neurofeedback outcomes, changes to sleep are noted, but not always highlighted or even reported. Sleep researchers are primarily unaware of neurofeedback and its implications for insomnia and other sleep disorders. Hopefully, cross-fertilization between clinically-oriented therapists and sleep researchers can occur. As in many academic areas, this kind of cross fertilization can take significant time and funding. Because of the vast amount of literature about brain regulation, sleep and the EEG, there is a solid basis for using neurofeedback with sleep problems. Hundreds of experienced licensed professionals have used this modality successfully to improve sleep for over 25 years. For general information on sleep issues see: http://www.ninds.nih.gov/find_people/ninds/organization.htm About the Author: Michael Cohen is Director of Education for Center for Brain Training in Florida. He has taught courses in EEG biofeedback to professionals around the world for the last eight years, including courses for psychiatrists at the annual American Psychiatric Conference. SLEEP AND FATIGUE During sleep, the brain has a chance to sort, prioritize and file all the information taken in during the day. Mental functioning decreases nearly twice as rapidly as physical performance with decreased sleep. The reasons for sleep difficulties are varied. It may be due to stress, anxiety, burnout, trauma, or habitual loop thinking. Whatever the cause, the brain has lost the ability to shift into the correct state for sleep. Neurofeedback helps you to restore your natural sleep rhythms. By training brain control and flexibility, the smooth transition of the central nervous system from activation to rest can happen naturally. In the case of fatigue related disorders neurofeedback sleep disorders insomnia such as CFS neurofeedback sleep disorders insomnia , it can be a long process to rebalance and re-strengthen the system. Proper nutrition is crucial as a supporting therapy in this case, as is a willingness to take it gently to give the system a chance to rebuild and recover. Sleep studies... For temporary relief, try this simple self-help tip. If you would like to arrange an assessment to see if we can help, contact us. I am sleeping better than I have for years - I feel like a human being again. It made a huge difference in my life. I'm calmer, more manageable and experiencing relationships in a different way. Neurofeedback at Brainworks was life-changing. Living in my brain is a very different experience now; no matter the circumstances I can maintain a sense of peace and clarity in my head. My resilience to stress and pressure has hugely improved, and my life-long insomnia is largely a thing of the past and when it crops up, I can overcome it. Thank you so much! Having suffered with post viral fatigue symptoms for years, I have had a great deal of success with Brainworks. After completing a block of treatments I found that my energy levels almost returned to normal. I would thoroughly recommend it. It's great - I honestly never imagined such a tangible result. So thank you for that, as sleep was my main area of concern. Neurofeedback for insomnia: a pilot study of Z-score SMR and individualized protocols. Hammer BU1, Colbert AP, Brown KA, Ilioi EC. Author information Abstract Insomnia is an epidemic in the US. Neurofeedback neurofeedback sleep disorders insomnia NFB neurofeedback sleep disorders insomnia is a little used, psychophysiological treatment with demonstrated usefulness for treating insomnia. Our objective was to assess whether two distinct Z-Score NFB protocols, a modified sensorimotor neurofeedback sleep disorders insomnia SMR neurofeedback sleep disorders insomnia protocol and a sequential, quantitative EEG neurofeedback sleep disorders insomnia sQEEG neurofeedback sleep disorders insomnia -guided, individually designed neurofeedback sleep disorders insomnia IND neurofeedback sleep disorders insomnia protocol, would alleviate sleep and associated daytime dysfunctions of participants with insomnia. Both protocols used instantaneous Z scores to determine reward condition administered when awake. Twelve adults with insomnia, free of other mental and uncontrolled physical illnesses, were randomly assigned to the SMR or IND group. Eight completed this randomized, parallel group, single-blind study. Both groups received fifteen 20-min sessions of Z-Score NFB. Pre-post assessments included sQEEG, mental health, quality of life, and insomnia status. ANOVA yielded significant post-treatment improvement for the combined group on all primary insomnia scores: Insomnia Severity Index neurofeedback sleep disorders insomnia ISI p neurofeedback sleep disorders insomnia .005 neurofeedback sleep disorders insomnia , Pittsburgh Sleep Quality Inventory neurofeedback sleep disorders insomnia PSQI p neurofeedback sleep disorders insomnia .0001 neurofeedback sleep disorders insomnia , PSQI Sleep Efficiency neurofeedback sleep disorders insomnia p neurofeedback sleep disorders insomnia .007 neurofeedback sleep disorders insomnia , and Quality of Life Inventory neurofeedback sleep disorders insomnia p neurofeedback sleep disorders insomnia .02 neurofeedback sleep disorders insomnia . Binomial tests of baseline EEGs indicated a significant proportion of excessively high levels of Delta and Beta power neurofeedback sleep disorders insomnia p neurofeedback sleep disorders insomnia .001 neurofeedback sleep disorders insomnia which were lowered post-treatment neurofeedback sleep disorders insomnia paired z-tests p neurofeedback sleep disorders insomnia .001 neurofeedback sleep disorders insomnia . Baseline EEGs showed excessive sleepiness and hyperarousal, which improved post-treatment. Both Z-Score NFB groups improved in sleep and daytime functioning. Post-treatment, all participants were normal sleepers. Because there were no significant differences in the findings between the two groups, our future large scale studies will utilize the less burdensome to administer Z-Score SMR protocol. Trouble Going to Sleep? Staying Asleep? Difficulty Waking? At least 40 million Americans each year suffer from chronic, long-term, sleep disorders. An additional 20 million experience occasional sleep problems. Good sleep is critical to good health. Do you find yourself lying awake at night worrying or being unable to shut off your mind? Maybe you don't feel rested or like you're always trying to "catch-up" on sleep? Do you wake multiple times throughout the night? Does your child struggle with a sleep problem like nightmares or bedwetting? Brain Training and Sleep Problems Neurofeedback is a powerful tool for helping people fall asleep and stay asleep. Over 3000 licensed health professionals now use this new technology daily with patients. They report significant and consistent improvements for clients' sleep problems. It's often remarkable how quickly sleep can improve with clients who have been to many different specialists and have struggled with sleep for years. At the Center for Brain Training, we take a comprehensive approach to helping clients with sleep. We review many different options with clients to help them assess what's most appropriate for their problem, including several brain regulating technologies like Alpha-Stim and Brain Music. If the problem is severe, we record a brain map to take a detailed look to see if there's a specific EEG problem in the brain that is interfering with sleep. Frankly, there just aren't many places that take a comprehensive look at sleep. The addition of neurofeedback is powerful, and most people can train their brain to sleep well again. Unfortunately many doctors and other health professionals are still unaware of neurofeedback and its effectiveness at treating sleep problems. As an alternative to medications, neurofeedback can help people reduce or eliminate drugs for insomnia and sleep disorders as their brains become more attuned to healthier sleep patterns. Common Sleep Issues that Improve with Neurofeedback Insomnia – Difficulty falling asleep; difficulty maintaining sleep during the night Difficulty waking from sleep Difficulty getting to bed Not feeling rested after sleep Sleeping too long neurofeedback sleep disorders insomnia over 10 hours neurofeedback sleep disorders insomnia Physically restless sleep Nightmares Bedwetting neurofeedback sleep disorders insomnia Nocturnal enuresis neurofeedback sleep disorders insomnia Sleepwalking Restless leg syndrome – Leg discomfort or sleep causing movement neurofeedback sleep disorders insomnia arousal Bruxism – teeth grinding during sleep Sleep terrors – Abrupt arousal with intense fear, difficult to awaken, no dream recall or memory of event Narcolepsy Dysregulated sleep patterns/cycles neurofeedback sleep disorders insomnia circadian rhythms neurofeedback sleep disorders insomnia Neurofeedback training helps these problems as it improves brain regulation. These are common reports: A 75 year-old reported recently that she "slept like a baby for the first time in 25 years" after neurofeedback training. Parents of children with Attention Deficit Hyperactivity Disorder neurofeedback sleep disorders insomnia ADHD neurofeedback sleep disorders insomnia often say it's easier to get their kids to sleep. Depressed clients remark they have a much easier time getting going in the morning. The Role of the Brain and Sleep The brain regulates sleep. The EEG neurofeedback sleep disorders insomnia brainwaves neurofeedback sleep disorders insomnia clearly reflects changes in sleep stages. Training brainwaves using neurofeedback to increase slow brainwave activity or to increase specific EEG activation patterns appears to help the brain normalize sleep. Based on reports from a large number of licensed health professionals, evidence shows that training the EEG impacts sleep regulatory mechanisms, and people sleep better. Since sleep is complex and involves many systems, it is not possible to suggest that sleep problems always improve as a result of neurofeedback. Yet, clinicians say they routinely expect positive changes to occur in sleep patterns after appropriate training for a large percentage of their clients. As with any program, a complete sleep assessment is helpful. Sleep hygiene issues neurofeedback sleep disorders insomnia including caffeine, alcohol and other behavioral factors neurofeedback sleep disorders insomnia , and other potential contributory factors such as possible sleep apnea also need to be carefully reviewed and corrected in combination with neurofeedback training. If you'd like to find out more about how the Center for Brain Training can help with your sleep problem, please call our office at 561-744-7616 or fill out the form in the sidebar. We look forward to hearing from you. Easy way to reset your sleep cycle: Stop eating neurofeedback sleep disorders insomnia Click here for information on a simple way to reset your sleep cycle. Neurofeedback, ADHD and sleep The article below is a pre-publication copy of the article published in Neuroscience neurofeedback sleep disorders insomnia Biobehavioral Reviews: Arns, M. neurofeedback sleep disorders insomnia Kenemans, J.L. neurofeedback sleep disorders insomnia 2012 neurofeedback sleep disorders insomnia . Neurofeedback in ADHD and insomnia: Vigilance Stabilization through sleep spindles and circadian networks. Neuroscience and Biobehavioral Reviews. doi: 10.1016/j.neubiorev.2012.10.006 Voor geïnteresseerden, lees hier ook het Nederlandstalige artikel over neurofeedback wat juni 2014 verscheen in De Psycholoog. Recent years have seen a re-emergence of research covering the application of neurofeedback. Neurofeedback is a method based on operant learning mechanisms neurofeedback sleep disorders insomnia Sherlin et al., 2011 neurofeedback sleep disorders insomnia which is hypothesized to 'normalize' deviant brain activity. Neurofeedback has been classified as an efficacious treatment for ADHD based on guidelines of the American Psychological Association neurofeedback sleep disorders insomnia APA neurofeedback sleep disorders insomnia neurofeedback sleep disorders insomnia Arns et al., 2009 neurofeedback sleep disorders insomnia . Neurofeedback has also been investigated in the treatment of epilepsy neurofeedback sleep disorders insomnia Tan et al., 2009 neurofeedback sleep disorders insomnia , insomnia