Neurofeedback in Depression

Neurofeedback for depression. Protocols

Depression is one of the most common mental disorders and the number one cause of disability worldwide. Traditionally, depression has been treated with therapy and medication, both of which have limitations. Even with medication, countless depression sufferers continue to struggle. Medication doesn’t teach the brain how to get out of the unhealthy brain pattern of depression. While drugs can serve some positive benefits, there are numerous problems with these medications, including unwanted side effects and reliance on the medication. Neurofeedback for depression can help restore healthier brain patterns and eliminate depression by teaching the brain to get “unstuck” and better modulate itself. It works on the root of the problem, altering the brain patterns affiliated with depression. It can bring lasting brain changes, is non-invasive, and produces no undesirable side effects.

Feeling down from time to time is a normal part of life. However, when emotions such as hopelessness and despair take hold and just won’t go away, you may have depression. More than just sadness in response to life’s struggles and setbacks, depression changes how you think, feel, and function in daily activities. It can interfere with your ability to work, study, eat, sleep, and enjoy life. Just trying to get through the day can be overwhelming. If depression is left untreated it can become a serious health condition.

Depression is one of the most common mental disorders and the number one cause of disability worldwide. It can affect anyone at almost any age. It is estimated that 10% to 15% of the general population will experience clinical depression in their lifetime. The World Health Organization estimates 5% of men and 9% of women experience depressive disorders in any given year. Over half of people who experience depression will experience anxiety at the same time. The financial costs of depression are tremendous with the global costs per year of depression and anxiety estimated to be $1.15 trillion.


There’s no single cause of depression. It can occur for a variety of reasons and it has many different triggers.
For some people, an upsetting or stressful life event, such as bereavement, divorce, illness, redundancy, and job or money worries, can be the cause.

Different causes can often combine to trigger depression. For example, you may feel low after being ill and then experience a traumatic event, such as a bereavement, which brings on depression.

People often talk about a “downward spiral” of events that leads to depression. For example, if your relationships with your partner break down, you’re likely to feel low, you may stop seeing friends and family and you may start drinking more. All of this can make you feel worse and trigger depression.

Some studies have also suggested that you’re more likely to get depression as you get older and that it’s more common in people who live in difficult social and economic circumstances.

Common causes of depression

Common causes of depression are reflected below.

Stressful events

Most people take time to come to terms with stressful events, such as bereavement or a relationship breakdown. When these stressful events occur, your risk of becoming depressed is increased if you stop seeing your friends and family and try to deal with your problems on your own.


You may be more vulnerable to depression if you have certain personality traits, such as low self-esteem or being overly self-critical. This may be because of the genes you’ve inherited from your parents, your early life experiences, or both.

Family history

Since it can run in families, it’s likely some people have a genetic susceptibility to depression. If someone in your family has had depression in the past, such as a parent or sister or brother, it’s more likely that you’ll also develop it. However, there is no single “depression” gene. Your lifestyle choices, relationships, and coping skills matter just as much as genetics.

Giving birth

Some women are particularly vulnerable to depression after pregnancy. The hormonal and physical changes, as well as the added responsibility of a new life, can lead to postnatal depression.

Loneliness and isolation

Feelings of loneliness, caused by things such as becoming cut off from your family and friends can increase your risk of depression. However, having depression can cause you to withdraw from others, exacerbating feelings of isolation.

Alcohol and drugs

When life is getting people down, some of them try to cope by drinking too much alcohol or taking drugs. This can result in a spiral of depression.
Cannabis can help you relax, but there’s evidence that it can also bring on depression, particularly in teenagers.

“Drowning your sorrows” with a drink is also not recommended. Alcohol affects the chemistry of the brain, which increases the risk of depression.

Chronic illness or pain

The mind and the body are clearly linked. If you are experiencing a physical health problem, you may discover changes in your mental health as well.
You may have a higher risk of depression if you have a longstanding or life-threatening illness, such as coronary heart disease or cancer.
Head injuries are also an often under-recognized cause of depression. A severe head injury can trigger mood swings and emotional problems.
Some people may have an underactive thyroid (hypothyroidism) resulting from problems with their immune system. In rarer cases, a minor head injury can damage the pituitary gland, which is a pea-sized gland at the base of your brain that produces thyroid-stimulating hormones.
This can cause a number of symptoms, such as extreme tiredness and a lack of interest in sex (loss of libido), which can, in turn, lead to depression.


Depression varies from person to person, but there are some common signs and symptoms. It’s important to remember that these symptoms can be part of life’s normal lows. But the more symptoms you have, the stronger they are, and the longer they’ve lasted – the more likely it is that you’re dealing with depression.

Depression is an ongoing problem, not a passing one. It consists of episodes during which the symptoms last for at least 2 weeks. Depression can last for several weeks, months, or years.

10 common symptoms of depression:

1. Feelings of helplessness, hopelessness, emptiness, despair, and sadness. A bleak outlook – nothing will ever get better and there’s nothing you can do to improve your situation.
2. Loss of interest in previously pleasurable daily activities. You don’t care anymore about former hobbies, pastimes, social activities, or sex. You’ve lost your ability to feel joy and pleasure.
3. Appetite or weight changes. Significant weight loss or weight gain – a change of more than 5% of body weight in a month.
4. Sleep changes. Either insomnia, especially waking in the early hours of the morning or oversleeping.
5. Anger or irritability. Feeling agitated, restless, or even violent. Your tolerance level is low, your temper short, and everything and everyone gets on your nerves.
6. Loss of energy. Feeling fatigued, sluggish, and physically drained. Your whole body may feel heavy, and even small tasks are exhausting or take longer to complete.
7. Self-loathing. Strong feelings of worthlessness or guilt. You harshly criticize yourself for perceived faults and mistakes.
8. Reckless behavior. You engage in escapist behavior such as substance abuse, compulsive gambling, reckless driving, or dangerous sports.
9. Concentration problems. Trouble focusing, making decisions or remembering things.
10. Unexplained aches and pains. An increase in physical complaints such as headaches, back pain, aching muscles, and stomach pain, breast tenderness, bloating.


Depression comes in many shapes and forms. While defining the severity of depression – whether it’s mild, moderate, or major – can be complicated, knowing what type of depression you have may help you manage your symptoms and get the most effective treatment.

Mild and moderate depression

Mild and moderate depression is the most common types of depression. More than simply feeling blue, the symptoms of mild depression can interfere with your daily life, robbing you of joy and motivation. Those symptoms become amplified in moderate depression and can lead to a decline in confidence and self-esteem.

Recurrent, mild depression (dysthymia)

Dysthymia is a type of chronic “low-grade” depression. More days than not, you feel mildly or moderately depressed, although you may have brief periods of normal mood.

• The symptoms of dysthymia are not as strong as the symptoms of major depression, but they last a long time (at least two years).
• Some people also experience major depressive episodes on top of dysthymia, a condition known as “double depression.”
• If you suffer from dysthymia, you may feel like you’ve always been depressed. Or you may think that your continuous low mood is “just the way you are.”

Major depression

Major depression is much less common than mild or moderate depression and is characterized by severe, relentless symptoms.
• Left untreated, major depression typically lasts for about six months.
• Some people experience just a single depressive episode in their lifetime, but major depression can be a recurring disorder.

Atypical depression

Atypical depression is a common subtype of major depression with a specific symptom pattern. It responds better to some therapies and medications than others, so identifying it can be helpful.
• People with atypical depression experience a temporary mood lift in response to positive events, such as after receiving good news or while out with friends.
• Other symptoms of atypical depression include weight gain, increased appetite, sleeping excessively, a heavy feeling in the arms and legs, and sensitivity to rejection.

Seasonal affective disorder (SAD)

For some people, the reduced daylight hours of winter lead to a form of depression known as seasonal affective disorder (SAD). SAD affects about 1% to 2% of the population, particularly women and young people. SAD can make you feel like a completely different person to who you are in the summer: hopeless, sad, tense, or stressed, with no interest in friends or activities you normally love. SAD usually begins in fall or winter when the days become shorter and remains until the brighter days of spring.

Understanding the underlying cause of your depression may help you overcome the problem. However, whether you’re able to isolate the causes of your depression or not, the most important thing is to recognize that you have a problem, reach out for support, and pursue the coping strategies that can help you to feel better.

Depression in children and teens

Depression affects also about 2% of preschool and school-age children. A depressive disorder in children does not have one specific cause. Biologically, depression is associated with a deficient level of the neurotransmitter serotonin in the brain, the smaller size of some areas of the brain and increased activity in other parts of the brain. Girls are more likely to be given the diagnosis of depression than boys, but that is thought to be due to, among other things, biological differences based on gender, and differences in how girls are encouraged to interpret their experiences and respond to it as opposed to boys. There is thought to be at least a partial genetic component to the pattern of children, and teens with a depressed parent are as much as four times more likely to also develop the disorder. Children who have depression or anxiety are more prone to have other biological problems, like low birth weight, suffering from a physical condition, trouble sleeping, etc.

Psychological contributors to depression include low self-esteem, negative social skills, negative body image, being excessively self-critical, and often feeling helpless when dealing with negative events. Children who suffer from conduct disorder, attention deficit hyperactivity disorder (ADHD), clinical anxiety, or who have cognitive or learning problems, as well as trouble engaging in social activities, also have more risk of developing depression.

Depression may be a reaction to life stresses, like trauma, including verbal, physical, or sexual abuse, the death of a loved one, school problems, bullying, or suffering from peer pressure.

Other contributors to this condition include poverty and financial difficulties in general, exposure to violence, social isolation, parental conflict, divorce, and other causes of disruptions to family life. Children who have limited physical activity, poor school performance, or lose a relationship are at higher risk for developing depression, as well.

General symptoms of depression in children

Depression often results in the sufferer being unable to perform daily activities, such as getting out of bed or getting dressed, performing well at school, or playing with peers. General symptoms of a major depressive episode regardless of age include having a depressed mood or irritability or difficulty experiencing pleasure for at least two weeks and having at least five of the following signs and symptoms:
• Feeling sad or blue and/or irritable or seeming that way as observed by others (for examples, tearfulness or otherwise looking persistently sad, or angry),
• Significant appetite changes, with or without significant weight loss, failing to gain weight appropriately or gaining excessive weight,
• Change in sleep pattern: trouble sleeping or sleeping too much,
• Physical agitation or retardation (for example, restlessness or feeling slowed down),
• Fatigue or low energy/loss of energy,
• Difficulty concentrating,
• Feeling worthless, excessively guilty, or tend to self-blame,
• Thoughts of death or suicide

Children with depression may also experience the classic symptoms but may exhibit other symptoms as well, including
• Impaired performance of schoolwork,
• Persistent boredom,
• Quickness to anger,
• Frequent physical complaints, like headaches and stomachaches,
• More risk-taking behaviors and/or showing less concern for their own safety (examples of risk-taking behaviors in children include unsafe play, like climbing excessively high or running in the street).

Parents of infants and children with depression often report noticing the following behavior changes in the child:
• Crying more often or more easily,
• Increased sensitivity to criticism or other negative experiences,
• More irritable mood than usual or compared to others their age and gender, leading to vocal or physical outbursts, defiant, destructive, angry or other acting out behaviors,
• Eating patterns, sleeping patterns, or significant increase or decrease in weight change, or the child fails to achieve appropriate gain weight for their age,
• Unexplained physical complaints (for examples, headaches or abdominal pain),
• Social withdrawal, in that the youth spends more time alone, away from friends and family,
• Developing more “clinginess” and more dependent on certain relationships,
• Overly pessimistic, hopeless, helpless, excessively guilty or feeling worthless,
• Expressing thoughts about hurting him or herself or engaging in self-injury behavior,
• Young children may act younger than their age or than they had before (regress).
• Younger children may have difficulty expressing how they feel in words. This can make it harder for them to explain their feelings of sadness.

Physical changes, peer pressure, and other factors can contribute to depression in teenagers. They may experience some of the following symptoms:
• Withdrawing from friends and family,
• Difficulty concentrating on schoolwork,
• Feeling guilty, helpless, or worthless,
• Restlessness, such as an inability to sit still

Hamilton Depression Rating Scale (HAM-D)

The Hamilton Rating Scale for Depression (often abbreviated to HRSD, HDRS or Ham-D) for more than 40 years was considered to be the ‘gold standard’ and most widely used clinician-administered depression assessment scale.
The scale is widely available and has two common versions with either 17 or 21 items and is scored between 0 and 4 points.
The first 17 items measure the severity of depressive symptoms and as examples, the interviewer rates the level of agitation clinically noted during the interview or how the mood is impacting an individual’s work or leisure pursuits.
The extra four items on the extended 21-point scale measure factors that might be related to depression, but are not thought to be measures of severity, such as paranoia or obsessional and compulsive symptoms.