neurofeedback sleep disorders insomnia Cortoos et al., 2010; Hauri et al., 1982; Hauri, 1981; Hoedlmoser et al., 2008; Sterman et al., 1970 neurofeedback sleep disorders insomnia and cognition. However, APA standards do not require single or double-blinded experimental designs. This certainly contributes to the limited understanding of how exactly neurofeedback exerts its clinical effects in these disorders. Fathoming the exact mechanisms underlying neurofeedback's effect is crucial for improving clinical trial designs investigating the efficacy of neurofeedback as well as for optimizing the efficacy of neurofeedback. Recently there have been new insights into the clinical pathophysiology of ADHD. These include insights from the EEG-Vigilance model, the role of sleep onset-insomnia and the possible efficacy of chronobiological treatments for ADHD such as melatonin and morning bright light neurofeedback sleep disorders insomnia Rybak et al., 2006; Van der Heijden et al., 2005; Van der Heijden et al., 2007; Van Veen et al., 2010 neurofeedback sleep disorders insomnia . These insights provoke new considerations regarding the specific effects of neurofeedback in ADHD and insomnia. This review paper will provide a review of neurofeedback research focused on the application in ADHD and sleep The new insights above will be further reviewed and integrated into a model that can explain the clinical effects of neurofeedback and circadian advancing treatments in ADHD and insomnia, and also provides insight into the development of new treatments for ADHD. 1.1. From EEG conditioning to Neurofeedback Classical conditioning of the EEG has been demonstrated as early as in 1935 in France neurofeedback sleep disorders insomnia Durup and Fessard, 1935 neurofeedback sleep disorders insomnia , and 1936 in the United States neurofeedback sleep disorders insomnia Loomis et al., 1936 neurofeedback sleep disorders insomnia , just a few years after the first description of the EEG by Berger in 1929. In the 1940's classical conditioning of the alpha blocking response in the EEG was more systematically investigated It was found that the EEG alpha blocking response fulfilled all of the Pavlovian types of conditioned responses neurofeedback sleep disorders insomnia Jasper and Shagass, 1941; Knott and Henry, 1941 neurofeedback sleep disorders insomnia . These early studies clearly demonstrate that principles of classical conditioning can be applied to EEG parameters such as the alpha blocking response. Further support for this comes from several recent studies demonstrating that not only cortical EEG can be conditioned neurofeedback sleep disorders insomnia reviewed in Sherlin et al., 2011 neurofeedback sleep disorders insomnia , but that it is also possible to condition more focal neuronal activity such as the activity in monkey frontal eye fields neurofeedback sleep disorders insomnia Schafer and Moore, 2011 neurofeedback sleep disorders insomnia , marmoset intra-cortical Sensori-Motor Rhythm or SMR neurofeedback sleep disorders insomnia Philippens and Vanwersch, 2010 neurofeedback sleep disorders insomnia , and human medial temporal cortex neurofeedback sleep disorders insomnia Cerf et al., 2010 neurofeedback sleep disorders insomnia and early visual processing areas such as V1 and V2 neurofeedback sleep disorders insomnia Shibata et al., 2011 neurofeedback sleep disorders insomnia . A first attempt of classical conditioning of spike-wave discharges in patients with epilepsy was unsuccessful neurofeedback sleep disorders insomnia Stevens and Stevens, 1960 neurofeedback sleep disorders insomnia or at least difficult neurofeedback sleep disorders insomnia Stevens et al., 1967 neurofeedback sleep disorders insomnia . Operant conditioning of epileptic multi-unit activity has been demonstrated, albeit without sustained effects of decreased seizure rates neurofeedback sleep disorders insomnia Fetz and Wyler, 1973; Wyler et al., 1974 neurofeedback sleep disorders insomnia . This was recently confirmed by Osterhagen et al. neurofeedback sleep disorders insomnia 2010 neurofeedback sleep disorders insomnia who were unable to demonstrate an increase in seizure rates in rats when the occurrence of spike-wave discharges was reinforced, suggesting that spike-wave discharges cannot be 'conditioned' or trained directly. The difficulty of this direct conditioning of epileptic states may be the result of the decreased level of consciousness during such states precluding efficient learning from taking place during the occurrence of a seizure. The first successful applications of EEG conditioning on seizures were not reported until the early 1960's by Barry Sterman. His work involved the training of Sensori-Motor Rhythm, also called SMR, in the cat. In a serendipitous finding the anticonvulsant effects of operant conditioning of this rhythm in cats exposed to the pro-convulsant Monomethylhydrazine was demonstrated neurofeedback sleep disorders insomnia Sterman et al., 1969; Sterman et al., 2010 neurofeedback sleep disorders insomnia . The movie above illustrates in more detail how neurofeedback works in practice and what the procedures look like. During those early days this technique was referred to as 'EEG Biofeedback'. The first demonstrations of SMR neurofeedback with potential clinical implications were reported in cats related to epilepsy neurofeedback sleep disorders insomnia Sterman et al., 1969; 2010 neurofeedback sleep disorders insomnia and sleep neurofeedback sleep disorders insomnia Sterman et al., 1970 neurofeedback sleep disorders insomnia , shortly followed by the clinical applications in humans with epilepsy neurofeedback sleep disorders insomnia Sterman and Friar, 1972 neurofeedback sleep disorders insomnia and ADHD neurofeedback sleep disorders insomnia Lubar and Shouse, 1976 neurofeedback sleep disorders insomnia . Contemporaneously Kamiya demonstrated voluntary control over alpha activity and alpha peak frequency neurofeedback sleep disorders insomnia APF neurofeedback sleep disorders insomnia neurofeedback sleep disorders insomnia Kamiya, 1968 neurofeedback sleep disorders insomnia . This work has resulted in, among others, the application of alpha/theta neurofeedback in the treatment of addictions and optimal performance neurofeedback sleep disorders insomnia reviewed in Gruzelier, 2009 neurofeedback sleep disorders insomnia and inspired several well controlled studies investigating training of upper-alpha power resulting in improved cognitive performance neurofeedback sleep disorders insomnia Hanslmayr et al. 2005; Zoefel et al., 2011 neurofeedback sleep disorders insomnia . In parallel with the development of SMR and alpha related 'frequency' neurofeedback or Alternating Current neurofeedback sleep disorders insomnia AC neurofeedback sleep disorders insomnia Neurofeedback, the first demonstration of voluntary control over the 'Contingent Negative Variation' or CNV was demonstrated in 1966 by McAdam and colleagues neurofeedback sleep disorders insomnia 1966 neurofeedback sleep disorders insomnia . Elbert and Birbaumer further pioneered the first studies on voluntary control of slow cortical potentials neurofeedback sleep disorders insomnia SCPs neurofeedback sleep disorders insomnia employing a biofeedback procedure, with the goal of investigating the functional relationship between SCP and the performance during a signal detection task neurofeedback sleep disorders insomnia Lutzenberger et al., 1979; Elbert et al., 1980 neurofeedback sleep disorders insomnia . Neurofeedback of these Slow Cortical Potentials, or SCP's is also referred to as Direct Current neurofeedback sleep disorders insomnia DC neurofeedback sleep disorders insomnia neurofeedback. The difference is that feedback is not provided based on the amplitude of a given frequency band, but rather on the polarity of the slow EEG content, e.g. surface-positivity or surface-negativity. Based on the observation that pro-convulsive procedures such as hyperventilation resulted in increased surface-negativity and anticonvulsants result in decreased surface-negativity, this SCP procedure was investigated in drug refractory epilepsy patients in a double-blind placebo controlled design. In this study SCP neurofeedback was compared to alpha-power neurofeedback, and only the group who received SCP neurofeedback demonstrated a significant reduction in seizure frequency neurofeedback sleep disorders insomnia Rockstroh et al., 1993 neurofeedback sleep disorders insomnia . In 2004, the first application of SCP neurofeedback in the treatment of ADHD was published neurofeedback sleep disorders insomnia Heinrich et al., 2004 neurofeedback sleep disorders insomnia . Generally the effects of SCP Neurofeedback appear similar to the effects of SMR and Theta/Beta neurofeedback for epilepsy neurofeedback sleep disorders insomnia Tan et al., 2009 neurofeedback sleep disorders insomnia and for ADHD neurofeedback sleep disorders insomnia Leins et al., 2007; Arns et al., 2009; Gevensleben et al., 2009 neurofeedback sleep disorders insomnia . Figure 1 visualizes this history further, by graphing the number of publications per year for 3 different keywords, which have historically been used to refer to neurofeedback related techniques since 1941. The early research focused on investigating classical conditioning of the EEG, in figure 1 this is visualized by the green bars and green trend line neurofeedback sleep disorders insomnia floating average, 2 points neurofeedback sleep disorders insomnia . During the 1940's and 1950's some research on this topic was published, but this research actually surged in the beginning of the 1960's with a peak in 1975. Following the first publications on operant conditioning of EEG by Wyrwicka and Sterman neurofeedback sleep disorders insomnia 1968 neurofeedback sleep disorders insomnia , as well as the work on conscious control of EEG alpha activity by Kamiya in 1968 neurofeedback sleep disorders insomnia Kamiya, 1968; 2011 neurofeedback sleep disorders insomnia and studies showing voluntary control over the CNV neurofeedback sleep disorders insomnia McAdam et al., 1966 neurofeedback sleep disorders insomnia , we see an increase in publications referring to 'EEG Biofeedback', which remained the pre-dominant term for neurofeedback until the end of the 1990's. The term 'neurofeedback' was first used by Nahmias, Tansey and Karetzky in 1994 neurofeedback sleep disorders insomnia Nahmias et al., 1994 neurofeedback sleep disorders insomnia . Since that time neurofeedback has become the predominant term as is clearly visible in figure 1, with the number of publications covering this term dramatically increasing in 2010 and 2011. Fig. 1: Frequency of different keywords related to neurofeedback and their frequency of occurrence in the scientific literature per year. Green reflects 'EEG AND conditioning', Red reflects 'EEG Biofeedback' and Blue reflects 'Neurofeedback'. Note that 2011* indicates the extrapolated number for 2011, based on the absolute numbers from August 15th 2011 neurofeedback sleep disorders insomnia obtained using SCOPUS neurofeedback sleep disorders insomnia . 1.2. Current status of Neurofeedback for ADHD and insomnia Since the initial report of Lubar and Shouse neurofeedback sleep disorders insomnia 1976 neurofeedback sleep disorders insomnia on SMR neurofeedback in ADHD and the initial report of Heinrich et al. neurofeedback sleep disorders insomnia 2004 neurofeedback sleep disorders insomnia of SCP Neurofeedback in ADHD, much research has been conducted on these 2 neurofeedback protocols in ADHD. SMR Neurofeedback is also referred to as Theta/Beta neurofeedback, where it is interesting to note that although the beta frequency band often used is broader neurofeedback sleep disorders insomnia e.g. 12-20 Hz neurofeedback sleep disorders insomnia than either Sterman's original 11-19 Hz range for SMR or the more traditional 12-15 Hz used for SMR; all studies still include the SMR band along with a theta inhibit used for both protocols. Furthermore, all these studies have trained at fronto-central locations neurofeedback sleep disorders insomnia also see Arns et al., 2009; Table 1 neurofeedback sleep disorders insomnia typical for SMR. Therefore, in this review where we refer to SMR Neurofeedback this also includes Theta/Beta neurofeedback. Currently, there are 8 published randomized controlled trials neurofeedback sleep disorders insomnia RCT's neurofeedback sleep disorders insomnia , which investigated SCP neurofeedback and/or SMR neurofeedback neurofeedback sleep disorders insomnia Linden, Habib, Radojevic, 1996; Levesque, Beauregard, Mensour, 2006; Leins et al., 2007; Gevensleben et al., 2009; Holtmann et al., 2009; Perreau-Link et al. 2010; Steiner et al., 2011; Bakshayesh et al., 2011 neurofeedback sleep disorders insomnia . All these studies except Perreau-Linck et al. neurofeedback sleep disorders insomnia 2010 neurofeedback sleep disorders insomnia demonstrated significant improvements on measures of inattention, hyperactivity or impulsivity compared to the control groups. This was confirmed by a meta-analysis conducted in 2009 by Arns and colleagues incorporating 15 studies neurofeedback sleep disorders insomnia total N=1194 neurofeedback sleep disorders insomnia where it was concluded that neurofeedback resulted in large and clinically relevant effect sizes neurofeedback sleep disorders insomnia ES neurofeedback sleep disorders insomnia for inattention and impulsivity and a low to medium ES for hyperactivity. Furthermore, the specificity of neurofeedback treatment in ADHD has been demonstrated by normalizations of Event Related Potentials neurofeedback sleep disorders insomnia ERP's neurofeedback sleep disorders insomnia after treatment, reflecting an improved information-processing neurofeedback sleep disorders insomnia Arns et al. 2012; Heinrich et al., 2004; Kropotov et al., 2005; Kropotov et al., 2007; Wangler et al., 2011 neurofeedback sleep disorders insomnia , normalizations of EEG power post-treatment neurofeedback sleep disorders insomnia Doehnert et al., 2008; Gevensleben et al., 2009 neurofeedback sleep disorders insomnia and effects on neural substrates of selective attention imaged with fMRI neurofeedback sleep disorders insomnia Lévesque et al., 2006 neurofeedback sleep disorders insomnia . Several studies have also directly compared the efficacy of neurofeedback with stimulant medication. Most have found the effects to be similar for measures of inattention, impulsivity and hyperactivity neurofeedback sleep disorders insomnia Rossiter neurofeedback sleep disorders insomnia LaVaque, 1995; Monastra et al., 2002; Fuchs et al., 2003; Rossiter, 2004 neurofeedback sleep disorders insomnia , which was also confirmed in the meta-analysis neurofeedback sleep disorders insomnia Arns et al., 2009 neurofeedback sleep disorders insomnia . However, none of these studies used a randomized group assignment design, and patients self-selected their preferred treatment. This may bias the results. Based on these studies it cannot be concluded that neurofeedback is as effective as stimulant medication. Interestingly, the ES reported for methylphenidate in a recent meta-analysis is comparable to the ES for neurofeedback neurofeedback sleep disorders insomnia NF neurofeedback sleep disorders insomnia for improvements in measurements of inattention neurofeedback sleep disorders insomnia ES NF=0.81; ES Methylphenidate=0.84 neurofeedback sleep disorders insomnia , whereas for impulsivity/hyperactivity the ES for methylphenidate is higher neurofeedback sleep disorders insomnia ES NF=0.4/0.69; ES Methylphenidate=1.01 neurofeedback sleep disorders insomnia neurofeedback sleep disorders insomnia Faraone and Buitelaar, 2009; Sherlin et al. 2010; Arns et al., 2009 neurofeedback sleep disorders insomnia . This suggests that the effects of neurofeedback and methylphenidate appear similar, at least for inattention. Further randomized controlled studies are required to substantiate this observation. The most adequately designed randomized controlled trials neurofeedback sleep disorders insomnia RCTs neurofeedback sleep disorders insomnia investigating neurofeedback in ADHD have used semi-active control groups such as attentional training neurofeedback sleep disorders insomnia Gevensleben et al., 2009 neurofeedback sleep disorders insomnia or EMG Biofeedback neurofeedback sleep disorders insomnia Bakhshayesh et al., 2011 neurofeedback sleep disorders insomnia , but none have used a double-blind placebo controlled design. The current controversy regarding the efficacy of neurofeedback in ADHD is centered around the appropriate design standards for these studies. Some suggest that neurofeedback should be evaluated as a psychological treatment using the APA guidelines neurofeedback sleep disorders insomnia Arns et al., 2009; Sherlin et al., 2010a; 2010b neurofeedback sleep disorders insomnia , though others prefer designs used for rating new drugs requiring a double-blind placebo controlled study neurofeedback sleep disorders insomnia e.g.: Lofthouse et al., 2010; 2011 neurofeedback sleep disorders insomnia . Given the fact that neurofeedback is based on operant conditioning principles, it is crucial that the active treatment and planned control condition be in line with principles of learning theory and conditioning principles. Adhering to these basic principles is required for any learning to take place, including paying heed to such aspects as latency of reinforcement, specificity of reinforcement, shaping and generalization. A double-blind design often demands a deviation from such principles. For example such studies often use auto-tresholding to remain double-blinded. With auto-tresholding the child will always be rewarded, whether active learning is taking place or whether the child is doing nothing, whereas motivating or coaching the child to perform better neurofeedback sleep disorders insomnia shaping or scaffolding neurofeedback sleep disorders insomnia will promote the occurrence of the reinforced behavior and thus facilitate learning. Another example is the use of non-contingent feedback or random reinforcement as a control condition. Though this is often interpreted as an inert condition, such a random reinforcement schedule is known to result in 'superstitious behavior' in pigeons neurofeedback sleep disorders insomnia Skinner, 1948 neurofeedback sleep disorders insomnia and man neurofeedback sleep disorders insomnia Koichi, 1987 neurofeedback sleep disorders insomnia , bringing into question whether these control conditions truly represent an inert condition. Four recent studies have employed a placebo-controlled design and failed to find a difference between neurofeedback and sham-neurofeedback neurofeedback sleep disorders insomnia Lansbergen et al., 2010; Perreau-Link et al., 2010; deBeus neurofeedback sleep disorders insomnia Kaiser, 2010; Arnold et al., In Press neurofeedback sleep disorders insomnia . Note that only Perreau-Link et al. neurofeedback sleep disorders insomnia 2010 neurofeedback sleep disorders insomnia employed SMR Neurofeedback, whereas the other studies employed an unconventional neurofeedback protocol such as 'QEEG-based' protocols with 2-channel training neurofeedback sleep disorders insomnia Lansbergen et al., 2010 neurofeedback sleep disorders insomnia or training of the 'engagement index' involving beta, theta and alpha neurofeedback sleep disorders insomnia deBeus neurofeedback sleep disorders insomnia Kaiser, 2010; Arnold et al., In Press neurofeedback sleep disorders insomnia . Furthermore, these studies employed: 1 neurofeedback sleep disorders insomnia a control condition consisting of non-contingent feedback or random-reinforcement neurofeedback sleep disorders insomnia DeBeus and Kaiser, 2011; Lansbergen et al., 2011; Perreau-Linck et al., 2010 neurofeedback sleep disorders insomnia ; and 2 neurofeedback sleep disorders insomnia auto-tresholding. As indicated above, these approaches deviate from principles of learning theory. DeBeus and Kaiser neurofeedback sleep disorders insomnia 2011 neurofeedback sleep disorders insomnia supported this notion further in their randomized double-blind placebo controlled study. They did not find a difference between neurofeedback and placebo groups on ADHD symptoms neurofeedback sleep disorders insomnia DeBeus, personal communication neurofeedback sleep disorders insomnia . However, when comparing 'learners', who demonstrated an increase of at least 0.5 SD in the 'engagement index' between baseline to end of treatment neurofeedback sleep disorders insomnia 74 neurofeedback sleep disorders insomnia of the sample neurofeedback sleep disorders insomnia vs. 'non-learners', there were significant effects of neurofeedback on teacher ratings and a CPT test. Thus further confirming the importance of implementing principles of learning theory in neurofeedback. None of the other placebo-controlled studies reported evidence of learning actually having taken place, such as learning curves. Non-specific or placebo effects as an explanation for the effects of neurofeedback in these studies cannot be ruled out at this moment and still requires further study. Future double-blind placebo controlled studies should employ well-investigated neurofeedback protocols such as SMR or SCP protocols and ensure that learning actually takes place. For a review proposing a double-blind design fulfilling these principles, also see The Collaborative Neurofeedback Group neurofeedback sleep disorders insomnia submitted neurofeedback sleep disorders insomnia . Long term effects of neurofeedback in ADHD Fig. 2: Within subject Hedges' D ES for 3 randomized studies who have performed 6 month and 2 year follow-up data for inattention neurofeedback sleep disorders insomnia left neurofeedback sleep disorders insomnia and hyperactivity neurofeedback sleep disorders insomnia right neurofeedback sleep disorders insomnia . For Post-Treatment and 6 month follow-up the ES for the control group from the Gevensleben et al. neurofeedback sleep disorders insomnia 2010 neurofeedback sleep disorders insomnia study has been plotted as a comparison for non-specific effects across time. For the comparison at 2 years follow-up the ES of 7-10 yr. vs 14-17 yr. children has been plotted as an indication of improvements of ADHD symptoms related to aging from neurofeedback sleep disorders insomnia Erhart et al., 2008 neurofeedback sleep disorders insomnia . Note that for all studies the effects of neurofeedback tend to increase with time, most specifically for hyperactivity. neurofeedback sleep disorders insomnia Error bars are Variability of the ES neurofeedback sleep disorders insomnia . Several randomized studies have demonstrated that the effects of neurofeedback in ADHD are maintained following training at the 6 month follow-up neurofeedback sleep disorders insomnia Gevensleben et al., 2010; Leins et al., 2007; Strehl et al., 2006 neurofeedback sleep disorders insomnia and 2-year follow-up neurofeedback sleep disorders insomnia Gani et al., 2008 neurofeedback sleep disorders insomnia . These results show a tendency to improve further with time, as seen in figure 2. This figure depicts the within-subject ES between pre- and post-treatment; between pre-treatment and 6 month follow-up and between pre-treatment and 2 years follow-up for 3 RCTs. The ES has been plotted for the control group from both the 6 month neurofeedback sleep disorders insomnia Gevensleben et al., 2010a neurofeedback sleep disorders insomnia and 2 year follow up, and they show the improvement on the FBB-HKS neurofeedback sleep disorders insomnia a German ADHD rating scale neurofeedback sleep disorders insomnia between 7-10 years and 14-17 years of age in a normative group neurofeedback sleep disorders insomnia Erhart et al., 2008 neurofeedback sleep disorders insomnia . These ES associated with long-term follow-up indicate improvements associated with non-specific effects and aging effects. It is interesting and promising to note that the effects of neurofeedback in ADHD tend to improve further with time. This also hints to perhaps the most attractive aspect of neurofeedback, namely the perspective that a finite treatment may yield permanent beneficial effects. A limitation of such studies is always the low follow-up rates, such as 63 neurofeedback sleep disorders insomnia of Neurofeedback treated, 66 neurofeedback sleep disorders insomnia of the control group in the Gevensleben study neurofeedback sleep disorders insomnia 2010a neurofeedback sleep disorders insomnia and the 44-55 neurofeedback sleep disorders insomnia rate after 2 years