Classification of symptoms can be expanded to:
• 0 – absent;
• 1 – mild;
• 2 – moderate;
• 3 – severe;
• 4 – incapacitating
In general the higher the total scores the more severe the depression.

The Hamilton Depression Rating Scale is designed to be administered by clinicians after a structured or unstructured interview of the patient to determine their symptoms. A total score is calculated by summing the individual scores from each question.
• Scores below 7 generally represent the absence or remission of depression,
• Scores between 7-17 represent the mild depression,
• Scores between 18-24 represent the moderate depression,
• Scores 25 and above represent the severe depression
The maximum score is 52 on the 17- point scale.


Brain Chemistry Imbalances

One potential biological cause of depression is an imbalance in the neurotransmitters which are involved in mood regulation. Certain neurotransmitters, including dopamine, serotonin, and norepinephrine, plays an important role in mood.

Neurotransmitters are chemical substances that help different areas of the brain communicate with each other. When certain neurotransmitters are in short supply, it may lead to the symptoms we recognize as clinical depression.
It’s often said that depression results from a chemical imbalance, but research suggests that depression doesn’t spring from simply having too much or too little of certain brain chemicals. Two people might have similar symptoms of depression, but the problem on the inside, and therefore what treatments will work best, may be entirely different.

Neurotransmitters are chemicals that relay messages from neuron to neuron. An antidepressant medication tends to increase the concentration of these substances in the spaces between neurons (the synapses). In many cases, this shift appears to give the system enough of a nudge so that the brain can do its job better.

A combination of electrical and chemical signals allows communication within and between neurons. When a neuron becomes activated, it passes an electrical signal from the cell body down the axon to its end (known as the axon terminal), where chemical messengers called neurotransmitters are stored. The signal releases certain neurotransmitters into the space between that neuron and the dendrite of a neighboring neuron. That space is called a synapse. 

As the concentration of a neurotransmitter rises in the synapse, neurotransmitter molecules begin to bind with receptors embedded in the membranes of the two neurons. Once the first neuron has released a certain amount of the chemical, a feedback mechanism (controlled by that neuron’s receptors) instructs the neuron to stop pumping out the neurotransmitter and start bringing it back into the cell. This process is called reabsorption or reuptake. Enzymes break down the remaining neurotransmitter molecules into smaller particles.

1. An electrical signal travels down the axon.
2. Chemical neurotransmitter molecules are released.
3. The neurotransmitter molecules bind to receptor sites.
4. The signal is picked up by the second neuron and is either passed along or halted.
5. The signal is also picked up by the first neuron, causing reuptake, the process by which the cell that released the neurotransmitter takes back some of the remaining molecules.

Brain cells usually produce levels of neurotransmitters that keep senses, learning, movements, and moods perking along. But in some people who are severely depressed or manic, the complex systems that accomplish this go awry.

Kinds of neurotransmitters

Scientists have identified many different neurotransmitters. Here is a description of a few believed to play a role in depression:
Acetylcholine enhances memory and is involved in learning and recall.
Serotonin helps regulate sleep, appetite, and mood and inhibits pain. Research supports the idea that some depressed people have reduced serotonin transmission. Low levels of a serotonin byproduct have been linked to a higher risk for suicide.
Norepinephrine constricts blood vessels, raising blood pressure. It may trigger anxiety and be involved in some types of depression. It also seems to help to determine motivation and reward.
Dopamine is essential to movement. It also influences motivation and plays a role in how a person perceives reality. Problems in dopamine transmission have been associated with psychosis, a severe form of distorted thinking characterized by hallucinations or delusions. It’s also involved in the brain’s reward system, so it is thought to play a role in substance abuse.
Glutamate is a small molecule believed to act as an excitatory neurotransmitter and to play a role in bipolar disorder and schizophrenia. Lithium carbonate, a well-known mood stabilizer used to treat bipolar disorder, helps prevent damage to neurons in the brains of rats exposed to high levels of glutamate. Other animal research suggests that lithium might stabilize glutamate reuptake, a mechanism that may explain how the drug smoothes out the highs of mania and the lows of depression in the long term.
Gamma-aminobutyric acid (GABA) is an amino acid that researchers believe acts as an inhibitory neurotransmitter. It is thought to be helpful in quell anxiety.

The neurotransmitter theory of depression suggests that having too much or too little of certain neurotransmitters causes, or at least contributes to, depression. While this explanation is often cited as a major cause of depression, it remains unproven and many experts believe that it doesn’t paint a complete picture of the complex factors that contribute to depression.

Medications to treat depression often focus on altering the levels of certain chemicals in the brain. Some of these treatments include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), monoamine oxidase inhibitors (MAOIs), and tricyclic antidepressants (TCAs).

Areas of the brain affected by depression

Certain areas of the brain help regulate mood. Researchers believe that the more important than levels of specific brain chemicals is the nerve cell connections, nerve cell growth, and the functioning of nerve circuits that have a major impact on depression.

Use of brain imaging technology (positron emission tomography (PET), single-photon emission computed tomography (SPECT), and functional magnetic resonance imaging (fMRI)) has led to a better understanding of which brain regions regulate mood and how other functions, such as memory, may be affected by depression. 

Many functional neuroimaging studies on mood disorders have sown the evidence for localizing the dysfunction on the medial (MFa and PFm) and the orbital frontal cortex (PFo), together with the medial and anterior temporal lobe. 

Compared to healthy controls, patients with MDD show altered activation in the orbital and medial frontal cortex during exposure to emotionally charged stimuli and during the performance of reward-processing tasks. Patients with cerebrovascular disease who develop depression have lesions in the orbital and medial frontal cortex, but other cerebrovascular patients – those without depression – do not. 

Patients with Parkinson’s disease who manifest depression show altered metabolism or blood flow in the orbital and medial frontal cortex compared to non-depressed Parkinson’s patients or healthy controls. Furthermore, reductions of cortical volume and thickness occur in several parts of the frontal cortex in depressed patients, with the most reliable and best characterized of these abnormalities occurring in PFo area, the sulcal part area, and the subgenual frontal cortex. In these key parts of the MFa, the reduction in cortical volume arises prior to the onset of symptoms in patients at high familial risk for depression, appears early in the course of the illness, persists across depressive episodes, and occurs consistently in the most severe cases.

Brain areas that play a significant role in depression are the amygdala, the thalamus, and the hippocampus.


The amygdala is part of the limbic system, a group of structures deep in the brain that’s associated with emotions such as anger, pleasure, sorrow, fear, and sexual arousal. The amygdala is activated when a person recalls emotionally charged memories, such as a frightening situation. Activity in the amygdala is higher when a person is sad or clinically depressed. This increased activity continues even after recovery from depression.


The thalamus receives most sensory information and relays it to the appropriate part of the cerebral cortex, which directs high-level functions such as speech, behavioral reactions, movement, thinking, and learning. Some research suggests that bipolar disorder may result from problems in the thalamus, which helps link sensory input to pleasant and unpleasant feelings.


The hippocampus is part of the limbic system and has a central role in processing long-term memory and recollection. The interplay between the hippocampus and the amygdala might account for the adage “once bitten, twice shy.” It is this part of the brain that registers fear when you are confronted by a barking, aggressive dog, and the memory of such an experience may make you wary of dogs you come across later in life. 

Research shows that the hippocampus 9% to 13% is smaller in some depressed people compared with those who were not depressed. Stress, which plays a role in depression, maybe a key factor here since experts believe that stress, can suppress the production of new neurons (nerve cells) in the hippocampus. Researchers are exploring possible links between the sluggish production of new neurons in the hippocampus and low moods. An interesting fact about antidepressants supports this theory. These medications immediately boost the concentration of chemical messengers in the brain (neurotransmitters). Yet people typically don’t begin to feel better for several weeks or longer. Experts have long wondered why, if depression were primarily the result of low levels of neurotransmitters, people don’t feel better as soon as levels of neurotransmitters increase. 

The answer may be that mood only improves as nerves grow and form new connections, a process that takes weeks. That is why the neurofeedback for depression is so effective. It is because the neurofeedback for depression boosts positive brain neuroplasticity, rewires neuron connections and creates a network, involves changes to structures and enhances the healthy functioning of the brain.

The changes in brain region activity in patients with depression can be registered by electroencephalographic (EEG) study. Special emphasis on the electroencephalographic (EEG) correlates of the disorder is open the venue to the use of EEG not only for diagnostic but for prognostic purposes, producing a new hope and excitement among patients and health practitioners, commonly seen today. In 2008 it was found that a very simple electroencephalographic marker (Alpha asymmetry) could be used to predict the response to antidepressants before the beginning of the pharmacologic treatment, in such a sense that it could serve as an aid in the choice of treatment.


Specific brain networks mediate different emotions and behaviors, and changes in patterns of interaction are associated with differential cerebral activation. The EEG studies provide useful information about patterns of brain functioning during cognitive or emotional tasks in patients with depression.

With a quantitative electroencephalogram (QEEG) it is possible to observe several patterns that include optimal states of psychic balance, but also states of fear, anxiety, panic, anger, impatience, and depression.

It was demonstrated that within the depressed population category it is possible to find specific symptoms for two types of depression: depression with symptoms of hopelessness and symptoms of agitated depression.

The symptoms of depression with hopelessness are sadness, loss or significant decline of interest in performing activities previously considered pleasurable, social withdrawal, altered appetite, and changes in sleep quality, slowing of speech and in some cases mutism, fatigue, guilty feelings, cognitive disorders and thoughts related to death. These symptoms are associated with a reversal or asymmetry of alpha waves (8- 12 Hz). Thus, in the normal non-depressed population, it was observed the importance of the right hemisphere represented by eight even points (Fp2, F4, F8, C4, T4, P4, T6, and O2) of the international 10-20 electroencephalography mapping system. These points, in normal non-depressed population contained around 10 to 15% more alpha waves when compared to the left hemisphere represented by eight odd points (Fp1, F3, F7, C3, T3, P3, T5, and O1) as the alpha waves emit less energy compared to beta waves. This same ideal alpha pattern is expected in the posterior region of the brain at five points (T5, P3, Pz, P4, and T6), when compared to the anterior region also at five points (F7, F3, Fz, F4, and F8), totaling 26 points, divided in two groups of 13.

The symptoms of agitated depression are irritation, impatience, overemotional and difficulty concentrating and paying attention and subjects have a struggle to create a routine and maintain it. These symptoms are linked to reversals of beta waves (15-23 Hz), which are in non-depressed population expected to be around 5% higher in the left hemisphere (Fp1, F3, F7, C3, T3, P3, T5 and O1) and in the anterior brain (F7, F3, Fz, F4 and F8) compared to the right hemisphere (Fp2, F4, F8, C4, T4, P4, T6 and O2) and posterior portion of the brain (T5, P3, Pz, P4 and T6), respectively. 

In 2008 it was found that a very simple electroencephalographic marker (Alpha asymmetry) could be used not only for diagnostic but prognostic purposes: to predict the response to antidepressants before the beginning of the pharmacologic treatment, in such a sense that it could serve as an aid in the choice of treatment.

While qEEG shows great promise in predicting antidepressant medication response and ending the need for lengthy “medication trials”, neurofeedback for depression has been repeatedly found effective in activating brain areas responsible for depression, and helping people re-engage with life.

The use of qEEG to map brain function makes the depressed brain visible. With the use of qEEG it can be seen the brain areas that have become less active, reflecting the disengagement of the patient. More importantly, we can target these areas with neurofeedback for depression to reactivate them, allowing the brain to normalize itself.


Traditionally, depression has been treated with therapy and medication, both of which have limitations.
Antidepressants can help treat moderate-to-severe depression. Several classes of antidepressants are available:
• selective serotonin reuptake inhibitors (SSRIs)
• monoamine oxidase inhibitors (MAOIs)
• tricyclic antidepressants
• atypical antidepressants
• selective serotonin and norepinephrine reuptake inhibitors (SNRIs).

Certain side effects of antidepressants can worsen depression in a small percentage of individuals:

• nausea
• headaches
• sleep disturbances
• agitation
• sexual problems
• suicidal thoughts
• irritability

Even with medication, countless depression sufferers continue to struggle. Medication doesn’t teach the brain how to get out of the unhealthy brain pattern of depression. While drugs can serve some positive benefits, there are numerous problems with these medications, including unwanted side effects and reliance on the medication making it difficult to stop taking it and manage mood on one’s own. If medications are stopped, symptoms often return. In addition, people can become tolerant of medications, necessitating a dosage increase or medication change which may produce new side effects. Despite the availability of effective clinical treatments for depression, 30-40% of these patients still fail to respond significantly to antidepressant treatment.

Depression is a multifaceted mental health condition that affects millions worldwide, impacting their emotional well-being, relationships, and daily functioning. While there are various therapeutic approaches to addressing depression, Cognitive Behavioral Therapy (CBT) stands out as one of the most effective and evidence-based treatments available.