follow up in the Gani et al neurofeedback sleep disorders insomnia 2008 neurofeedback sleep disorders insomnia study. Furthermore, the number of studies where follow-up was conducted is very limited, making generalization of these findings difficult and requiring further study. After the first report on operant conditioning of SMR in cat neurofeedback sleep disorders insomnia Wyrwicka and Sterman, 1967 neurofeedback sleep disorders insomnia , Sterman, Howe and Macdonald in 1970 convincingly demonstrated that SMR enhancement training during wakefulness resulted in increased sleep spindle density, accompanied by a reduction of phasic movements during sleep. Conversely, rewarding beta neurofeedback sleep disorders insomnia excluding SMR neurofeedback sleep disorders insomnia , did not demonstrate this effect during sleep. Furthermore, after SMR training the sleep spindle density during sleep, remained increased at post-assessment, suggesting these effects were long-lasting. Hoedlmoser et al. neurofeedback sleep disorders insomnia 2008 neurofeedback sleep disorders insomnia replicated this finding in humans in a placebo controlled RCT where SMR enhancement training resulted in shorter sleep latencies, accompanied by an increased sleep spindle density during sleep and improvements in declarative memory. More recently, Cortoos et al neurofeedback sleep disorders insomnia 2010 neurofeedback sleep disorders insomnia conducted a RCT where patients were randomized to EMG Biofeedback or SMR Neurofeedback. Improvements were initially expected for both groups, based on Sterman's work and relaxation related improvements of EMG Biofeedback. They demonstrated that SMR neurofeedback in patients with primary insomnia resulted in increased total sleep time as compared to EMG biofeedback. These studies provide clear evidence of SMR neurofeedback's effect of improving sleep. Placebo-effects in these studies are ruled out due to the placebo-control design used in these studies including randomized frequency conditioning neurofeedback sleep disorders insomnia Hoedlmoser et al. 2008 neurofeedback sleep disorders insomnia and EMG biofeedback neurofeedback sleep disorders insomnia Cortoos et al., 2010 neurofeedback sleep disorders insomnia as well as by the observation that SMR training during wakefulness resulted in increased sleep spindle density during sleep, only for the SMR Neurofeedback group neurofeedback sleep disorders insomnia Sterman et al., 1970; Hoedlmoser et al., 2008 neurofeedback sleep disorders insomnia . The clinical relevance of these effects in insomnia should be investigated further by replicating these effects in a group of clinical insomnia patients, investigating the usefulness of this approach in actual clinical practice. 2. Impaired vigilance regulation in ADHD The most consistent EEG findings reported in the literature on ADHD are those of increased absolute power in Theta neurofeedback sleep disorders insomnia Bresnahan et al., 1999; Chabot, Serfontein., 1996; Clarke et al., 1998; Clarke et al., 2001; DeFrance et al., 1996; Janzen et al., 1995; Lazzaro et al., 1998; Lazzaro et al., 1999; Mann et al., 1992; Matsuura et al., 1993 neurofeedback sleep disorders insomnia and sometimes increased absolute Delta EEG power neurofeedback sleep disorders insomnia Bresnahan et al., 1999; Clarke et al., 2001; Kuperman et al., 1996; Matsuura et al., 1993 neurofeedback sleep disorders insomnia . Conceptually, these EEG findings in ADHD are consistent with the EEG Vigilance model originally developed by Bente neurofeedback sleep disorders insomnia 1964 neurofeedback sleep disorders insomnia . More specifically these findings of slower EEG content reflect impaired vigilance regulation neurofeedback sleep disorders insomnia Sander et al., 2010 and reviewed below neurofeedback sleep disorders insomnia . The EEG is considered the gold standard for classifying the sleep stages based on the Rechtshaffen neurofeedback sleep disorders insomnia Kales criteria neurofeedback sleep disorders insomnia 1968 neurofeedback sleep disorders insomnia . Qualitatively different stages are defined such as stages 1-4, which are non-rapid eye movement sleep neurofeedback sleep disorders insomnia NREM neurofeedback sleep disorders insomnia with increasing sleep depth from stage I through stage 4. Stage 3 and 4 are referred to as Slow Wave Sleep neurofeedback sleep disorders insomnia SWS neurofeedback sleep disorders insomnia , and rapid eye movement sleep neurofeedback sleep disorders insomnia REM neurofeedback sleep disorders insomnia represents "dreaming". The EEG Vigilance model can be regarded as an extension of this sleep stage model with a focus on the transition from relaxed wakefulness through drowsiness to sleep onset, which is seen in stage 2. These vigilance model stages find their origins in the early work of Loomis et al. neurofeedback sleep disorders insomnia 1937 neurofeedback sleep disorders insomnia , later modified by Roth neurofeedback sleep disorders insomnia 1961 neurofeedback sleep disorders insomnia and Bente neurofeedback sleep disorders insomnia 1964 neurofeedback sleep disorders insomnia . In this model the EEG stages described reflect decreasing levels of vigilance from A1, to A2, A3, B1, B2 to B3. The three A stages reflect stages where alpha activity is dominant posterior neurofeedback sleep disorders insomnia A1 neurofeedback sleep disorders insomnia , followed by alpha anteriorisation neurofeedback sleep disorders insomnia A3 neurofeedback sleep disorders insomnia , whereas B stages are reflective of the lowest vigilance stages, which are characterized by an alpha drop-out or low-voltage EEG neurofeedback sleep disorders insomnia B1 neurofeedback sleep disorders insomnia followed by increased frontal theta and delta activity neurofeedback sleep disorders insomnia B2/3 neurofeedback sleep disorders insomnia . These vigilance stages are followed by the occurrence of K-complexes and sleep spindles, which mark the transition to stage C in the vigilance model, or classically to stage II sleep neurofeedback sleep disorders insomnia NREM neurofeedback sleep disorders insomnia . This EEG Vigilance regulation is a reflection of the process of 'falling asleep' and is measured during an eyes closed condition. EEG Vigilance regulation can be 'rigid', meaning that an individual remains in higher vigilance stages for an extended time and does not exhibit lower vigilance stages. This would be seen as rigid parietal alpha neurofeedback sleep disorders insomnia stage A1 neurofeedback sleep disorders insomnia , which is often seen in Depression neurofeedback sleep disorders insomnia Ulrich et al., 1999; Hegerl et al., 2011 neurofeedback sleep disorders insomnia . On the other hand, EEG Vigilance regulation can be 'labile' or 'unstable', meaning that an individual very quickly drops to lower EEG Vigilance stages, displaying the characteristic drowsiness EEG patterns such as frontal theta neurofeedback sleep disorders insomnia stage B2/3 neurofeedback sleep disorders insomnia , and they switch more often between EEG Vigilance stages. This labile or unstable pattern is often seen in ADHD neurofeedback sleep disorders insomnia Sander et al., 2010 neurofeedback sleep disorders insomnia . The often-reported 'excess theta' in ADHD mentioned above should thus be viewed as a predominance of the low B2/3 vigilance stages. These different EEG stages and their relationship to vigilance have been well described in the literature neurofeedback sleep disorders insomnia e.g. theta as a sign of drowsiness neurofeedback sleep disorders insomnia . Several recent validation studies have demonstrated the validity of these EEG Vigilance stages neurofeedback sleep disorders insomnia e.g. Olbrich et al., 2009; 2011; 2012 neurofeedback sleep disorders insomnia and are reviewed in a recent publication neurofeedback sleep disorders insomnia Arns et al., 2010 neurofeedback sleep disorders insomnia . The EEG Vigilance model explains the relationship between EEG states and behavior by means of vigilance regulation, which is a phenomenon we are all familiar with. The following example illustrates this further: After a tiring day, EEG vigilance regulation in a healthy individual will become unstable and demonstrate more of the lower vigilance stages. This has a classical EEG signature often referred to as 'fatigue' or 'drowsiness', which is expressed as alpha anteriorisation neurofeedback sleep disorders insomnia Broughton and Hasan, 1995; Connemann et al., 2005; De Gennaro et al., 2001; 2004; 2005; Pivik and Harman, 1995 neurofeedback sleep disorders insomnia and increased frontal slow waves neurofeedback sleep disorders insomnia Strijkstra et al., 2003; Tanaka et al., 1996; 1997 neurofeedback sleep disorders insomnia . In the EEG vigilance model these changes seen in drowsiness are referred to as stage A2-A3 for the anterior alpha and B2-B3 for the anterior theta respectively neurofeedback sleep disorders insomnia see Hegerl et al., this issue neurofeedback sleep disorders insomnia . In young children we all know the example of the hyperactive, 'high-spirited' behavior in over-tired children. This is a clear example of vigilance autostabilization behavior neurofeedback sleep disorders insomnia i.e. keeping himself awake by moving neurofeedback sleep disorders insomnia . A healthy adult displaying this type of EEG at home and near bedtime will feel sleepy and decide to 'withdraw', seeking an environment with low external stimulation, thus increasing the probability of falling asleep. However, when this same healthy adult is driving a car with the same reduced EEG Vigilance, he will: turn up the volume of the music, open the window, turn-down the air-conditioning, and so on, all to avoid further drowsiness. Hence the healthy adult will exhibit autostabilization or externalizing behavior in order to keep himself awake. Furthermore, when the car in front of him unexpectedly brakes, he is more likely to respond slowly neurofeedback sleep disorders insomnia impaired sustained attention neurofeedback sleep disorders insomnia and the likelihood of a car accident is increased due to this reduced vigilance or drowsiness neurofeedback sleep disorders insomnia Miller, 1995 neurofeedback sleep disorders insomnia . A summary of this model is depicted in figure 3. An unstable vigilance regulation explains the cognitive deficits that characterize ADHD and ADD, such as impaired sustained attention. This vigilance stabilization behavior explains the hyperactivity aspect of ADHD as an attempt to up regulate vigilance. Fig. 3: Overview of the relation between an unstable vigilance regulation and the behavioral symptoms of ADHD. To summarize, in the majority of ADHD patients an EEG pattern is observed illustrative of a reduced and unstable vigilance regulation neurofeedback sleep disorders insomnia i.e. the same EEG signature a healthy, but fatigued person would demonstrate at the end of the day neurofeedback sleep disorders insomnia . In turn, some unknown factor induces autostabilisation or externalizing behavior, which can be either adaptive neurofeedback sleep disorders insomnia i.e. keeping oneself awake while driving a car neurofeedback sleep disorders insomnia or mal-adaptive neurofeedback sleep disorders insomnia i.e. the hyperactivity in ADHD neurofeedback sleep disorders insomnia , depending on the circumstance. Conceptually, unstable vigilance has repercussions for the cortical vigilance network as proposed by Posner and Petersen neurofeedback sleep disorders insomnia 1990 neurofeedback sleep disorders insomnia and Corbetta and Shulman neurofeedback sleep disorders insomnia 2002 neurofeedback sleep disorders insomnia . Part of this network is the right inferior frontal gyrus, which is hypothesized to control a flexible inhibitory link between cortical sensory and motor systems; this link is in turn instrumental in processing of eternal signals that prompt a change in behavioral priorities or strategies neurofeedback sleep disorders insomnia Bekker et al., 20056a neurofeedback sleep disorders insomnia . Off medications, adult ADHD patients are characterized by impairments in both the behavioral and electrocortical aspects of this flexibly controlled inhibitory link neurofeedback sleep disorders insomnia Aron et al., 2003; Bekker et al., 2005b; Overtoom et al., 2009 neurofeedback sleep disorders insomnia . 2.1. Sleep and ADHD Reduced EEG Vigilance is observed in our earlier example of driving a car very late at night while being tired, but reduced vigilance can also be caused by enduring sleep restriction. A recent meta-analysis incorporating data from 35,936 healthy children reported that sleep-duration is positively correlated with school performance, executive function, and negatively correlated with internalizing and externalizing behavior problems neurofeedback sleep disorders insomnia Astill, van der Heijden, van Ijzendoorn neurofeedback sleep disorders insomnia van Someren, 2012 neurofeedback sleep disorders insomnia . ADHD has also been associated with daytime sleepiness neurofeedback sleep disorders insomnia Golan et al., 2004 neurofeedback sleep disorders insomnia and primary sleep disorders, sleep related movement disorders and parasomnias neurofeedback sleep disorders insomnia Chervin et al., 2002; Konofal et al., 2010; Walters et al., 2008 neurofeedback sleep disorders insomnia . Symptoms associated with ADHD can be induced in healthy children by sleep restriction neurofeedback sleep disorders insomnia Fallone et al., 2001; 2005; Sadeh et al., 2003; Beebe et al., 2008 neurofeedback sleep disorders insomnia , suggesting an overlap between ADHD symptoms and sleep-disruptions. Several open-label studies have demonstrated dramatic improvements in ADHD symptoms after normalizing sleep. For example, Walters and colleagues reported that ADHD children who were unresponsive to stimulant medication, and were treated with levodopa or a dopamine-agonist for restless legs syndrome neurofeedback sleep disorders insomnia resulting in normalized sleep neurofeedback sleep disorders insomnia demonstrated dramatic improvements in ADHD symptoms measured with the Conners Rating Scale neurofeedback sleep disorders insomnia CRS neurofeedback sleep disorders insomnia and Child Behavior Checklist neurofeedback sleep disorders insomnia CBCL neurofeedback sleep disorders insomnia neurofeedback sleep disorders insomnia Walters et al., 2000 neurofeedback sleep disorders insomnia . Huang and colleagues neurofeedback sleep disorders insomnia 2007 neurofeedback sleep disorders insomnia reported that in ADHD children with sleep apnea, adenotonsillectomy resulted in substantial clinical improvements in attention and ADHD complaints neurofeedback sleep disorders insomnia measured with the CBCL and TOVA neurofeedback sleep disorders insomnia . These improvements were larger when compared to stimulant medication. These studies suggest that a sub-group of children with 'ADHD complaints' actually suffers from a sleep disorder, and if the sleep disorder is treated effectively the 'ADHD complaints' improve. However, these specific sleep disorders, e.g. restless legs and breathing disorders, present in a limited percentage of the ADHD patients, estimated between 20 neurofeedback sleep disorders insomnia for sleep related breathing disorders neurofeedback sleep disorders insomnia Silvestri et al., 2009 neurofeedback sleep disorders insomnia and 26 neurofeedback sleep disorders insomnia for restless legs syndrome neurofeedback sleep disorders insomnia Konofal et al., 2010; Silvestri et al., 2009 neurofeedback sleep disorders insomnia . 2.2. Sleep onset insomnia and Circadian Phase Delay in ADHD Several studies have investigated the occurrence of 'idiopathic sleep-onset insomnia' neurofeedback sleep disorders insomnia SOI neurofeedback sleep disorders insomnia also called 'delayed sleep phase syndrome' in ADHD neurofeedback sleep disorders insomnia Van der Heijden et al., 2005 neurofeedback sleep disorders insomnia . SOI is defined as a difficulty falling asleep at a desired bedtime and/or a sleep onset latency of more than 30 minutes for at least 4 nights a week, existing for at least 6-12 months and leading to impairment in several areas neurofeedback sleep disorders insomnia Smits et al., 2001; Van Veen et al., 2010 neurofeedback sleep disorders insomnia . SOI should not be regarded as a full-blown sleep disorder, but rather as an inability or difficulty falling asleep. In general SOI is not related to 'sleep hygiene' neurofeedback sleep disorders insomnia van der Heijden et al., 2006 neurofeedback sleep disorders insomnia , is already present before the age of 3 years in 70 neurofeedback sleep disorders insomnia of children neurofeedback sleep disorders insomnia Van der Heijden et al., 2005 neurofeedback sleep disorders insomnia , and is also associated with a delayed Dim Light Melatonin Onset neurofeedback sleep disorders insomnia DLMO neurofeedback sleep disorders insomnia suggesting a circadian phase delay neurofeedback sleep disorders insomnia Van der Heijden et al., 2005; Van Veen et al., 2010 neurofeedback sleep disorders insomnia . Van Veen et al. neurofeedback sleep disorders insomnia 2010 neurofeedback sleep disorders insomnia reported SOI in 78 neurofeedback sleep disorders insomnia of a sample of adult ADHD patients, and a similar rate of 72-75 neurofeedback sleep disorders insomnia SOI has been reported in large samples of unmedicated pediatric ADHD neurofeedback sleep disorders insomnia Van der Heijden et al., 2005 neurofeedback sleep disorders insomnia . In further agreement with these findings, Rybak et al. neurofeedback sleep disorders insomnia 2007 neurofeedback sleep disorders insomnia reported that adult ADHD is characterized by a higher prevalence of 'evening types', characteristic for a delayed circadian phase, strongly correlated with self-reported and neuropsychological measures of ADHD symptoms neurofeedback sleep disorders insomnia CPT impulsivity errors neurofeedback sleep disorders insomnia . These studies suggest that at least a subgroup of patients with ADHD is characterized by a circadian phase delay, associated with delayed sleep onset, already present before the age of 3. These ADHD patients during the day are characterized by lower vigilance stages neurofeedback sleep disorders insomnia e.g. more frontal theta and frontal alpha neurofeedback sleep disorders insomnia and these EEG subtypes also respond well to stimulant medication neurofeedback sleep disorders insomnia Arns et al., 2008 neurofeedback sleep disorders insomnia , by virtue of its vigilance stabilizing properties. However, stimulant medications do not affect the core-symptomatology in the circadian phase delay subgroup, which is the cause of the lower vigilance levels. 2.3. Chronic sleep-restriction and the effects on attention and externalizing behavior. Van Dongen et al. neurofeedback sleep disorders insomnia 2003 neurofeedback sleep disorders insomnia systematically investigated the cumulative effects of sleep restriction in healthy volunteers over the course of 14 days, and found clear dose-response effects on cognition of restricting sleep to 4, 6 or 8 hours per night. Furthermore, they also reported that these effects progressively eroded performance on a psychomotor vigilance task and working memory over time, where performance was still worsening at day 14. This suggests that a chronic but slight reduction in total sleep time can result in cumulative effects across time on vigilance, attention and cognition. Similar findings have also been reported after 5-7 days of restricted sleep neurofeedback sleep disorders insomnia Axelsson et al., 2008; Belenky et al., 2003 neurofeedback sleep disorders insomnia . Performance improved after 3 recovery nights albeit not to pre-sleep restriction levels as opposed to 1 night of total sleep deprivation, which does normalize after a recovery night neurofeedback sleep disorders insomnia Belenky et al., 2003 neurofeedback sleep disorders insomnia . Normalization was also reported for reaction times and sleepiness within 7 recovery days, but 'lapses' neurofeedback sleep disorders insomnia reflective of inattention neurofeedback sleep disorders insomnia did not normalize after 7 recovery nights neurofeedback sleep disorders insomnia Axelsson et al., 2008 neurofeedback sleep disorders insomnia , demonstrating that the effects of chronic sleep restriction do not normalize after few recovery nights of sleep. Sleep restriction studies have also been conducted in children, albeit not as extensively as in adults. In general sleep restriction studies in healthy children have all demonstrated impairments of attention neurofeedback sleep disorders insomnia Fallone et al., 2001; 2005; Sadeh et al., 2003; Beebe et al., 2008 neurofeedback sleep disorders insomnia , whereas only Beebe et al. neurofeedback sleep disorders insomnia 2008 neurofeedback sleep disorders insomnia found increased externalizing behavior neurofeedback sleep disorders insomnia e.g. hyperactivity and oppositional/irritable behaviors rated with the BRIEF neurofeedback sleep disorders insomnia after 1 week of sleep restriction. Interestingly, in a replication study with a more naturalistic design neurofeedback sleep disorders insomnia simulated classroom set-up and blinded video-ratings neurofeedback sleep disorders insomnia , they replicated the findings for inattention but also found that Theta EEG power tended to be increased after a week of sleep restriction neurofeedback sleep disorders insomnia effect size=0.53 neurofeedback sleep disorders insomnia neurofeedback sleep disorders insomnia Beebe et al., 2010 neurofeedback sleep disorders insomnia demonstrating that sleep restriction resulted in impaired vigilance regulation neurofeedback sleep disorders insomnia excess theta neurofeedback sleep disorders insomnia as well as impaired attention. The relationship with externalizing behaviors such as hyperactivity and impulsivity was only found in Beebe et al. neurofeedback sleep disorders insomnia 2008 neurofeedback sleep disorders insomnia but not in other studies. On the other hand, the earlier mentioned meta-analysis by Astill, van der Heijden, van Ijzendoorn and van Someren neurofeedback sleep disorders insomnia 2012 neurofeedback sleep disorders insomnia did clearly demonstrate a relationship between total sleep time and externalizing behavior. This meta-analysis failed to find a relationship with sustained attention in children, whereas large effects sizes for this measure are found in adults neurofeedback sleep disorders insomnia Lim and Dinges, 2010 neurofeedback sleep disorders insomnia . The interventional sleep restriction studies above clearly indicated that attentional problems are caused by chronic sleep restriction, whereas the meta-analytic results suggest an effect from decreased sleep duration on externalizing behavior. Obviously these studies have been performed in healthy children and this may not generalize to ADHD children. This suggests that interventions aimed at restoring the SOI and/or circadian phase delay might not have immediate effects, as opposed to psychostimulants which acutely increase vigilance during the day, but might take more time to exert their effects on behavior. In this view, SOI caused by a circadian phase delay is the underlying pathophysiology in a significant number of patients with ADHD, for which normalizing the circadian phase delay may result in clinical improvements, albeit with a delayed onset. A large placebo controlled RCT investigation of ADHD showed the effects of 4-weeks melatonin on sleep-onset latency and circadian phase, as assessed with the DLMO neurofeedback sleep disorders insomnia Van der Heijden et al., 2007 neurofeedback sleep disorders insomnia . Post-treatment sleep-onset and DLMO latencies were shorter relative to placebo, which may be due to melatonin-enhanced signals from the nucleus suprachiasmaticus neurofeedback sleep disorders insomnia SCN neurofeedback sleep disorders insomnia to the pineal gland. However, no improvements of ADHD symptoms and cognition were reported after this period of 4 weeks neurofeedback sleep disorders insomnia Van der Heijden et al., 2007 neurofeedback sleep disorders insomnia . A follow-up study revealed that after long-term treatment neurofeedback sleep disorders insomnia 2-3 years neurofeedback sleep disorders insomnia improvements of behavior and mood were present only for children still using melatonin. It also showed that discontinuation of melatonin resulted in a relapse of sleep onset insomnia, probably also in a delayed circadian phase neurofeedback sleep disorders insomnia Hoebert et al., 2009 neurofeedback sleep disorders insomnia . In a study of Rybak and colleagues neurofeedback sleep disorders insomnia 2006 neurofeedback sleep disorders insomnia , adult ADHD patients were treated with early morning bright light, which also has circadian phase advancing effects. They reported improvements on the Brown adult ADD scale and neuropsychological measures neurofeedback sleep disorders insomnia e.g. CPT, Wisconsin Card Sorting Test neurofeedback sleep disorders insomnia after 3 weeks of morning bright light therapy, with medium effect sizes neurofeedback sleep disorders insomnia Rybak et al., 2006 neurofeedback sleep disorders insomnia . These effects appeared faster compared to the effects of melatonin, suggesting bright light might have faster effects. On the other hand, these were only medium effect sizes, and might have increased when a follow-up was performed after 6 months. These results suggest that in this sub-group of ADHD patients, normalizing SOI can be achieved by advancing the circadian phase delay by using melatonin or morning bright light, albeit with a delayed-onset of effect on ADHD symptoms for melatonin compared to bright light. The fact that these complaints are already present in the majority of ADHD patients with SOI before the age of 3 neurofeedback sleep disorders insomnia Van der Heijden et al., 2005 neurofeedback sleep disorders insomnia , and that ADHD is most often diagnosed after the age of 5 or 6, further suggests that SOI results in an accumulation of impaired sleep neurofeedback sleep disorders insomnia extended sleep restriction neurofeedback sleep disorders insomnia across time which eventually results in unstable EEG vigilance regulation, as demonstrated by Beebe et al. neurofeedback sleep disorders insomnia 2010 neurofeedback sleep disorders insomnia . 