By understanding the underlying mechanisms of CBT and its application in treating depressive symptoms, mental health professionals can equip themselves with powerful tools to assist individuals in overcoming this debilitating condition.

Through a collaborative and empowering approach, CBT offers hope and healing to those navigating the complex terrain of depression, guiding them towards a brighter and more fulfilling future.

Neurofeedback for depression can help restore healthier brain patterns and eliminate depression by teaching the brain to get “unstuck” and better modulate itself. It teaches the brain to regulate mood. Neurofeedback for depression works on the root of the problem, altering the brain patterns affiliated with depression. It can bring lasting brain changes, is non-invasive, and produces no undesirable side effects.


People who have depression show asymmetry in their frontal lobe. Specifically, the left frontal lobe has significantly less activation in people with depression than in people without depression. Decreased left-sided frontal activation is thought to be associated with a deficit in the approach system (which can generate positive moods). Hence people with these deficits are more prone to depressive disorders.

Right-sided frontal activation is related to withdrawal-related emotion such as anxiety disorders. Interestingly this right-sided activation was associated with selective spatial deficits, which are often reported to accompany depression, and may account for the issues with the decoding of nonverbal behavior in people with depression.

Underlying pathophysiological mechanisms have been identified in depression and research has shown that neurofeedback for depression can target these physiological mechanisms in order to reduce depressive symptoms.

In 2016 Wang and colleagues highlighted the benefits of neurofeedback for depression on the left and right frontal activity alpha asymmetry in patients with major depressive disorder.

In 2017, studies by Young and colleagues found evidence to suggest that neurofeedback for depression can significantly decrease depressive symptoms by the increasing activity surrounding positive memories. The study suggests a strong correlation between the roles of the amygdala and the recovery of depression.

Young and colleagues (2018) investigated the correlations between changes in depression scores and changes in amygdala connectivity and the effects of neurofeedback training on these changes. They had found that neurofeedback for depression increased connectivity of the amygdala with regions involved in self-referential, salience, and reward processing. Results showed that the specific amygdala connectivity was significantly correlated with improvement in depressive symptoms.


Neurofeedback represents an exciting complementary option in the treatment of depression that builds upon a huge body of research on electroencephalographic correlates of depression. 

The most used neurofeedback training protocols in depression focus on Alpha inter-hemispheric asymmetry and Theta/Beta ratio within the left prefrontal cortex. In some cases to reduce anxiety, it may be necessary to reinforce the decrease of Beta-3.

The Hammond depression neurofeedback training protocol – reinforce beta arousal while inhibiting alpha and theta arousal in the left frontal area at electrode sites Fp1 and F3.

Patients should receive active neurofeedback from the left amygdala (LA) or from the left horizontal segment of the intraparietal sulcus (control region). Pre-/post- resting-state functional connectivity measures showed that abnormal LA hypo-connectivity in patients with depression was reversed after neurofeedback training. 

Clinical experience demonstrated that occasionally a patient-reported becoming over-activated from the reinforcement of 15-18 Hz beta, reporting feeling somewhat more irritable, anxious, and having some difficulty falling asleep. Therefore, the protocol was modified so that while inhibiting alpha and theta activity, 15-18 Hz beta was reinforced for 20-22 minutes and then the reinforcement band was changed to 12-15 Hz for the last 8-10 minutes.

Key Electrode Application Sites for Depression Neurofeedback

1. F3 (Left Dorsolateral Prefrontal Cortex – DLPFC):

• Location: Frontal lobe, 30% of the distance from the nasion (bridge of the nose) to the inion (the prominent bump at the back of the head) and 20% from the midline.
• Relevance: Associated with positive mood regulation and approach behavior. Activity in this area is often reduced in individuals with depression.

2. F4 (Right Dorsolateral Prefrontal Cortex – DLPFC):

• Location: Frontal lobe, analogous to F3 on the right side of the head.
• Relevance: While F4 is often related to negative emotions, balancing activity between F3 and F4 can be crucial in mood regulation.

3. Fp1 (Left Prefrontal Cortex):

• Location: Frontal pole, 10% of the distance from the nasion.
• Relevance: Involved in executive function and mood regulation. Targeting Fp1 can help enhance positive affect and cognitive control.

4. Cz (Central Midline):

• Location: The vertex of the scalp, halfway between the nasion and inion and equally spaced between the left and right preauricular points (just above the ears).
• Relevance: Often used as a reference or ground electrode in neurofeedback sessions.

Neurofeedback Protocols for Depression Management

Alpha Asymmetry Protocol

This protocol aims to balance the alpha wave activity between the left and right prefrontal cortex, particularly at F3 (left) and F4 (right).

• Target Brainwaves: Alpha waves (8-12 Hz)
• Goal: Increase alpha activity at F3 and/or decrease alpha activity at F4 to reduce left-right asymmetry, as greater left alpha activity relative to the right is often associated with depression.


1. Electrode Placement: Place electrodes at F3, F4, and Cz (reference).
2. Baseline Recording: Record baseline alpha activity for 5-10 minutes.
3. Feedback Mechanism: Provide real-time feedback using visual (e.g., a moving bar or video) or auditory (e.g., tone) cues. When the desired alpha asymmetry is achieved (i.e., more balanced alpha activity), the feedback becomes positive (e.g., the bar grows, the video plays, or the tone changes pleasantly).
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use depression rating scales and follow-up qEEG to assess changes.

Alpha-Theta Training

This protocol focuses on increasing alpha and theta waves to promote relaxation and reduce anxiety, which can help alleviate depressive symptoms.

• Target Brainwaves: Alpha waves (8-12 Hz) and Theta waves (4-8 Hz)
• Goal: Increase the amplitude of alpha and theta waves, particularly during relaxed wakefulness.


1. Electrode Placement: Place electrodes at Fp1 and Cz (reference).
2. Baseline Recording: Record baseline alpha and theta activity for 5-10 minutes.
3. Feedback Mechanism: Provide feedback through a calming visual (e.g., a serene landscape) or auditory (e.g., nature sounds) stimuli. Positive feedback occurs when alpha and theta amplitudes increase.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use depression rating scales and follow-up qEEG to track progress.

Beta/SMR Training Protocol

This protocol focuses on increasing low beta (12-15 Hz) or sensorimotor rhythm (SMR, 12-15 Hz) waves to enhance cognitive function and stabilize mood.

• Target Brainwaves: Beta waves (12-15 Hz)
• Goal: Increase low beta/SMR activity, which is associated with calm focus and emotional stability.


1. Electrode Placement: Place electrodes at F3 (for left DLPFC) and Cz (reference).
2. Baseline Recording: Record baseline beta/SMR activity for 5-10 minutes.
3. Feedback Mechanism: Use visual (e.g., a moving object) or auditory (e.g., a musical tone) feedback. Positive feedback is provided when beta/SMR activity increases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Utilize depression rating scales and follow-up qEEG to monitor changes.

High Beta Downtraining Protocol

This protocol aims to reduce high beta (18-30 Hz) activity, which is often associated with anxiety and ruminative thinking in depression.

• Target Brainwaves: High beta waves (18-30 Hz)
• Goal: Decrease high beta activity to reduce anxiety and rumination.


1. Electrode Placement: Place electrodes at Fz (midline frontal) and Cz (reference).
2. Baseline Recording: Record baseline high beta activity for 5-10 minutes.
3. Feedback Mechanism: Use visual or auditory feedback. Negative feedback (e.g., screen dims, tone lowers) occurs when high beta activity is excessive, encouraging reduction.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use depression and anxiety scales along with follow-up qEEG to track progress.


Neurofeedback for depression actually retrains the dysfunctional brain patterns associated with depression, making it a powerful treatment tool. With neurofeedback for depression, the brain practices healthier patterns of mood regulation. Sessions can range from twice a week to several times a week and average 30 minutes each.

Those with depression often notice improvement after only a few sessions, but for the brain to fully learn to make healthier patterns consistently, a number of brain training sessions are required. With sufficient practice, the brain learns to make these healthy patterns on its own and regulate mood independently.

Neurofeedback can help depression sufferers get their lives back. Your brain changes when you are depressed and neurofeedback can help it relearn healthier patterns, giving those who suffer from depression a way out of the prison of their minds.

Before treatment

HAM (Hamilton Depression Scale)=28
HAS((Hamilton Anxiety Scale)=20

After treatment

HAM (Hamilton Depression Scale)=10
HAS((Hamilton Anxiety Scale)=8

The maps before treatment indicate significant over-activation for alpha and beta frequencies, shown in red on the first row. The rating scale for depression (HAM) indicates severe depression and the anxiety scale (HAS) indicates moderate severity. The maps after treatment show that alpha and beta frequencies are no longer significantly elevated. The HAM score indicates mild depression and the anxiety scale is within the normal range.

After neurofeedback for depression, about 77.8% of the patients made significant improvements. During 1 year of the follow-up not only symptoms of depression, but also anxiety, obsessive rumination, withdrawal, and introversion, while ego-strength has improved.


Reach out to other people. Isolation fuels depression, so reach out to friends and loved ones, even if you feel like being alone or don’t want to be a burden to others. The simple act of talking to someone face-to-face about how you feel can be an enormous help. The person you talk to doesn’t have to be able to fix you. They just need to be a good listener – someone who’ll listen attentively without being distracted or judging you.

Get moving. When you’re depressed, just getting out of bed can seem daunting, let alone exercising. But regular exercise can be as effective as antidepressant medication in countering the symptoms of depression. Take a short walk or put some music on and dance around. Start with small activities and build up from there.

Eat a mood-boosting diet. Reduce your intake of foods that can adversely affect your moods, such as caffeine, alcohol, trans-fats, sugar and refined carbs. And increase mood-enhancing nutrients such as Omega-3 fatty acids.

Find ways to engage again with the world. Spend some time in nature, care for a pet, volunteer, and pick up a hobby you used to enjoy (or take up a new one). You won’t feel like it at first, but as you participate in the world again, you will start to feel better.


Ribas VR, De Souza MV, Tulio VW, Pavan MD, Castagini GA, et al. (2017) Treatment of Depression with Quantitative Electroencephalography (QEEG) of the TQ-7 Neuro-feedback System Increases the Level of Attention of Patients. J Neurol Disord 5:340. doi:10.4172/2329-6895.1000340

Bruder et al., 2008 – Bruder, G. E., Sedoruk, J. P., Stewart, J. W., McGrath, P. J., Quitkin, F. M., & Tenke, C. E. (2008). Electroencephalographic alpha measures predict therapeutic response to a selective serotonin reuptake inhibitor antidepressant: pre- and post- treatment findings. Biological Psychiatry, 63(12), 1171-1177. doi:10.1016/j.biopsych.2007.10.009

Wang, S. Y., Lin, I. M., Peper, E., Chen, Y. T., Tang, T. C., Yeh, Y. C., … & Chu, C. C. (2016). The efficacy of neurofeedback among patients with major depressive disorder: preliminary study. NeuroRegulation, 3(3), 127

Young, K. D., Siegle, G. J., Zotev, V., Phillips, R., Misaki, M., Yuan, H., Drevets, W. C., & Bodurka, J. (2017). Randomized clinical trial of real-time fMRI amygdala neurofeedback for major depressive disorder: Effects on symptoms and autobiographical memory recall. The American Journal of Psychiatry. Vol.174(8), pp. 748-755.)

Young, K. D., Siegle, G. J., Misaki, M., Zotev, V., Phillips, R., Drevets, W. C., & Bodurka, J. (2018). Altered task-based and resting state amygdala functional connectivity following real-time fMRI amygdala neurofeedback training in major depressive disorder. Neuroimage: Clinical, 691-703. doi: 10.1016/j.nicl.2017.12.004

Neurofeedback for migraine vs medicine

Neurofeedback for Migraines. Neurofeedback Protocols.

Migraine is a debilitating illness with long term consequences for the brain. Researches had explored the origins of migraine and suggest that it is an electrical phenomenon initiated in the occipital cortex. Assessments of the brain using the EEG have found abnormal electrical activity supporting this idea. Neurofeedback for migraines is a treatment targeting electrical firing patterns in the brain. Many research data had shown that NFB training/treatment successfully suppresses abnormal brain wave activity leading to a significant decrease in migraine frequency and improvement in associated psychoneurological states such as anxiety, depression, and sleep.


Migraine is a severe health problem which is the second most common one among the primary headaches, which affects 3-10 to 30-38% of the world’s population and which affects the quality of life negatively. Migraine is a disabling neurological condition characterized by episodic attacks of usually unilateral headache, with pulsating character and light and sound intolerance, associated with nausea and vomiting.

The tendency to suffer from migraine has a genetic component, but attacks can be triggered by a series of internal and external factors.

Migraine is a disease with many faces. The most common form is migraine without aura, occurring in about 80% of patients, while migraine with aura occurs in about 20% of the patients.