2.4 Sleep spindles and Sensori-motor rhythm Sensori-motor rhythm or SMR is characterized by a frequency of 12-15 Hz being most pronounced across the sensorimotor strip neurofeedback sleep disorders insomnia EEG locations C3, Cz and C4 neurofeedback sleep disorders insomnia . This rhythm is too date still used in most neurofeedback studies in ADHD along with changing other frequencies such as Theta. Interestingly, this rhythm shares overlap with sleep-spindles during stage-2 NREM sleep which have an identical topographical distribution but also an identical frequency. The first report of sleep spindles, also referred to as sigma waves, stems from the work by Loomis in 1935 where he described: '…but frequently very regular bursts lasting 1 to 1.5 seconds of 15 per second frequency appear. The amplitude builds regularly to a maximum and then falls regularly so that we have designated these "spindles", because of their appearance...'. Sleep spindles are considered the hallmark of stage 2 NREM sleep neurofeedback sleep disorders insomnia De Gennaro et al., 2001; De Gennaro and Ferrara, 2003 neurofeedback sleep disorders insomnia and are reduced in the night after sleep deprivation neurofeedback sleep disorders insomnia Borbély et al., 1981; De Gennaro and Ferrara, 2003; Dijk et al., 1993; Huber et al., 2008 neurofeedback sleep disorders insomnia , perhaps due to increased SWS pressure after deprivation. Furthermore, the density of sleep spindle occurrence exhibits a strong circadian modulation comparable to the melatonin rhythm neurofeedback sleep disorders insomnia De Gennaro and Ferrara, 2003; Dijk et al., 1997 neurofeedback sleep disorders insomnia . Full-developed sleep spindles are already present at 8-9 weeks after birth and stabilize at 23 weeks neurofeedback sleep disorders insomnia De Gennaro and Ferrara, 2003 neurofeedback sleep disorders insomnia and hence do not display the typical maturational effects on frequency, characteristic for posterior alpha activity neurofeedback sleep disorders insomnia Niedermeyer and Lopes Da Silva, 2004 neurofeedback sleep disorders insomnia . As pointed out in section 1.2 several studies have demonstrated that SMR neurofeedback, results in increased sleep spindle density during sleep neurofeedback sleep disorders insomnia Hoedlmoser et al., 2008; Sterman et al., 1970 neurofeedback sleep disorders insomnia , decreased sleep latency neurofeedback sleep disorders insomnia Hoedlmoser et al., 2008 neurofeedback sleep disorders insomnia increased total sleep time neurofeedback sleep disorders insomnia Cortoos et al., 2010; Hoedlmoser et al., 2008 neurofeedback sleep disorders insomnia and sleep improvements in ADHD neurofeedback sleep disorders insomnia Arns, 2011 neurofeedback sleep disorders insomnia . Research has also demonstrated that melatonin results in an increased sleep spindle density neurofeedback sleep disorders insomnia Dijk et al., 1995 neurofeedback sleep disorders insomnia and decreased sleep latency neurofeedback sleep disorders insomnia Van der Heijden et al., 2007 neurofeedback sleep disorders insomnia , suggesting overlap in the working mechanisms of SMR neurofeedback and melatonin. Could there also be an overlap with SCP's and sleep spindles? 2.5 Sleep spindles and Slow Cortical Potentials neurofeedback sleep disorders insomnia SCP's neurofeedback sleep disorders insomnia . Given that the results of SCP neurofeedback and SMR neurofeedback in ADHD are rather similar, and no differential effects have been reported on measures such as inattention, impulsivity and hyperactivity neurofeedback sleep disorders insomnia Arns et al., 2009; Gevensleben et al., 2009 neurofeedback sleep disorders insomnia , it has been speculated that these two forms of neurofeedback might share a similar working mechanism. In SCP neurofeedback surface positivity and surface negativity are both trained. That is, patients are required to demonstrate surface positivity or negativity within a 6-8 sec. time frame, depending on the instruction provided by the software neurofeedback sleep disorders insomnia 'activation' or 'deactivation' neurofeedback sleep disorders insomnia . However, both have different neurophysiological implications. Surface negativity indicates depolarization of apical dendrites reflective of increased excitation, whereas surface positivity probably reflects inhibition or a reduction of cortical excitation neurofeedback sleep disorders insomnia Birbaumer et al. 1990 neurofeedback sleep disorders insomnia . SCP neurofeedback hence seems to differ from SMR neurofeedback in that patients are taught 'self regulation'. Currently there is no published evidence that SMR neurofeedback results in increased EEG power in this frequency range post-treatment. Several studies have demonstrated learning curves of SMR power increases within training sessions e.g. Sterman neurofeedback sleep disorders insomnia Friar neurofeedback sleep disorders insomnia 1972 neurofeedback sleep disorders insomnia and Lubar and Shouse neurofeedback sleep disorders insomnia 1976 neurofeedback sleep disorders insomnia reflective of a learning process. One recent study actually reported a decreased SMR power post-treatment with SMR enhancement neurofeedback in ADHD patients who all were responders to treatment neurofeedback sleep disorders insomnia Arns et al., 2012 neurofeedback sleep disorders insomnia . Furthermore, Pineda et al. neurofeedback sleep disorders insomnia 2008 neurofeedback sleep disorders insomnia in a double-blind, placebo controlled design demonstrated that mu-enhancement training neurofeedback sleep disorders insomnia 8-13 Hz neurofeedback sleep disorders insomnia in autism resulted in improved mu-suppression post-treatment as well as improvement in autism symptoms. Therefore, these results rather suggest that SMR neurofeedback is not about increasing the EEG power in a specific frequency range, but rather about regulating activity within a functional network neurofeedback sleep disorders insomnia reticulo-thalamocortical network, also see section 2.6 below neurofeedback sleep disorders insomnia , thereby increasing the synaptic strength within this network, resulting in long-term potentiation neurofeedback sleep disorders insomnia LTP neurofeedback sleep disorders insomnia which increases synaptic sensitivity and the probability of future activation in this network neurofeedback sleep disorders insomnia Sterman an Egner, 2006 neurofeedback sleep disorders insomnia . This is further supported by studies that actually trained SMR neurofeedback in the exact same way as SCP's are trained, e.g. patients had to increase or decrease their Theta/Beta ratio during a pre-set interval depending on the instructions from the software neurofeedback sleep disorders insomnia arrow up, 'activation' or arrow down, 'deactivation' neurofeedback sleep disorders insomnia , and these studies also demonstrated clinical effects in ADHD neurofeedback sleep disorders insomnia Leins et al., 2007; Holtmann et al., 2009 neurofeedback sleep disorders insomnia . The sleep EEG during NREM sleep is not only characterized by sleep spindles and delta oscillations, but also by cortically generated slow oscillations at frequencies lower then 1 Hz neurofeedback sleep disorders insomnia Amzica and Steriade, 1997; Evans, 2003; Sinha, 2011 neurofeedback sleep disorders insomnia . Although the sleep spindle oscillations are generated in a reticulo-thalamocortical network neurofeedback sleep disorders insomnia Sinha et al. 2011 neurofeedback sleep disorders insomnia , neocortical control over this sleep spindle circuit is established via generation of slow oscillations, where the depolarizing phase is associated with increased neuronal firing, which drives the thalamic spindle generator via cortico-thalamic efferents neurofeedback sleep disorders insomnia Marshall et al., 2003; Steriade and Amzica, 1998; Steriade, 1999; Timofeev et al., 2000 neurofeedback sleep disorders insomnia . The transition from wakefulness to sleep in humans is characterized by a negative DC shift neurofeedback sleep disorders insomnia Marshall et al. 1996, 2003 neurofeedback sleep disorders insomnia . Furthermore, clear temporal interrelations between the occurrence of sleep-spindles and brief shifts to surface negativity have been described neurofeedback sleep disorders insomnia Caspers neurofeedback sleep disorders insomnia Schulze, 1959; Marshall, Molle and Born, 2003 neurofeedback sleep disorders insomnia and a clear cross-correlation between the negative DC potential and sleep spindle activity across time with correlation coefficients around .80 with zero time lag have been reported neurofeedback sleep disorders insomnia Marshall et al., 2003 neurofeedback sleep disorders insomnia . Furthermore, Molle et al. neurofeedback sleep disorders insomnia 2002 neurofeedback sleep disorders insomnia concluded that slow oscillations serve a function in 'grouping' sleep related EEG activities such as sleep spindles neurofeedback sleep disorders insomnia Molle et al., 2002 neurofeedback sleep disorders insomnia in agreement with the conclusion that these cortical slow waves are known to trigger sleep spindles and control the faster delta waves originating from the thalamus neurofeedback sleep disorders insomnia Amzica and Steriade, 1997; Evans, 2003; Sinha, 2011 neurofeedback sleep disorders insomnia . Interestingly, transcranial slow oscillation stimulation neurofeedback sleep disorders insomnia 0.75 Hz neurofeedback sleep disorders insomnia during NREM sleep, but not stimulation at 5 Hz, improved declarative memory neurofeedback sleep disorders insomnia Marshall et al., 2004; 2006 neurofeedback sleep disorders insomnia and resulted in increased sleep spindle density neurofeedback sleep disorders insomnia both increased power in the sleep spindle range and increased spindle counts neurofeedback sleep disorders insomnia neurofeedback sleep disorders insomnia Marshall et al., 2006 neurofeedback sleep disorders insomnia , further demonstrating the causal nature between these slow oscillations and sleep spindle generation, or as Marshall et al. neurofeedback sleep disorders insomnia 2006 neurofeedback sleep disorders insomnia concluded: '…agrees well with the notion that neocortical slow oscillations drive the thalamic generation of spindles…' neurofeedback sleep disorders insomnia Marshall et al., 2006; p 611 neurofeedback sleep disorders insomnia . Therefore, it is proposed that SCP neurofeedback and SMR neurofeedback share their mechanism by both tapping into a network related to induction and triggering of sleep spindles. 2.6 Sleep spindles and circadian regulation Sleep spindles are generated by the GABA-ergic thalamic reticular neurons and are synchronized through glutamatergic cortico-thalamic projections neurofeedback sleep disorders insomnia De Gennaro and Ferrara, 2003 neurofeedback sleep disorders insomnia . The spindle oscillation generated in the reticular neurons is transferred to thalamocortical relay cells in the dorsal thalamic nuclei through GABAergic synapses, producing inhibitory postsynaptic potentials neurofeedback sleep disorders insomnia IPSPs neurofeedback sleep disorders insomnia and travel through glutamatergic thalamocortical axons to generate rhythmic excitatory postsynaptic potentials neurofeedback sleep disorders insomnia EPSPs neurofeedback sleep disorders insomnia in the cortex neurofeedback sleep disorders insomnia Sinha, 2011 neurofeedback sleep disorders insomnia . As pointed out above, cortical slow oscillations trigger sleep spindles from the thalamus neurofeedback sleep disorders insomnia Amzica and Steriade, 1997; Evans, 2003; Sinha, 2011; Marshall et al., 2006 neurofeedback sleep disorders insomnia , thereby explaining how SCP neurofeedback training might influence sleep spindle generation. Furthermore, SMR neurofeedback is hypothesized to directly train the sleep spindle circuit given the overlap in frequency and location and as evidenced by studies demonstrating an increase in sleep spindle density after SMR neurofeedback neurofeedback sleep disorders insomnia Hoedlmoser et al., 2008; Sterman et al., 1970 neurofeedback sleep disorders insomnia . As stated earlier, there is a strong circadian modulation of sleep spindles neurofeedback sleep disorders insomnia De Gennaro and Ferrara, 2003; Dijk et al., 1997 neurofeedback sleep disorders insomnia and melatonin has been demonstrated to result in increased sleep spindle density neurofeedback sleep disorders insomnia Dijk et al., 1995 neurofeedback sleep disorders insomnia suggesting an interplay between the SCN and the sleep spindle circuitry. Interestingly, Aston-Jones et al. neurofeedback sleep disorders insomnia 2001 neurofeedback sleep disorders insomnia have described an indirect connection from the SCN to the noradrenergic locus coeruleus neurofeedback sleep disorders insomnia LC neurofeedback sleep disorders insomnia via projections to the dorsomedial nucleus of the hypothalamus neurofeedback sleep disorders insomnia DMH neurofeedback sleep disorders insomnia . In turn the noradrenergic LC is part of a set of subcortical nuclei that regulate activation of the sleep spindle generating circuitry neurofeedback sleep disorders insomnia Sinha 2011 neurofeedback sleep disorders insomnia . Furthermore, as explained in more detail by Hegerl in this same issue, the noradrenergic LC plays a crucial role in vigilance stabilization. Fig. 4: This figure summarizes the proposed model for how chronobiological treatments neurofeedback sleep disorders insomnia left top neurofeedback sleep disorders insomnia and neurofeedback neurofeedback sleep disorders insomnia right top neurofeedback sleep disorders insomnia impact on the vigilance system and thereby resulting in vigilance stabilization. Chronobiological treatments have short term effects, for the duration of the treatment, whereas neurofeedback has long-term effects by increasing the synaptic strength within this network, resulting in long-term potentiation neurofeedback sleep disorders insomnia LTP neurofeedback sleep disorders insomnia which increases synaptic sensitivity and the probability of future activation in this network neurofeedback sleep disorders insomnia Sterman an Egner, 2006 neurofeedback sleep disorders insomnia . 3. Conclusion In this review article the history and current status of neurofeedback for the treatment of ADHD and insomnia have been summarized. We have demonstrated that SMR and SCP neurofeedback have the ability to directly impact the sleep spindle circuit resulting in increased sleep spindle density during sleep. Increased sleep spindle density has been demonstrated to be associated with improved sleep quality, including decreased sleep latency and increased sleep duration, resulting in normalization of SOI. This normalization of SOI neurofeedback sleep disorders insomnia and thus the relief of sustained sleep restriction neurofeedback sleep disorders insomnia will eventually result in vigilance stabilization mediated by the noradrenergic locus couruleus neurofeedback sleep disorders insomnia LC neurofeedback sleep disorders insomnia in turn resulting in improvements of inattention, hyperactivity and impulsivity in ADHD. The effects of activation neurofeedback sleep disorders insomnia e.g. LC neurofeedback sleep disorders insomnia on the sleep spindle circuitry have been documented neurofeedback sleep disorders insomnia Sinha 2011 neurofeedback sleep disorders insomnia , however to the authors knowledge no direct link from the sleep spindle circuitry on the LC has been documented, therefore we speculate this is a reciprocal link and LC activation will occur along with the normalization of sleep and the model predicts that this will occur with a time lag, and will not occur during neurofeedback but will be seen better at follow-up. In this view then, a circadian phase delay characterized by SOI is considered the core pathophysiology in this sub-group of ADHD, with an estimated prevalence of 72-78 neurofeedback sleep disorders insomnia neurofeedback sleep disorders insomnia Van der Heijden et al., 2005; Van Veen et al., 2010 neurofeedback sleep disorders insomnia . Although neurofeedback does not target this circadian phase delay in the SCN or pineal gland directly, it does so at the level of subcortical and cortical structures, which mediate sleep spindle production and sleep onset. These improvements on ADHD symptoms will most likely occur with a delayed effect of onset, as was found for melatonin treatment in ADHD neurofeedback sleep disorders insomnia Hoebert et al., 2009 neurofeedback sleep disorders insomnia . This is also supported by the tendency for further improvements at follow-up for neurofeedback, which was seen in figure 2 and by the effects of long-term sleep restriction in healthy volunteers where the impairments on attention take more recovery nights to normalize than the actual number of nights of sleep restriction neurofeedback sleep disorders insomnia Axelsson et al., 2008; Belenky et al., 2003 neurofeedback sleep disorders insomnia . The model also predicts that QEEG normalizations such as reduced frontal theta and frontal alpha seen after neurofeedback will be most prominent at follow-up, rather than directly at outtake. In line with this delayed onset of effect of ADHD symptoms, an interesting hypothesis deserving further study is that neurofeedback might require fewer sessions. Sessions might be terminated when SOI is normalized, with other findings normalizing over time with no additional neurofeedback. Improvements in sleep are the most often reported 'side-effects' of children and adults with ADHD treated with neurofeedback, and the biggest improvements in sleep take place in approximately 20 sessions as measured with the Pittsburgh Sleep Quality Inventory neurofeedback sleep disorders insomnia PSQI neurofeedback sleep disorders insomnia neurofeedback sleep disorders insomnia Arns 2011 neurofeedback sleep disorders insomnia . Note that, in the present view, once sleep-onset latencies and sleep quality have been normalized, it takes an additional amount of time for ADHD symptoms to improve neurofeedback sleep disorders insomnia see figure 2 neurofeedback sleep disorders insomnia . In contrast to the persistent and improving findings in Neurofeedback studies, the effects of melatonin disappear when the treatment is discontinued. Hence future studies should incorporate polysomnography, and actigraphy neurofeedback sleep disorders insomnia Hoebert et al., 2009; Van der Heijden et al., 2007; Van Veen et al., 2010 neurofeedback sleep disorders insomnia , and investigate whether the normalization of SOI is consistently related to improvements in ADHD symptoms and to quantify the delay in onset more completely. Furthermore, clinical trials of new treatments for ADHD should consider evaluating primary treatment endpoints at follow-up, after 6-12 months, rather than directly at the end of treatment, in order to identify treatments that have lasting effects. Differentiating long term versus temporary treatment effects is especially important since it was recently concluded based on the large NIMH-MTA trial that conventional treatments in ADHD such as stimulant medication, multicomponent behavior therapy and combined treatment had no effects beyond 2 years following treatment neurofeedback sleep disorders insomnia Molina et al., 2009 neurofeedback sleep disorders insomnia . This identification of the longer term failure of conventional ADHD treatment approaches further stresses the need for the identification and development of new treatments with long-term effects. 4. Limitations and directions for future research This review provides a model which can explain the behavioral complaints in a sub-group of ADHD, and how chronobiological treatments and neurofeedback exert their clinical effects in ADHD and insomnia. Obviously such a model results in more testable questions than answers. Obviously there are also inherent limitations and weaknesses to this model. The effects of sleep restriction in children have been most clearly replicated for inattention, but only 1 study found effects on externalizing behaviors such as hyperactivity. On the other hand, the extensive meta-analysis by Astill et al. neurofeedback sleep disorders insomnia 2012 neurofeedback sleep disorders insomnia in 35.936 children found clear relationships between sleep duration and school performance, executive function and externalizing behavior, but not for sustained attention. Therefore, this aspect of the model requires further study such as longer sleep restriction studies, sleep restriction studies in 'ADHD risk' populations. The implications of this model thus are clearest for the circadian delay sub-group of ADHD patients, and might not generalize to explain all of the forms of ADHD. Currently the debate about whether neurofeedback has specific effects beyond a 'sham' condition continues. This debate is mainly centered around whether to evaluate neurofeedback based on APA norms, or based on pharmaceutical norms which require a double-blind placebo controlled study. Although this pharmaceutical standard based approach is not impossible, there are considerable methodological issues to address. One such design-proposal was recently submitted for publication by the Collaborative Neurofeedback Group, which is constituted by Neurofeedback experts, mainstream ADHD investigators and clinical trial experts neurofeedback sleep disorders insomnia The Collaborative Neurofeedback Group, submitted neurofeedback sleep disorders insomnia . Such a study might provide more definitive answers though this requires further implementation of their proposed study. We have construed our review and model narrowly around ADHD and insomnia. There is a rich literature on many other applications for which this framework might not provide a valid explanation. Some of these include SMR Neurofeedback resulting in reduction of seizures neurofeedback sleep disorders insomnia Tan et al., 2009 neurofeedback sleep disorders insomnia , in improving micro-surgical skills neurofeedback sleep disorders insomnia Ros et al. 2009 neurofeedback sleep disorders insomnia and creative acting performance neurofeedback sleep disorders insomnia Gruzelier et al., 2010 neurofeedback sleep disorders insomnia . Therefore, other effects and explanations of SMR and SCP neurofeedback should not be ruled out. Furthermore, this review focused on the effects of SCP's and SMR, and the effects of the often included inhibition of Theta, as well as rewarding of the higher beta-band and inhibition of EMG activity, none of which have been covered in this review. Further research should focus on investigating the independent contribution of these additional inhibits and rewards. This review focused on the relationship between