The annual costs of migraines such as diagnosis, treatment, reduced productivity, and absence from work are estimated to be 5 billion euros in the European Union and about 29 billion in the USA.

The incidence of migraine before puberty is greater in boys than in girls. It grows up to 12 years in both sexes and is the highest in the age range of 30–40 years. After puberty, the ratio changes and increases in favor of women, and with 40 is 3.5:1. After 40 years, the strength of the symptoms is reduced (except for women in perimenopause), and the beginning of migraine headaches in the fifties are rare.

Migraine trigger checklist

Migraine trigger checklist

The main symptoms of migraine are recurring, severe, most often localized in one half of the head (hemicrania), and throbbing headache, which can last from 4 to 72 hours. It usually begins in the temporal region, in the eyeballs, or in the frontal region. Pain may also occur in the face, and neck. During a migraine attack, visual disturbances, increased sensitivity in the hands, dizziness, tinnitus, and increased sensitivity to light or noise may be observed. At the end of an attack, nausea and vomiting may occur.

There are migraines with and without aura. Aura is a complex of neuropsychological symptoms that anticipate the onset of pain, become the first signs of a migraine, or develop simultaneously with a headache. They are caused by a spasm of cerebral vessels, which occurs at the initial stage of an attack.

Symptoms associated with Migraine are:

  • Severe pain in the head or eyes;
  • Being worse on one side of the head;
  • Nausea
  • Vomiting;
  • Dizziness ;
  • Perceiving an aura;
  • Blurred or tunnel vision;
  • Seeing auras;
  • Photophobia (sensitivity to light);
  • Phonophobia (sensitivity to sound);
  • Osmophobia (sensitivity to smells);
  • Poor concentration;
  • Ringing in the ears;
  • Sweating;
  • Feeling very hot or very cold;
  • Abdominal pain (which can sometimes cause diarrhea);
  • A frequent need to urinate. 

The pathogenesis of migraine

The pathogenesis of migraine has long been a subject of discussion among scientists. It has been considered that typical headaches are caused by intracranial vasodilation preceded by vasoconstriction causing aura—vascular theory. Today it is known that this is not the case, and although new findings have emerged, the exact mechanism and genetic determinants are not yet fully clarified.

For a long time, it was thought that the cause of the aura, which precedes headaches, is cerebral vasoconstriction. Today, this theory is denied, and the aura is explained by neural dysfunction rather than ischemia due to vasoconstriction.

The frequency with which migraine attacks occur may vary from once in a lifetime to almost daily, an indication that the degree of migraine predisposition varies individually. It is necessary to consider both the factors that influence the threshold of a person’s susceptibility to a migraine attack and also the mechanisms that trigger the attack and the associated symptoms.

Acute migraine attacks occur in the context of an individual’s inherent level of vulnerability. The greater the vulnerability/lower the threshold, the more frequent attacks occur. Attacks are initiated when internal or environmental triggers are of sufficient intensity to activate a series of events that culminate in the generation of a migraine headache. Many migraineurs experience vague vegetative or affective symptoms as much as 24 hours before the onset of a migraine attack. This phase is called the prodrome and should not be confused with the aura phase.

The aura phase consists of focal neurological symptoms that persist for up to one hour. Symptoms may include visual, sensory, or language disturbance, as well as symptoms, localizing to the brainstem.

Within an hour of the resolution of the aura symptoms, the typical migraine headache usually appears with its unilateral throbbing pain and associated nausea, vomiting, photophobia, or phonophobia. Without treatment, the headache may persist for up to 72 hours before ending in a resolution phase often characterized by deep sleep.

For up to twenty-four hours after the spontaneous throbbing has resolved, many patients may experience malaise, fatigue, and transient return of the head pain in a similar location for a few seconds or minutes following coughing, sudden head movement, or Valsalva movements. This phase is sometimes called the migraine hangover (postdrome).

It is becoming increasingly clear that much of the vulnerability to migraine is inherited.

Migraine is, in essence, a familial episodic disorder whose key marker is a headache, with certain associated features. One of the most important aspects of the pathophysiology of migraine is the inherited nature of the disorder. It is clear from clinical practice that many patients have first-degree relatives who also suffer from migraines. Transmission of migraines from parents to children has been reported as early as the seventeenth century, and numerous published studies have reported a positive family history.

In approximately 50% of the reported families, Familial hemiplegic migraine (FHM) has been assigned to chromosome 19p13. The biological basis for the linkage to chromosome 19 is mutations involving the Ca 2.1 (P/Q) type voltage-gated calcium channel CACNA1A gene. Dysfunction of these channels might impair serotonin release and predispose patients to migraine or impair their self-aborting mechanism.

Migraine aura

A migraine aura is defined as a focal neurological disturbance manifesting as visual, sensory, or motor symptoms. It is seen in about 30% of patients, and it is neurally driven. Visual aura has been described as affecting the visual field, suggesting the visual cortex, and it starts at the center of the visual field, propagating to the periphery at a speed of 3 mm/min. Blood flow studies in patients have also shown that focal hyperemia tends to precede the spreading of oligemia. However, some researchers conclude that migraine aura is evoked by aberrant firing of neurons.

Shown is the entire hemisphere, from a posterior-medial view. The aura-related changes appeared first in extrastriatal cortex. The spread of the aura began and was most systematic in the representation of the lower visual field, becoming less regular as it progressed into the representation of the upper visual field.


The study of anatomy and physiology of pain-producing structures in the cranium and the central nervous system modulation of the input have led to the conclusion that migraine involves alterations in the subcortical aminergic sensory modulatory systems that influence the brain widely.

Available research data had shown that no structural differences have been found in individuals with migraine compared to individuals without migraine. This research suggests that migraine is an electrical phenomenon initiated within the cortex of the brain. This phenomenon is known as Cortical Spreading Depression (CSD) referring to a wave of electrophysiological hyperactivity that spreads through the brain from the occipital lobes forward. This wave affects the cortex in several ways: altering the electrical polarity of neurons, decreasing blood flow and associated levels of oxygen in the cortex and altering the degree of vasodilation within the vascular system of the cortex. These changes release of nerve irritating chemicals into the brain. These chemicals irritate the pain transmitting the “trigeminal” nerve system in the meninges, the sensitive membranes that cover the brain. The result is severe blinding pain.

Consequences of migraine to the brain are:

  • impaired ability in tests of short and long-term memory,
  •  small areas of stroke-like damage to the brain,
  • with a high frequency of Migraine (more than three attacks per month) show significantly more areas of damage than those with fewer attacks,
  • with a history of Migraines, longer than 15 years were found to have more changes in the brain than those with a shorter history,
  • higher frequency migraines show abnormalities in both white and gray matter of the brain,
  • people with migraine are more at risk for future strokes,
  • show a predilection toward damage in the following sites:
    – frontal lobe
    – limbic system
    – parietal lobes
    – brainstem
    – cerebellum

Chronic migraine comorbidities


There are two ways in which anomalies in the EEG have been associated with migraine: via the relationship of migraine to seizure activity and as a function of slow brain waves found elsewhere in the brain. Migraine and epilepsy frequently coexist and are often difficult to differentiate. Both migraine and seizure-prone individuals show abnormal occipital discharges that are typically high voltage (200–300 mV), with a diphasic morphology, and a unilateral or bilateral occipital and postero-temporal distribution.

Migraine has been associated with abnormal EEG activity elsewhere in the brain. Both unilateral and bilateral increased delta wave activity has been recorded during a hemiplegic migraine and attacks of migraine with disturbed consciousness. It is shown that in the waking, non-migraine state there are slow waves in the theta range (48 hertz). Neurofeedback for migraines has been used to target and suppress this slow-wave activity in both adults and children with a concomitant reduction in frequency and intensity of migraine. Some research has shown that neurofeedback blood flow-up training in the frontal cortex results in a 70% reduction in the frequency of migraines compared with a 50% reduction using medication alone. NFB training is also associated with decreases in anxiety, depression, and improved sleep, each of which has been associated with migraines.

Newer methods, i.e. EEG frequency analysis and topographic brain mapping, are promising tools in this field. So far, mostly small studies have been published with somewhat inconsistent results. A pattern of increased alpha rhythm variability (and/or asymmetry) in the headache-free phase seems to emerge, however. Significant asymmetry of alpha and theta during headache has been reported in a topographic brain mapping study.

The EEG patterns observed in migraine patients seem to suggest a possible physiological connection between sleep, hyperventilation, and migraine.

EEG activity seems to change shortly before the attack. This suggests that migraineurs are most susceptible to attack when anterior QEEG delta power and posterior alpha asymmetry values are high.
Occipitoparietal and temporal alpha power were more asymmetric before the attack compared with the interictal baseline

Different research found the increased power in 19 cortical areas in delta (1.5-3.5 Hz), theta (4.0-7.5 Hz), and high-frequency beta (21-30 Hz) bands. Multiple types of research have shown significant abnormalities in the high-frequency beta band (21-30 Hz) in the parietal, central, and frontal regions.

How Neurofeedback Training Manage Migraines?

Despite a large number of medications being used to treat migraine today, only 20% of patients report their effectiveness. Many develop resistance to medications, and therefore the dose of the drug is gradually increasing, which is required to achieve the effect of relieving headache. Often the medication is accompanied by side effects.

In patients with migraine, changes in the biological parameters of brain activity, brain waves, are often recorded. Neurofeedback is a recently developed technology for treating migraines based on recording these changes in brain wave activity and transmitting information about their condition in the form of audio and video signals to the patient. Based on these audio and video signals, the patient learns how to manage his condition to regulate brain wave activity and normalize it. Normalization of wave activity leads to a significant decrease in both the frequency and intensity of headaches. At first, these changes are not stable but gradually become stable and permanent. It becomes possible (after about 10 sessions of treatment) to manage the condition without the support of special equipment and computer programs.

Migraine research points to electrophysiological anomalies in the brain as correlates of migraine headaches. Neurofeedback, as a therapy, is specifically designed to target dysregulated firing patterns in the brain. Research has demonstrated the ability of NFB to successfully treat anomalous brainwave patterns in a variety of conditions most specifically with migraines.

After performing diagnostic scanning and getting brain mapping patterns of the patients with migraine some clinicians provide neurofeedback training with an increase of SMR and low beta 12-15 Hz and decreased theta (4-7Hz) and high beta (21-30 Hz) at each affected site; 5 sessions for each affected site.

qEEG Before and after Neurofeedback for Migraines

Electrode Placement and Detailed Neurofeedback Protocols for Migraine Management

Key Electrode Sites for Migraine Neurofeedback

1. Fz (Frontal Midline):

• Location: Frontal lobe, on the midline, 20% of the distance from the nasion (bridge of the nose).
• Relevance: Associated with emotional regulation and autonomic control. Targeting this site can help manage stress and reduce the frequency and intensity of migraines.

2. Cz (Central Midline):

• Location: The scalp vertex, halfway between the nasion and inion and equally spaced between the left and right preauricular points (just above the ears).
• Relevance: Central region involved in general arousal regulation. Often used as a reference or active site for enhancing overall neural stability.


Electrode Application Sites for Migraine Neurofeedback Management

3. Pz (Parietal Midline):

• Location: Parietal lobe, on the midline, 50% of the distance from the nasion to the inion.
• Relevance: Involved in sensory processing and pain perception. Targeting Pz can help modulate sensory processing related to migraine pain.

4. T3 (Left Temporal Lobe):

• Location: Temporal lobe, 20% above the preauricular point.
• Relevance: Associated with stress and emotional regulation. Training in this area can help manage triggers related to emotional stress.

5. T4 (Right Temporal Lobe):

• Location: Temporal lobe, analogous to T3 on the right side.
• Relevance: Similar to T3, it helps balance activity related to emotional stress and can assist in reducing migraine frequency.

Neurofeedback Protocols for Migraine

The protocol involves training individuals to increase or decrease specific brainwave activity at the targeted locations to promote relaxation, improve stress management, and reduce migraine symptoms.

1. Alpha Enhancement Protocol

This protocol focuses on increasing alpha (8-12 Hz) activity to promote relaxation and reduce stress, which are common migraine triggers.

• Target Brainwaves: Alpha waves (8-12 Hz)
• Goal: Increase alpha activity to enhance relaxation and reduce stress-related migraine triggers.

1. Electrode Placement: Place electrodes at Fz and Pz with Cz as the reference.
2. Baseline Recording: Record baseline alpha activity for 5-10 minutes.
3. Feedback Mechanism: Provide real-time feedback using visual (e.g., calming images) or auditory (e.g., soothing sounds) cues. Positive feedback is given when alpha activity increases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use headache frequency and intensity diaries along with follow-up qEEG to assess changes.

2. SMR Training Protocol

This protocol focuses on increasing sensorimotor rhythm (SMR, 12-15 Hz) activity to promote calmness and reduce hyperarousal that can trigger migraines.

• Target Brainwaves: SMR (12-15 Hz)
• Goal: Increase SMR activity to enhance motor inhibition and promote calmness.


1. Electrode Placement: Place electrodes at Cz with reference electrodes at mastoids (A1 and A2).
2. Baseline Recording: Record baseline SMR activity for 5-10 minutes.
3. Feedback Mechanism: Provide real-time feedback using visual or auditory cues. Positive feedback is given when SMR activity increases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use headache frequency and intensity diaries and follow-up qEEG to monitor changes.

3. Theta/Beta Ratio Training

This protocol aims to balance theta (4-8 Hz) and beta (15-20 Hz) wave activity to improve cognitive control and reduce stress, which can contribute to migraine frequency.

• Target Brainwaves: Theta (4-8 Hz) and Beta (15-20 Hz)
• Goal: Decrease theta activity and increase beta activity to improve cognitive control and reduce stress.


1. Electrode Placement: Place electrodes at T3 and T4 with Cz as the reference.
2. Baseline Recording: Record baseline theta and beta activity for 5-10 minutes.
3. Feedback Mechanism: Provide feedback using visual or auditory stimuli. Positive feedback occurs when theta decreases and beta increases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use headache frequency and intensity diaries along with follow-up qEEG to track progress.

4. Alpha/Theta Training

This protocol focuses on increasing alpha (8-12 Hz) and theta (4-8 Hz) waves to promote relaxation and reduce anxiety, which are common migraine triggers.

• Target Brainwaves: Alpha waves (8-12 Hz) and Theta waves (4-8 Hz)
• Goal: Increase alpha and theta activity to reduce stress and improve overall emotional regulation.


1. Electrode Placement: Place electrodes at Fz and Cz (reference).
2. Baseline Recording: Record baseline alpha and theta activity for 5-10 minutes.
3. Feedback Mechanism: Use calming visual or auditory feedback. Positive feedback is provided when alpha and theta waves increase.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use headache frequency and intensity diaries along with follow-up qEEG to monitor changes.

Frequently used Neurofeedback Protocol for migraine management as follows:

Left-sided headaches – at C3 (T3)

  • down-trained: 2-7 Hz and high-frequency beta
  • up-trained: 15-18 Hz

Right-sided headaches – at C4 (T4)

  • down-trained: 2-7 Hz and high-frequency beta
  • up-trained: 12-15 Hz

An average number of neurofeedback sessions to get a significant change to occur are around 20-30 sessions. A person can get a neurofeedback session as much as twice a day with at least a two-hour break in between. It is recommended that a person try to do neurofeedback at least two or three times a week until the sessions are completed. Results appear to solidify and happen faster when done more frequently.

How effective is neurofeedback for migraines?

Neurofeedback for migraines can help with dysfunctions in the central nervous system, such as the increased excitability of the cerebral cortex. Because of working directly with the central nervous system, Neurofeedback training can be very effective in stabilizing the excitability of the cerebral cortex what will result in reduced headaches, less sensitivity, and improvements in other symptoms associated with Migraine.
The researchers concluded, “Neurofeedback appears to be dramatically effective in abolishing or significantly reducing headache frequency in patients with recurrent migraine”.

Walker (Walker, J. E. (2011). QEEG‐Guided Neurofeedback for Recurrent Migraine Headaches. Clinical EEG and Neuroscience, 42(1), 59‐61. doi:10.1177/155005941104200112) examined the effects of neurofeedback therapy versus drug therapy in 71 patients with recurrent migraine headaches. After completion of a quantitative electroencephalogram (QEEG) procedure, all results indicated an excess of high-frequency beta activity (21‐30 Hz). Twenty‐five patients chose to continue with drug therapy for their recurring migraines, whilst 46 of the 71 patients selected neurofeedback training. Of those who chose neurofeedback therapy, the majority (54%) reported complete abolishment of their migraines, 39% experienced a significant reduction in migraine frequency of greater than 50%, and 4% experienced a decrease in the frequency of less than 50%. Only one patient did not report a reduction in headache frequency. The control group of participants who opted to continue drug therapy as opposed to neurofeedback experienced no change in headache frequency (68%), a reduction of less than 50% (20%), or a reduction greater than 50% (8%). Overall, the study demonstrates that neurofeedback is significantly effective in abolishing or substantially reducing the frequency of headaches in patients with recurrent migraines.

Effectiveness of Neurofeedback vs. Drug Management of the Migraine

Effectiveness of Neurofeedback for Migraines

Complete abolishment of the migraines
Significant reduction in migraine frequency of greater than 50%
Decrease in migraine frequency of less than 50%
No change in migraine frequency
Web Designer 0.5%

Effectiveness of Drug Therapy for Migraines

Complete abolishment of the migraines
Web Designer 1%
Significant reduction in migraine frequency of greater than 50%
Decrease in migraine frequency of less than 50%
No change in migraine frequency

After Neurofeedback for migraines, the reduction of frequency and intensity of headaches usually was sustained at the 14.5 months follow‐up assessment.

Some of the benefits of neurofeedback for migraines:

  • It helps to retrain the brain and or optimize the functioning of the entire brain by removing barriers and improving the connections and brainwave activity in a certain region of the brain or among different regions of the brain.
  • It releases the old stuck or abnormal patterns to create new and more effective, stronger, and organized patterns.
  • Training protocols are generated from the initial QEEG brain mapping. Training involves audiovisual feedback that INVOLUNTARILY teaches the individual to self-regulate the abnormal brain wave patterns that are presented to them on a computer screen in several ways.
  • There are no contraindications or side effects of neurofeedback for migraines.

Effective Use of Various Biofeedback Modalities for Migraine Management

Various modalities of biofeedback, including Electromyography (EMG), Heart Rate Variability (HRV), Temperature, and Galvanic Skin Response (GSR), can also be effectively utilized in the management of migraines. EMG biofeedback helps individuals become aware of and reduce muscle tension, which can alleviate headache symptoms. HRV biofeedback trains individuals to regulate their heart rate variability, promoting autonomic balance and reducing stress, a common migraine trigger. Temperature biofeedback involves monitoring peripheral skin temperature to enhance relaxation and decrease physiological arousal, thus helping to prevent migraines. GSR biofeedback measures the skin’s electrical conductance, which varies with sweat gland activity, providing insights into stress and arousal levels. By learning to modulate these physiological responses, individuals with migraines can manage their symptoms more effectively, complementing traditional neurofeedback approaches. For more detailed information regarding various biofeedback modalities used in Migraine Management, please visit the Article “Biofeedback for Migraines. How to choose”.

ADHD in boys

Neurofeedback for ADHD Management

Attention Deficit Hyperactivity Disorder (ADHD) has become one of the most common neurodevelopmental and psychiatric disorders of childhood (3% to 7% of school-age children), that persists to adolescence and adulthood in 40-60% cases. ADHD treatment main strategies are the use of pharmacological therapy, omega 3, multivitamins, and multi-minerals. Stimulants work by causing the brain to synthesize more norepinephrine; non-stimulants by slowing the rate at which norepinephrine is broken down. Once the level is where it should be, the brain functions normally, and the individual becomes less hyperactive, inattentive, and/or impulsive. Once the drug wears off, the level falls — and symptoms return. In addition, side-effects, resistance to pharmacological therapy have raised interest in non-pharmacological treatment options. Neurofeedback for ADHD management is a non-pharmacological intervention, based on neuroplasticity characteristics of the brain and utilizes cognitive behavioral therapeutic elements to gain access on and practice brain activity. In fact, several organizations worldwide are looking into claims that neurofeedback such effective as pharmacological therapy, but with significantly long-lasting effectiveness and free of side-effects. This became more actual if take into consideration existing today friendly use technology of neurofeedback devices for ADHD management at home, school, university, and workplace.

Attention-deficit hyperactivity disorder (ADHD) is the most commonly diagnosed behavioral disorder in children, but it is often misunderstood as well as the subject of controversy. Confusion surrounding the disorder has led to both under- and overtreatment of children. Currently, the disorder is primarily diagnosed by referring to the criteria of the Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition Text Revision (DSM-IV, 1994) or the International Statistical Classification of Mental Disorders (ICD-10, World Health Organization, 1992).

Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset, clinically heterogeneous disorder of inattention, hyperactivity, and impulsivity. Its impact on society is enormous in terms of its financial cost, stress to families, adverse academic and vocational outcomes, and negative effects on self-esteem. Children with ADHD are easily recognized in clinics, in schools, and in the home. Their inattention leads to daydreaming, distractibility, and difficulties in sustaining effort on a single task for a prolonged period. Their impulsivity makes them accident-prone, creates problems with peers, and disrupts classrooms. Their hyperactivity, often manifested as fidgeting and excessive talking is poorly tolerated in schools and is frustrating to parents, who can easily lose them in crowds and cannot get them to sleep at a reasonable hour. In their teenage years, symptoms of hyperactivity and impulsivity diminish, but in most cases, the symptoms and impairments of ADHD persist. The teen with ADHD is at high risk of low self-esteem, poor peer relationships, conflict with parents, delinquency, smoking, and substance abuse.

The validity of diagnosing ADHD in adults has been a source of much controversy. Some investigators argue that most cases of ADHD remit by adulthood (3), a view that questions the validity of the diagnosis in adulthood. Others argue that the diagnosis of ADHD in adults is both reliable and valid.
Longitudinal studies have found that as many as two-thirds of children with ADHD have impaired ADHD symptoms as adults. In adults, inner restlessness rather than hyperactivity may occur. Throughout the life cycle, a key clinical feature observed in patients with ADHD is comorbidity with conduct, depressive, bipolar, and anxiety disorders.

ADHD Symptoms in Children and Teenagers

ADHD is divided into three subtypes:

  • predominantly inattentive (ADHD-PI or ADHD-I),
  • predominantly hyperactive-impulsive (ADHD-PH or ADHD-HI), and
  • combined type (ADHD-C).

The symptoms of ADHD in children and teenagers are well-defined, and they’re usually noticeable before the age of 6. They occur in more than one situation, such as at home and school.


The main signs of inattentiveness are:
• having a short attention span and being easily distracted
• making careless mistakes – for example, in schoolwork
• appearing forgetful or losing things
• being unable to stick to tasks that are tedious or time-consuming
• appearing to be unable to listen to or carry out instructions
• constantly changing activity or task
• having difficulty organizing tasks

Hyperactivity and impulsiveness

The main signs of hyperactivity and impulsiveness are:
• being unable to sit still, especially in calm or quiet surroundings
• constantly fidgeting
• being unable to concentrate on tasks
• excessive physical movement
• excessive talking
• being unable to wait their turn
• acting without thinking
• interrupting conversations
• little or no sense of danger

These symptoms can cause significant problems in a child’s life, such as underachievement at school, poor social interaction with other children and adults, and problems with discipline.

A common symptom of ADHD in children and adults is the inability to focus at length on the task at hand. Those who have ADHD are easily distracted, which makes it difficult to give sustained attention to a specific activity, assignment, or chore. But a lesser-known, and more controversial, symptom that some people with ADHD demonstrate is known as hyperfocus. Although other conditions include hyperfocus as a symptom, here we will look at hyperfocus as it relates to a person with ADHD.
Hyperfocus is the experience of intense concentration in some people with ADHD. ADHD is not necessarily a deficit of attention, but rather a problem with regulating one’s attention span to desired tasks. So, while mundane tasks may be difficult to focus on, others may be completely absorbing. An individual with ADHD who may not be able to complete homework assignments or work projects may instead be able to focus for hours on video games, sports, or reading.

People with ADHD may immerse themselves so completely in an activity that they want to do or enjoy doing to the point that they become oblivious to everything around them. This concentration can be so intense that an individual loses track of time, other chores, or the surrounding environment. While this level of intensity can be channeled into difficult tasks, such as work or homework, the downside is that ADHD individuals can become immersed in unproductive activities while ignoring pressing responsibilities. No one’s going to mind if someone spends hours solving math problems or painting the house. But hyperfocus can cause trouble if someone gets so wrapped up in a project at work that misses a dinner date, or the child can’t break away from a video game to do his homework.

It also can make it harder to diagnose ADHD, especially in kids considered gifted. They do better in school because their high IQs help them get past the learning issues that usually go along with the disorder, and their ability to hyperfocus can make it even harder to spot. 

It is very important to find ways to manage the focus of children with ADHD and direct it for their development and good performance, finding an interest that removes them from isolated time and fosters social interaction, such as music, sports, or other. 

Adults with ADHD also have to deal with hyperfocus, on the job, and at home. The best way to cope with hyperfocus is not to fight it by forbidding certain activities, but rather to harness it. Making work or school stimulating can capture their focus in the same way as their favorite activities. This may be difficult for a growing child but can ultimately become advantageous for an adult in the workplace. By finding a job that caters to one’s interests, an individual with ADHD can truly shine, using hyperfocus to their advantage.