circadian phase delay resulting in sleep restriction and changes in vigilance. As pointed out earlier, other sleep disorders are also prevalent in ADHD, such as restless legs, sleep apneas and parasomnias. Such sleep disorders obviously require a different treatment approach. Chronobiological treatments, such as light therapy and melatonin, as well as treatment with neurofeedback are not indicated for these sleep disorders. For a review of these as well as other sleep disorders, see Miano, Parisi and Villa neurofeedback sleep disorders insomnia 2012 neurofeedback sleep disorders insomnia who have described in more detail the different 'sleep phenotypes' in ADHD as well as their related treatments. Want to learn more about Neurofeedback in ADHD and how to apply this technique? Click here. Reference: Arns, M. neurofeedback sleep disorders insomnia Kenemans, J.L. neurofeedback sleep disorders insomnia 2012 neurofeedback sleep disorders insomnia . Neurofeedback in ADHD and insomnia: Vigilance Stabilization through sleep spindles and circadian networks. Neuroscience and Biobehavioral Reviews. doi: 10.1016/j.neubiorev.2012.10.006 Treatment of chronic insomnia and sleep problems Approximately five to seven percent of the people in the Netherlands suffers from a chronic sleep problem neurofeedback sleep disorders insomnia insomnia neurofeedback sleep disorders insomnia . People with insomnia report trouble falling asleep, maintaining sleep and early awakenings. But also daytime symptoms such as fatigue, complaints about the mood, memory problems, concentration problems and drowsiness. We speak of insomnia as the symptoms occur at least three times per week and are accompanied by daytime symptoms. There are many individual differences between how people experience their sleep. The same sleep patterns for one person may be experienced as pleasant, while for another it is rated as poor sleep. There is no such thing as a standard for healthy sleep, therefore sleep complaints are subjective. Often we will use actigraphy to get a better view of the sleep problems. The client wears the "Actiwatch' for a few days. This is a watch that measures sleep, light and physical activity. The results of this measurement give more objective information regarding the complaints, leading to a better understanding by the client as well as the therapist. Additionally Brainclinics offers various treatments for sleep problems depending on the symptoms: Cognitive behavioral therapy for adults Research shows that cognitive behavioral therapy is an effective treatment for insomnia. A recently conducted research into the effectiveness of this treatment shows that the positive effects on sleep, number of awakenings at night, duration of waking after sleep and sleep quality are high and that the positive effect on total sleep time is average neurofeedback sleep disorders insomnia Riemann neurofeedback sleep disorders insomnia Perlis , 2008 neurofeedback sleep disorders insomnia . The reported effects are comparable or better than sleeping medication. Cognitive behavioral therapy can be helpful for anyone who suffers from sleep problems, when all physical causes are excluded. Many sleep problems are traced to false expectations, perceptions and behavior. This form of guidance is aimed at neurofeedback sleep disorders insomnia wrong neurofeedback sleep disorders insomnia expectations of sleep, insight into their own sleep patterns and to learn other sleep behavior. This treatment consists of 10 sessions in total, where as the first 7 sessions will take place on a weekly basis. Before the treatment starts, an intake will take place to identify complaints and to assess whether cognitive behavioral therapy is appropriate for you. See below a video outlining the different treatment approaches at Brainclinics neurofeedback sleep disorders insomnia English version neurofeedback sleep disorders insomnia . Neurofeedback in insomnia Neurofeedback is a proven effective treatment in the treatment of ADHD / ADD and sleep problems, where training the brain will decrease the symptoms of ADHD and ADD or of insomnia. Research on neurofeedback in the treatment of chronic insomnia is clinically relevant and improvements are shown neurofeedback sleep disorders insomnia Cortoos et al, 2009 neurofeedback sleep disorders insomnia . Several studies have also shown that neurofeedback leads to an increase in sleeping spindles during sleep neurofeedback sleep disorders insomnia Sterman et al, 1970 ; Hoedlmoser et al, 2008 neurofeedback sleep disorders insomnia which is an important measure of improved sleep. The working mechanism of neurofeedback in sleep is studied intensly. In adults and children with ADHD / ADD and associated sleep problems, a combination of neurofeedback and CBT can be used as treatment. Adults with primary chronic insomnia will initially be advised to have cognitive behavioral therapy. If neccessary, neurofeedback can be used later. For more information see the section on neurofeedback. Furthermore, in some in stance we also apply light-therapy, especially when there are problems related to an advanced circadian phase. Sleep and Brain Training Alternative Insomnia Treatment At least 40 million Americans each year suffer from chronic, long-term, sleep disorders. An additional 20 million experience occasional sleep problems. The impact on their health, work, and relationships is immeasurable. Neurofeedback is a powerful tool for helping people fall asleep and stay asleep. Over 3,000 licensed health professionals, such as psychologists, therapists, and doctors now use this brain training daily with their patients. As a group, they report significant and consistent improvements for clients' sleep problems. Why Is Neurofeedback Effective for Insomnia? Neurofeedback has a powerful ability to positively impact sleep because it works on the areas of the brain that allow and regulate sleep. With neurofeedback, most people can train their brain to allow sleep again by rewarding it for creating healthier patterns. Sleep can improve surprisingly quickly for clients who have seen numerous specialists and struggled with sleep for years. Falling asleep and staying asleep is clearly the job of the brain. Many brain training options can help, as well as making lifestyle changes and changes in sleep "hygiene". A skilled neurofeedback clinician can review different options with clients to help them assess what's most appropriate for them, including several brain regulating technologies such as Alpha-Stim and Brain Music. Neurofeedback is non-invasive, and produces no undesirable side effects. What are the most common sleep issues that improve with neurofeedback? Woman with insomnia taking sleeping pillInsomnia – Difficulty falling asleep or maintaining sleep during the night Difficulty waking from sleep Difficulty getting to bed Not feeling rested after sleep Sleeping too long neurofeedback sleep disorders insomnia over 10 hours neurofeedback sleep disorders insomnia Physically restless sleep Nightmares Bedwetting neurofeedback sleep disorders insomnia Nocturnal enuresis neurofeedback sleep disorders insomnia Sleepwalking Restless leg syndrome – Leg discomfort or a need to move legs, disrupting sleep Bruxism – Teeth grinding during sleep Sleep terrors – Abrupt arousal with intense fear, no dream recall or memory of event Narcolepsy Dysregulated sleep patterns/cycles neurofeedback sleep disorders insomnia circadian rhythms neurofeedback sleep disorders insomnia Brain training often helps these problems as it improves brain regulation. For instance, a 75-year-old woman reported that she "slept like a baby for the first time in 25 years" after neurofeedback training. Parents of children with Attention Deficit Hyperactivity Disorder neurofeedback sleep disorders insomnia ADHD neurofeedback sleep disorders insomnia often say it's easier to get their kids to sleep when they've had neurofeedback, and depressed clients remark they have a much easier time getting going in the morning. These are common reports, and just a few examples of the improvements reported. The Role of the Brain and Sleep Insomnia brain image with brain wavesThe brain regulates sleep. The EEG, which shows brainwaves, clearly reflects changes in sleep stages. Training brain patterns using neurofeedback to decrease or increase brainwave activity appears to help the brain normalize sleep. Based on reports from a large number of health professionals, the evidence shows that training brain patterns impacts sleep regulatory mechanisms, and people sleep better. Since sleep is complex and involves many systems, it's not possible to affirm that sleep problems always improve as a result of neurofeedback. Yet, clinicians say they routinely expect changes to occur in sleep patterns after appropriate training for a large percentage of their clients. As with any program, a complete sleep assessment is helpful. Sleep hygiene issues neurofeedback sleep disorders insomnia including caffeine, alcohol, and other behavioral factors neurofeedback sleep disorders insomnia among other potential contributory factors, such as possible sleep apnea, also need to be carefully reviewed and corrected in combination with neurofeedback training. To learn more about how neurofeedback can help with insomnia or other sleep problems, please visit our Neurofeedback Provider List to see if we have a clinician listed near you. Neurofeedback trains your brain for sleep Research shows that people with insomnia have different brain activity than people who sleep well. Neurofeedback is a computer-based technology that re-trains the brain to allow deep, natural, restorative sleep. Neurofeedback: Is relaxing and pleasant. Results in long-term insomnia improvement. Can help people with sleep apnea adjust more easily to CPAP treatment. Can improve sleep after several trainings, with long-term change after continued training. Has a positive impact on many aspects of life and well-being. Here's how it works. Biofeedback's cousin — Neurofeedback is an advanced type of biofeedback. It works with brain waves rather than heart rate, skin temperature or the other bodily measures used in traditional biofeedback. Everyone's different – Each of us has a unique pattern of brain wave activity, with variations in frequencies depending on how smoothly and flexibly the brain functions. When there is mental struggle or symptoms, it can be seen – using sophisticated technology — as turbulence or surges in brain wave activity. The goal — Neurofeedback training gradually improves the brain's efficiency and resiliency to reduce or eliminate the turbulence that's contributing to sleep problems Wider benefits – In addition to overcoming insomnia and other sleep disorders, the method used at Sleep HealthCare trains the brain and also provides positive results for the entire central nervous system. This is similar to how aerobic exercise and yoga train the body, mind, and spirit. This method was developed by the Zengar Institute, a highly respected scientific research organization. What to expect Your brain does all the work – Neurofeedback training takes place directly with your brain, and does not require that you do anything more than to sit back and relax. It's painless and non-invasive. In fact, it's delightful and refreshing. You just get comfy – You'll be settled into a very comfortable chair. Tiny sensors will be attached to your scalp, similar to the way sensors are affixed with adhesive during an EKG. A couple of other sensors are clipped gently to the ears and you get little ipod-type earbuds for listening to music while your brain trains. The technology is cool – Your technician will show you a 'before' view of your brain activity on a computer screen in front of you to get a 'before' picture against which to measure your brain's progress. The training session – You'll just relax and listen to some soft, rhythmic music. You may close your eyes or choose to watch a visual representation of the music on the computer screen. Every so often you may notice a split-second gap in the music – like a tiny bit of static. That's the feedback to your brain helping it to become more efficient. And after the training – Many people experience a sense of extreme relaxation and well-being – particularly when they see progress in the 'after' view of their brain waves.