Correlation between ADHD and high levels of cell phone use

If you’re a parent of a child with attention deficit hyperactivity disorder, you know that their attention can be directed quite intensely onto technology they find fascinating, which includes cell phone games, texting, the internet, and social media. These facets of mobile phone use provide an endless supply of feedback and enticements that keep the pleasure center of the brain very happy, which can make pulling a child away from their phone or yours a real struggle.

Though researchers do not yet know whether excessive phone use increases the risk of ADHD, encouraging thoughtful and limited cell phone use is considered an important life skill for any child. However, there is a correlation between ADHD and high levels of cell phone use, and the increase in children diagnosed with the disorder make researchers wonder how the rise of mobile technology impacts the attention levels of young children and teens. One study found that children who make calls and play games on cell phones were at increased risk for ADHD. However, it is possible that children may play more games on their phone because they already have symptoms of ADHD, such as inattention and hyperfocus.

Some children can become engrossed with a particular smartphone game or app and later toss it aside, but kids with ADHD are at higher risk for becoming behaviorally and cognitively dependent on their device. This can be a cause for concern, as researchers have linked cell phone dependence to symptoms of anxiety, depression, sleep disturbances, and low self-esteem.
Being dependent or overinvolved with a cell phone isn’t just about the number of games a child plays or the texts they send. Kids with ADHD can become caught in a behavioral loop, mindlessly checking different social media apps or seeking to achieve the reach level in a difficult game. Dependence has a cognitive component as well, with the child thinking about or becoming hyperfocused on being able to access and use their phone. For example, they might become distressed when the battery dies, when their phone is not in sight, or when they cannot sleep with their cell phone at night.

Although hyperfocus can have a detrimental effect on a person’s life by distracting them from important tasks, it can also be used positively, as evidenced by many scientists, artists, and writers. Like all symptoms of ADHD, hyperfocus needs to be delicately managed.

When in a hyperfocused state, a child may lose track of time and the outside world may seem unimportant.
It is very important to find ways to manage the focus of children’s with ADHD and direct it for their development and good performance. First of all, for parents, it is necessary to monitor the length of use and the content accessed on their child’s phone and to keep mobile devices out of a child’s bedroom to ensure healthy sleep habits. Less phone use won’t feel like a punishment if kids and teens have flexible, fun options when it comes to their attention. What activities does your child enjoy that don’t involve screens, and how can they be utilized when your child seems particularly dependent on their phone? A day at the park, a museum, or the pool can prove a much-needed break in hyper-focus. Help your child find an interest that removes them from isolated time and fosters social interaction, such as music or sports.

Neurofeedback management of ADHD gives excellent results and leads to significant improvement of memory, attention, concentration, and focus. These improvements will provide the possibility to stop addiction to phones and computers.

Video – More screen tine leads to ADHD

Related conditions in children and teenagers with ADHD

Although not always the case, some children may also have signs of other problems or conditions alongside ADHD, such as:
• Anxiety disorder – which causes your child to worry and be nervous much of the time; it may also cause physical symptoms, such as a rapid heartbeat, sweating, and dizziness
• Oppositional defiant disorder (ODD) – this is defined by negative and disruptive behavior, particularly towards authority figures, such as parents and teachers
• Conduct disorder – this often involves a tendency towards highly antisocial behavior, such as stealing, fighting, vandalism, and harming people or animals
• Depression
• Sleep problems – finding it difficult to get to sleep at night, and having irregular sleeping patterns
• Autistic spectrum disorder (ASD) – this affects social interaction, communication, interests, and behavior
• Epilepsy – a condition that affects the brain and causes repeated fits or seizures
• Tourette’s syndrome – a condition of the nervous system, characterized by a combination of involuntary noises and movements (tics)
• Learning difficulties – such as dyslexia

ADHD Symptoms in Adults

In adults, the symptoms of ADHD are more difficult to define. This is largely due to a lack of research into adults with ADHD.
As ADHD is a developmental disorder, it’s believed it cannot develop in adults without it first appearing during childhood. However, it’s known that symptoms of ADHD often persist from childhood into a person’s teenage years and then adulthood.
Any additional problems or conditions experienced by children with ADHD, such as depression or dyslexia, may also continue into adulthood. By the age of 25, an estimated 15% of people diagnosed with ADHD as children still have a full range of symptoms, and 65% still have some symptoms that affect their daily lives. Hyperactivity tends to decrease in adults, while inattentiveness tends to get worse as the pressures of adult life increase. Adult symptoms of ADHD also tend to be far more subtle than childhood symptoms.
Some specialists have suggested the following as a list of symptoms associated with ADHD in adults:

• Impulsiveness
• Excessive activity or restlessness and edginess
• Carelessness and lack of attention to detail
• Continually starting new tasks before finishing old ones
• Poor organizational skills and problems prioritizing
• Poor time management skills
• Problems focusing on a task
• Poor planning
• Trouble multitasking
• Continually losing or misplacing things
• Forgetfulness
• Difficulty keeping quiet, and speaking out of turn
• Blurting out responses and often interrupting others
• Frequent mood swings, irritability, and a quick temper
• Low frustration tolerance
• Trouble coping with stress
• Extreme impatience
• Taking risks in activities, often with little or no regard for personal safety or the safety of others – for example, driving dangerously

Related conditions in adults with ADHD

Although ADHD doesn’t cause other psychological or developmental problems, as with ADHD in children and teenagers, ADHD in adults can occur alongside several related problems or conditions and make treatment more challenging.

Mood disorders. Many adults with ADHD also have depression, bipolar disorder, or another mood disorder. While mood problems aren’t necessarily due directly to ADHD, a repeated pattern of failures and frustrations due to ADHD can worsen depression.
Anxiety disorders. Anxiety disorders occur fairly often in adults with ADHD. Anxiety disorders may cause overwhelming worry, nervousness, and other symptoms. Anxiety can be made worse by the challenges and setbacks caused by ADHD.
Learning disabilities. Adults with ADHD may score lower on academic testing than would be expected for their age, intelligence, and education. Learning disabilities can include problems with understanding and communicating.
Other psychiatric disorders. Adults with ADHD are at increased risk of other psychiatric disorders, such as personality disorders, intermittent explosive disorder, and substance abuse.
– personality disorders – conditions in which an individual differs significantly from the average person in terms of how they think, perceive, feel, or relate to others
– bipolar disorder – a condition affecting your mood, which can swing from one extreme to another
– obsessive-compulsive disorder (OCD) – a condition that causes obsessive thoughts and compulsive behavior.

The behavioral problems associated with ADHD can also cause problems such as difficulties with relationships and social interaction.

The exact cause of attention deficit hyperactivity disorder (ADHD) is not fully understood, although a combination of factors is thought to be responsible.
Researchers suspect that a gene involved in the creation of dopamine, a chemical that controls the brain’s ability to maintain regular and consistent attention may be traced back to ADHD. ADHD tends to run in families and, in most cases, it’s thought the genes you inherit from your parents are a significant factor in developing the condition.

Research shows that parents and siblings of a child with ADHD are more likely to have ADHD themselves. However, the way ADHD is inherited is likely to be complex and is not thought to be related to a single genetic fault.

Among the factors that are thought to contribute to ADHD are:

• Brain injury or infection
• a lack of oxygen, or exposure to alcohol or nicotine before birth
• premature birth
• difficult experiences in early childhood.


Does My Child Have Attention Deficit Hyperactivity Disorder (ADHD or ADD)?

Only a mental health professional can tell for sure whether symptoms of distractibility, impulsivity, and hyperactivity are severe enough to suggest a positive ADHD diagnosis. But this test may provide some behavior clues and suggestions about the next steps. This questionnaire is designed to determine whether your child demonstrates symptoms similar to those of attention deficit disorder (ADHD). Download and print out the Assessment Scale.  If you answer yes to a significant number of these questions, consult a licensed mental health practitioner. An accurate diagnosis can only be made through clinical evaluation.

Scoring Instructions for the NICHQ Vanderbilt Assessment Scales

These scales should NOT be used alone to make any diagnosis. You must take into consideration information from multiple sources. Scores of 2 or 3 on a single Symptom question reflect often-occurring behaviors. Scores of 4 or 5 on Performance questions reflect problems in performance.

The initial assessment scales, parent and teacher, have 2 components: symptom assessment and impairment in performance.
On both the parent and teacher initial scales, the symptom assessment screens for symptoms that meet the criteria for both inattentive (items 1–9) and hyperactive ADHD (items 10–18).
To meet DSM-IV criteria for the diagnosis, one must have at least 6 positive responses to either the inattentive 9 or hyperactive 9 core symptoms or both. A positive response is a 2 or 3 (often, very often) (you could draw a line straight down the page and count the positive answers in each subsegment). There is a place to record the number of positives in each subsegment, and a place for a total score for the first 18 symptoms (just add them up).
The initial scales also have symptom screens for 3 other comorbidities — oppositional-defiant, conduct, and anxiety/ depression. These are screened by the number of positive responses in each of the segments separated by the “squares.” The specific item sets and numbers of positives required for each co-morbid symptom screen set are detailed in the pdf file.
The second section of the scale has a set of performance measures, scored 1 to 5, with 4 and 5 being somewhat of a problem.
To meet the criteria for ADHD there must be at least one item of the Performance set in which the child scores a 4 or 5; ie, there must be impairment, not just symptoms to meet diagnostic criteria. The sheet has a place to record the number of positives (4s, 5s) and an Average Performance Score—add them up and divide by the amount of Performance criteria answered.

Adult ADHD Self-Report Scale (ASRS) Symptom Checklist

Many adults have been living with Adult Attention-Deficit/Hyperactivity Disorder (Adult ADHD) and don’t recognize it. Why? Because its symptoms are often mistaken for a stressful life. If you’ve felt this type of frustration most of your life, you may have Adult ADHD.
The following questionnaire can be used as a starting point to help you recognize the signs/symptoms of Adult ADHD but is not meant to replace consultation with a trained healthcare professional. An accurate diagnosis can only be made through a clinical evaluation. Regardless of the questionnaire results, if you have concerns about diagnosis and treatment of Adult ADHD, please discuss your concerns with your physician.

The Adult Self-Report Scale  Screener is intended for people aged 18 years or older.


In children with ADHD, several brain regions and structures (pre-frontal cortex, striatum, basal ganglia, and cerebellum) tend to be smaller by roughly 5%.
ADHD brains have low levels of a neurotransmitter called norepinephrine. Norepinephrine is linked arm-in-arm with dopamine. The ADHD brain has impaired neurotransmitter activity in four functional regions of the brain.

1. Frontal Cortex
This region controls high-level functions:
• Attention
• Executive Function
• Organization
This region orchestrates our high-level functioning: maintaining attention, organization, and executive function. A deficiency of dopamine within this brain region might cause inattention, problems with organization, and/or impaired executive functioning.

2. Limbic System
This region is located deeper in the brain. It regulates our emotions and attention. A dopamine deficiency in this region might result in restlessness, inattention, or emotional volatility.

3. Basal Ganglia
These neural circuits regulate communication within the brain. Information from all regions of the brain enters the basal ganglia and is then relayed to the correct sites in the brain. A dopamine deficiency in the basal ganglia can cause inter-brain communication and information to “short-circuit,” resulting in inattention or impulsivity.

4. Reticular Activating System
This is the major relay system among the many pathways that enter and leave the brain. A dopamine deficiency here can cause inattention, impulsivity, or hyperactivity.
These four regions interact with one another, so a deficiency in one region may cause a problem in one or more of the others. ADHD results from problems in one or more of these regions.


The human brain consists of a million neurons secreting dopamine. The cells are scattered in different regions, and each area is responsible for different functions, including movement, cognitive functions, memory, and management skills such as decision-making and planning which enables attention and learning.
Dopamine is also secreted when feeling pleasure and success as part of positive feedback regulation. This miraculous system enables us to strengthen our desired behavior and progress in achieving our goals. The system works in the neural pathways that create a sense of pleasure, motivation, and concentration. When we have an interest or desire to succeed in the task, we secrete dopamine and the secretion of dopamine increases our motivation and attention and of course the feeling of success.
The reinforcement system operates under the mechanism of positive feedback, dopamine secretion is enhanced in response to success, and as a result, we are highly motivated and focused on the task.

ADHD is associated with several neurophysiological deficits. More recent theoretical approaches integrate clinical symptoms and neuropsychological difficulties within a framework of specific brain dysfunctions: cognitive deficits may emerge from dysfunctions particularly in fronto-striatal or mesocortical brain networks dopaminergic system, while problems with reward processing may be associated with dysfunctions in the mesolimbic dopaminergic system (Sagvolden et al., 2005; Sonuga-Barke, 2005).

However, deficits in ADHD may already be seen in the resting brain, and a more fundamental neuronal network approach suggests that in ADHD particularly Default Mode-Network (DMN) activity (usually prominent during rest) may interfere with activity in neuronal networks engaged in task processing, leading to difficulties in state regulation and periodic attentional lapses (Sonuga-Barke and Castellanos, 2007; Castellanos and Proal, 2012). That is why neurofeedback in ADHD management is very effective with long-lasting results. 

Pharmacological interventions, particularly with stimulants such as methylphenidate and amphetamine sulfate, as well as non-stimulants like Atomoxetine, are highly effective in reducing ADHD symptoms (Banaschewski et al., 2006; King et al., 2006). What do ADHD medications do? In simple terms, they raise the level of norepinephrine within the brain. Stimulants work by causing the brain to synthesize more norepinephrine; non-stimulants by slowing the rate at which norepinephrine is broken down. Once the level is where it should be, the brain functions normally, and the individual becomes less hyperactive, inattentive, and/or impulsive. Once the drug wears off, the level falls — and symptoms return.
That’s because dopamine is hooked into the brain’s reward system. Having more dopamine circulating are feels like getting a bonus. It feels like that extra ten points on the test, right then. That means not only feel focused and content during the study but also to continue feeling that way. “The more you use it,” one student reported, “the more of it you want to use.”
The problem is that the good feelings, feeling in control and focused — these stop when the drug passes through your system a few hours later. The problem with drugs like Adderall and Ritalin is that you have to get more to feel better. That’s an addiction.
As report many researchers the long-term effectiveness is still questionable (Molina et al., 2009; van de Loo-Neus et al., 2011). In addition, side-effects, non-response, and prejudice have raised interest in non-pharmacological treatment options (Sonuga-Barke et al., 2013; Daley et al., 2014).


ADHD has been associated with certain clinical behavioral symptoms for many years. Recently, interest has been focused on ADHD, to determine whether certain abnormal EEG patterns correlate with clinical manifestations of ADHD.
Multiple studies have determined that compared to gender and age-matched controls, children with ADHD have greater theta activity. Other studies showed an increase in delta activity, coupled with decreased alpha and beta activities.

Additionally, abnormalities in the theta/beta ratio are one of the most significant measures of EEG alterations in ADHD.
Some researchers describe that in patients with ADHD theta/low beta ratio, and theta/alpha ratios were significantly increased.
Brain scans show that ADHD brains produce more low-frequency delta or theta brain waves than do neurotypical brains, and often show a shortage of the high-frequency beta brain waves linked to focus and impulse control.


Neurofeedback (NFB) as a non-pharmacological intervention for ADHD management utilizes cognitive behavioral therapeutic elements to gain access to and practice brain activity. Several organizations worldwide are looking into claims that neurofeedback works just as well as pharma when it comes to helping kids with ADHD. A course of Neurofeedback sessions can have the same effect as the ongoing intake of psychostimulant medications like Ritalin, for example. The benefit of Neurofeedback, however, is that ongoing treatment is rarely needed after the course length and medications can be avoided altogether.

The functioning of the brain and a person’s behavior are connected. Changes in behavior can change the brain, and changes in the brain can change behavior. Neurofeedback aims to change a person’s behavior by changing their brain. With neurofeedback, it is possible to train the brain in a positive, natural way. The goal of neurofeedback is to increase the brain’s capacity for beta waves while diminishing the frequency of delta and theta waves.

Most recently, clinical trials have garnered interesting results attesting to both the presence of unique EEG patterns in the ADHD brain and the efficacy of theta suppression/beta enhancement and theta suppression/alpha enhancement protocols on ADHD symptoms reduction (see different NFB protocols detailed description on “NFB Protocol” page of this website, which will continuously update with the arrival of new research data).

In theta/beta training the goal is to decrease activity in the theta band (4–8 Hz) and to increase activity in the beta band (13–20 Hz) of the electroencephalogram (EEG) which corresponds to an alert and focused but relaxed state. Thus, this training paradigm addresses tonic aspects of cortical arousal. Alpha enhancement protocol was more effective in suppressing omission errors.

Practicing the neurofeedback allows the trainee to change his brainwave frequency to the desired frequency while using his self-regulation system. Today in the market there are a lot of Home Use Neurofeedback Headset Devices that can be used for home-based training and treatment. The neurofeedback trainee is wearing a headset that measures his brain frequency in real-time while he is playing a computer game that responds to the sensor (practically it responds to the user’s brain waves). Only when the NFB trainee’s brainwave frequency is as expected for attention or relaxation, he will score in the video game he is playing. When the trainee achieves points (meaning he has reached the desired frequency in the brainwaves), he experiences success the reinforcement system is activated and the excretion of dopamine increases naturally. The excreted dopamine increases attention and the trainee gets motivated to maintain the right frequency of the brainwaves. The flexibility of the brain is reflected in its ability to remember the way it changed frequency and by learning to reach the desired frequency even when the computer game is no longer there. This allows the trainee to keep the achieved attitude in everyday life and decrease symptoms of ADHD. 

Neurofeedback has been introduced to treat ADHD and can improve attention levels and alleviate hyperactivity symptoms. The process provides a mechanism by which the patient can normalize the cortical activity profile by decreasing slow-wave activity and increasing fast-wave activity. It is expected that compensation of the dysfunctional electroencephalogram (EEG) enhances concentration and attention and increases the arousal level. Patients will learn how to enhance the desirable EEG frequencies associated with relaxed attention and how to reduce the undesirable frequencies that are associated with under- or over-arousal.

Key Electrode Sites for ADHD Neurofeedback

1. Fz (Frontal Midline):

Location: Frontal lobe, on the midline, 20% of the distance from the nasion (bridge of the nose).
Relevance: Associated with attention, impulse control, and executive function. Targeting Fz can help improve these areas.

2. Cz (Central Midline):

• Location: The scalp vertex, halfway between the nasion and inion and equally spaced between the left and right preauricular points (just above the ears).
• Relevance: Central region involved in motor control and general arousal regulation. Often used as a reference site.

Electrode Application Sites for ADHD Neurofeedback Management

3. C3 (Left Sensorimotor Cortex):

• Location: Left hemisphere, 20% of the distance from the midline along the central line.
• Relevance: Involved in motor control and coordination, relevant for reducing hyperactivity.

4. C4 (Right Sensorimotor Cortex):

• Location: Right hemisphere, analogous to C3 on the right side.
• Relevance: Also involved in motor control; balancing neural activity related to motor functions.

Neurofeedback Protocols for ADHD Management

The protocol involves training individuals to increase or decrease specific brainwave activity at the targeted locations to improve attention, impulse control, and executive function.

1. Theta/Beta Ratio Training

This protocol aims to balance theta (4-8 Hz) and beta (15-20 Hz) wave activity to improve attention and reduce impulsivity.

• Target Brainwaves: Theta (4-8 Hz) and Beta (15-20 Hz)
• Goal: Decrease theta activity and increase beta activity to improve cognitive control and reduce symptoms of ADHD.


1. Electrode Placement: Place electrodes at Fz and Cz (reference).
2. Baseline Recording: Record baseline theta and beta activity for 5-10 minutes.
3. Feedback Mechanism: Provide real-time feedback using visual (e.g., a game or moving bar) or auditory (e.g., tone) cues. Positive feedback occurs when theta decreases and beta increases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Utilize attention and impulse control scales along with follow-up qEEG to track progress.

2. SMR Training Protocol

This protocol focuses on increasing sensorimotor rhythm (SMR, 12-15 Hz) activity to enhance motor inhibition and reduce hyperactivity.

• Target Brainwaves: SMR (12-15 Hz)
• Goal: Increase SMR activity to enhance motor inhibition and promote calmness.


1. Electrode Placement: Place electrodes at C3 (left sensorimotor cortex) and Cz (reference).
2. Baseline Recording: Record baseline SMR activity for 5-10 minutes.
3. Feedback Mechanism: Provide real-time feedback using visual or auditory cues. Positive feedback is given when SMR activity increases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use attention and hyperactivity rating scales and follow-up qEEG to monitor changes.

3. Alpha/Theta Training

This protocol focuses on balancing alpha (8-12 Hz) and theta (4-8 Hz) waves to promote relaxation and improve cognitive control.

• Target Brainwaves: Alpha waves (8-12 Hz) and Theta waves (4-8 Hz)
• Goal: Increase alpha activity and decrease theta activity to enhance relaxation and attention.


1. Electrode Placement: Place electrodes at Fz and Cz (reference).
2. Baseline Recording: Record baseline alpha and theta activity for 5-10 minutes.
3. Feedback Mechanism: Use calming visual or auditory feedback. Positive feedback is provided when alpha increases and theta decreases.
4. Training Sessions: Conduct sessions for 20-30 minutes, 2-3 times per week, for 20-40 sessions.
5. Progress Monitoring: Use attention and relaxation scales along with follow-up qEEG to monitor changes.

Effectiveness of Neurofeedback for ADHD management

After 2 sessions of NFB 37%
After 10 sessions of NFB 60%
After 20 sessions of NFB 78%

Moreover, long-term follow-up studies with children successfully treated with neurofeedback have shown that the improved attention ability and memory improvement of these children remain stable long after treatment has ended. These children also learn easier manage their emotional status in different stressful situations. In other words, abnormal brainwave patterns are permanently normalized without the use of toxic drugs. It is also important to note that drugs do not improve the child’s ability to learn but neurofeedback does.
The research shows that neurofeedback works best for children over 6 years of age with normal or high intelligence. Usually, some 30-50 treatment sessions (30-45 minutes each) are required for successful treatment, at a rate of 2-3 sessions per week.

After 1-5 sessions 


After 6-10 sessions 


After 11-20 sessions  


After 20+ sessions 



Neurofeedback devices and systems are used for both medical and non-medical uses, and the dividing line between them may be thin. Non-medical application of neurofeedback can be considered primarily as personal improvement and conditioning for the brain and mind: to improve relaxation, attention, focus, concentration, and self-awareness, or as an adjunct to meditation, counseling, hypnosis, or achieving altered states of consciousness. It can be done without professional intervention. In cases where it is desired to relieve the conditions of a medical problem, professional help should be sought.

It is a fact that Neurofeedback systems are designed to allow the user to control a computer for recreational, educational, or entertainment purposes and are not medical instruments. You can find detailed information regarding indications, methods, and descriptions of different neurofeedback devices for home use here. However, if direct benefits are claimed for relaxation or relief from the symptoms of disorders, then the device is considered medical.

In the nonclinical embodiment, most of the same functions and capabilities are present, but they are presented in the context of an educational and recreational device. It is nonetheless true that the actual benefits may be essentially the same in both embodiments depending on how the user configures and applies the device, although the labeling and claims are different. The same instrument is being provided in both cases but with different intent.

The difference between the medical and non-medical embodiment of NFB devices lies primarily in the claims and the expectations and applications of the user.

For example, although neurofeedback can be used to improve attention and concentration, and this can be considered a personal improvement application, in cases of suspected or diagnosed Attention Deficit Hyperactivity Disorders the use of this procedure might be regarded as a medical procedure.

It may thus be argued that neurofeedback treatment intended to reduce the symptoms of ADHD, especially when the removal from stimulants (Ritalin, etc) is desired, that neurofeedback is being used in a medical context. However, if a parent, teacher, or counselor uses neurofeedback in a home or educational setting to educate a child on how to reach a state of relaxed attentiveness and improve academic success, the treatment may be considered education, not treatment.

Neurofeedback takes advantage of the brain’s ability to change itself through a process known as Neuroplasticity. It utilizes the same learning process that occurs whenever we acquire a new skill. The brain learns by forming connections between nerve cells and utilizing important pathways that connect different locations in the brain.

The more frequently you utilize these pathways the better the brain becomes at performing the associated task.

This type of learning is a type in which responses come to be controlled by their consequences. Quite simply, Neurofeedback offers the perfect learning conditions, since it facilitates awareness of when the brain is producing healthier brainwave patterns, reinforces the positive change, and multiple opportunities to provide practice during a training session.

You can choose and change electrode location.

Excellent Brain ADHD Neurofeedback Home Training Kit

Neurosky Puzzlebox Orbit Bundle EEG Headset

Biofeedback Home Use Device

Various modalities of biofeedback, including Electromyography (EMG), Heart Rate Variability (HRV), Temperature, and Galvanic Skin Response (GSR), can also be utilized in the management of Attention-Deficit/Hyperactivity Disorder (ADHD). EMG biofeedback helps individuals gain awareness and control over muscle tension, which can reduce physical restlessness and hyperactivity often associated with ADHD. HRV biofeedback trains individuals to regulate their heart rate variability, promoting autonomic balance and improving emotional regulation and stress resilience. Temperature biofeedback involves monitoring peripheral skin temperature to enhance relaxation and decrease physiological arousal, thereby aiding concentration and impulse control. GSR biofeedback measures the electrical conductance of the skin, which varies with sweat gland activity and can provide insights into stress and arousal levels. By learning to modulate these physiological responses, individuals with ADHD can improve their focus, reduce impulsivity, and manage stress more effectively, complementing traditional neurofeedback approaches.

EMG Biofeedback home-use device

Temperature Biofeedback home-use device



• Balanced Meals
• B Vitamins
• Zinc, Iron, and Magnesium
• Multivitamins/ Multimineral
• Picamilon

• Proteins

Foods rich in protein: lean beef, pork, poultry, fish, eggs, beans, nuts, soy, and low-fat dairy products — can have beneficial effects on ADHD symptoms. Protein-rich foods are used by the body to make neurotransmitters, the chemicals released by brain cells to communicate with each other. Protein can prevent surges in blood sugar, which increases hyperactivity.

• Balanced Meals

A well-balanced diet, including vegetables, complex carbohydrates, fruits, and plenty of protein, leads to behavior that tends to be more consistently under control.

• B Vitamins

Studies suggest that B vitamin supplements may improve IQ scores and reduce aggression and antisocial behavior in children who are B-vitamin deficient. Vitamin B-6 may also increase the brains’
levels of dopamine, a neurotransmitter that improves alertness.

• Zinc, Iron, and Magnesium

Zinc synthesizes dopamine and boosts the effects of some ADHD stimulant medications, such as Ritalin and Concerta; low levels of zinc correlate with inattention. Iron is also necessary for making dopamine; low levels of iron may cause cognitive deficits and severe ADHD. Adequate levels of magnesium keep the brain calm

  • Multivitamins/Multiminerals

Daily recommended a value of vitamins and minerals are important for any child, especially one with ADHD. A daily multivitamin/multimineral will ensure that he gets what he needs.

• Picamilon

A combination of the B-vitamin niacin and gamma-aminobutyric acid, picamilon improves blood flow to the brain. It’s been shown to improve alertness and attention, as well as reduce aggressive behavior.


It is rapidly becoming acknowledged that omega-3 fatty acids are good for the brain. Our requirements for EPA (Eicosapentaenoic Acid) and DHA (Docosahexaenoic Acid) change throughout life and so does the optimal amount of each fatty acid in our diet.

Children require DHA for growth and development, and the brain, CNS, and retina rely heavily on the adequate supply of DHA during growth in the womb.

Children continue to need DHA up until the age they start school, so if children under the age of five are taking an omega-3 supplement, it should contain DHA.

After the age of five, the development of the brain and CNS starts to reduce and the body’s need for DHA reduces. This is a good time to increase EPA in the diet, as studies show that EPA can help with childhood behavior and academic performance, as well as focus, attention, and reducing aggression.

Research has shown that EPA levels are under constant demand and low EPA levels in adolescents and adults correlate strongly with the development of mental health issues, including depression, dyslexia and dyspraxia, heart problems, joint and bone conditions, as well as neurodegenerative diseases such as MS and Parkinson’s.

The majority of the body’s needs can be met by using EPA-rich oils and eating fish, marine products, organic greens, and pastured animal products.

Recent studies suggest that ADHD children may be deficient in omega-3 and that a daily supplement may decrease ADHD symptoms while improving focus and cognitive function.

Studies have yet to determine an optimum dosage of omega-3, or fish oil, in children or adults with attention deficit hyperactivity disorder (ADHD). It is recommended that children four to six years of age start with a daily supplement of 500 mg of omega-3; for children seven years and older, 1000 mg.

It is determined that supplements with an EPA: DHA ratio of 2:1 with Vitamin E are the more effective for ADHD management (85% effectiveness with extension of effect over the following 6 months). Such a supplement is eVitamins Ultra Omega 3 – 750 mg with EPA/DHA  – 500/ 250 that is very effective for the management of ADHD symptoms.


Thirty minutes to a full hour of physical activity per day can make a huge difference in anyone’s mental and physical health, but especially for a child with ADHD. A child with ADHD who is regularly active may sleep better and experience fewer emotional outbursts at home and school. They may see benefits from the structure and organization of being part of a team and learning the rules of a new game or activity. Kids can also learn communication and social skills, increase coordination skills, and build up their self-esteem by being part of a sport or other activity. Because people with ADHD are at increased risk for developing depression, activities that involve exercise can lower their risk for depressive symptoms.
Sports offer lots of social interaction in addition to physical fitness. This helps kids with ADHD bond with their peers, and it helps get them out of their shell. A common issue with ADHD kids is to find something to help them gain confidence and self-esteem. They can use sports as a vehicle for making and having friends. Healthy activities like sports are better than sitting alone or in front of the television.
How do you know what sport will be best for your child? Ask him what he wants to do. Always support the choices and decisions of your child, because if he chooses to do something because he likes it then he will do it right and have a great time with it.
Many kids will see or try a lot of different athletic activities, whether at school, during camp, or in after-school programs. That gives them the chance to decide what appeals the most.
These are the best after-school activities for kids with ADHD: Swimming, Track and Cross-country, Horseback riding, Tennis, Baseball, Basketball, Gymnastics, Martial arts, Soccer, Wrestling, Archery, etc.
It’s important to remember that it might take several tries before your child finds the right sport or activity for them. It may be too much to try multiple things at once, so consider trying different sports or activities in different seasons and then letting your child decide what they like best. Never underestimate your child’s abilities because they have ADHD.
Many successful athletes like Michael Phelps, Simone Biles, Michael Jordan, and Terry Bradshaw have shared their experiences with the disorder. Artists like actor Jim Carrey, musician Adam Levine, and writer Jenny Lawson have gone on to create inspiring things while living with an ADHD diagnosis.

Anxiety Disorders

Neurofeedback for Anxiety Disorders

Anxiety is a normal and often healthy emotion. Anxiety is a natural human reaction that involves the mind and body. It serves an important basic survival function. Anxiety is an alarm system that is activated whenever a person perceives danger or threat. When a person feels threatened, under pressure, or are facing a stressful situation the body makes automatic fight-or-flight response. Because anxiety makes a person alert, focused, and ready to head off potential problems, a little anxiety can help us do our best in situations that involve performance and motivate to solve problems.
But anxiety that’s too strong and long-lasting can interfere with doing our best. Too much anxiety can cause people to feel overwhelmed, tongue-tied, or unable to do what they need to do. When a person regularly feels disproportionate levels of anxiety, then it is likely to cross the line from normal anxiety into the territory of an anxiety disorder and it might become a medical disorder. Anxiety Disorders are among the most common mental health issues and can be disabling, preventing a person from living a life that they want. But the good things are that Anxiety Disorders are highly treatable. Neurofeedback for anxiety disorders management is very effective with long-lasting results.

Symptoms of Anxiety Disorders

To treat anxiety it is necessary to timely recognize the symptoms and manifestations. The symptoms may not go away on their own and if left untreated, they can start to take over the person’s life. It’s important to seek support early if you’re experiencing anxiety.

Anxiety disorders often are a group of related conditions and symptoms may vary from person to person. One person can get panicky at the thoughts of some problem, others may struggle with a disabling fear or uncontrollable, intrusive thoughts, someone else may suffer from intense anxiety attacks that strike without warning. Yet another may live in a constant state of tension, worrying about anything and everything. But despite their different forms, all anxiety disorders illicit an intense fear or worry out of proportion to the situation at hand.

The symptoms of anxiety disorder often include the following:

  • restlessness, and a feeling of being “on-edge”;
  • uncontrollable feelings of worry;
  • increased irritability;
  • concentration difficulties;
  • sleep difficulties, such as problems in falling or staying asleep.

In addition to the primary symptom of excessive and irrational fear and worry, other common emotional symptoms of an anxiety disorder include:

  • Feelings of apprehension or dread;
  • Watching for signs of danger;
  • Anticipating the worst;
  • Trouble concentrating;
  • Feeling tense and jumpy;
  • Irritability;
  • Feeling like your mind’s gone blank.

But anxiety is more than just a feeling. As a product of the body’s fight-or-flight response, anxiety also involves a wide range of physical symptoms, including:

  • Pounding heart;
  • Sweating;
  • Headaches;
  • Stomach upset;
  • Dizziness;
  • Frequent urination or diarrhea;
  • Shortness of breath;
  • Muscle tension or twitches;
  • Shaking or trembling;
  • Insomnia

Because of these physical symptoms, anxiety sufferers often mistake their disorder for a medical illness. They may visit many doctors and make numerous trips to the hospital before their anxiety disorder is finally recognized.

Types of Anxiety Disorders

There are different types of anxiety. The most common is the follow.

Generalized Anxiety Disorder (GAD)

A person feels anxious on most days, worrying about lots of different things, for a period of six months or more.
If constant worries and fears distract a person from his day-to-day activities, or he is troubled by a persistent feeling that something bad is going to happen, this person may be suffering from generalized anxiety disorder (GAD). People with GAD are chronic worrywarts who feel anxious nearly all of the time, though they may not even know why.
Anxiety related to GAD often manifests in physical symptoms like chest pain, headache, tiredness, tight muscles, insomnia, stomach upset or vomiting, restlessness, and fatigue. Generalized anxiety can lead a person to miss school or avoid social activities. With generalized anxiety, worries can feel like a burden, making life feel overwhelming or out of control.

Social Anxiety Disorder

A person with a social anxiety disorder has an intense fear of being viewed negatively by others, being criticized, embarrassed or humiliated, even in everyday situations, such as speaking publicly, eating in public, being assertive at work or making small talk. It is also known as social phobia.

Social anxiety disorder can be thought of as extreme shyness. In severe cases, social situations are avoided altogether. Performance anxiety is the most common type of social phobia.

Phobias and Irrational Fears

A person with phobia feels unrealistic or exaggerated fear of a particular object, activity or situation that in reality presents little to no danger. He may go to great lengths to avoid the object of the fear. Unfortunately, avoidance only strengthens the phobia.
There are many different types of phobias. Common phobias include fear of animals (such as snakes and spiders), fear of flying, fear of heights, and etc.

Panic Attacks and Panic Disorder

A person has panic attacks, which are intense, overwhelming and often uncontrollable feelings of anxiety combined with a range of physical symptoms. Someone having a panic attack may experience shortness of breath, chest pain, dizziness, and excessive perspiration. Sometimes, people experiencing a panic attack think they are having a heart attack or are about to die.
If a person has recurrent panic attacks or persistently fears for more than a month, they’re said to have panic disorder. Panic disorder is characterized by repeated, unexpected panic attacks, as well as fear of experiencing another episode. Agoraphobia is an intense fear of panic attacks that causes a person to avoid going anywhere a panic attack could possibly occur.

Other Conditions Where Anxiety is Present

Obsessive-Compulsive Disorder (OCD)

A person has ongoing unwanted/intrusive thoughts and fears that cause anxiety and seem impossible to stop or control. Although the person may acknowledge these thoughts as silly, they often try to relieve their anxiety by carrying out certain behaviors or rituals.

For a person with OCD, anxiety takes the form of obsessions (bad thoughts) and compulsions (actions that try to relieve anxiety). For example, a fear of germs and contamination can lead to constant washing of hands and clothes.

Post-Traumatic Stress Disorder (PTSD)

Post-traumatic stress disorder (PTSD) can happen after a person experiences a traumatic or life-threatening event (e.g. war, assault, accident, disaster). Symptoms of PTSD can include difficulty relaxing, nightmares or flashbacks of the event, hypervigilance, startling easily, withdrawing from others, and avoidance of anything related to the event. PTSD is diagnosed when a person has symptoms for at least a month.

Separation Anxiety Disorder

While separation anxiety is a normal stage of development, if anxieties intensify or are persistent enough to get in the way of school or other activities, your child may have a separation anxiety disorder. Children with a separation anxiety disorder may become agitated at just the thought of being away from mom or dad and complain of sickness to avoid playing with friends or going to school.

Anxiety Disorder Risk Factors

Researchers are finding that both genetic and environmental factors contribute to the risk of developing an anxiety disorder. Although the risk factors for each type of anxiety disorder can vary, some general risk factors for all types of anxiety disorders include:

  • Temperamental traits of shyness or behavioral inhibition in childhood;
  • Exposure to stressful and negative life or environmental events in early childhood or adulthood;
  • A history of anxiety or other mental illnesses in biological relatives;
  • Some physical health conditions, such as thyroid problems or heart arrhythmias, or caffeine or other
    substances/medications can produce or aggravate anxiety symptoms.
  • Inflammation affects subcortical and cortical brain circuits associated with motivation and motor activity as well as cortical brain regions associated with arousal, anxiety, and alarm.
    There is a surprising specificity on the impact of inflammation on behavior. Researches show that inflammation not only occurs in depression but also in multiple other psychiatric diseases including anxiety disorders, bipolar disorder, personality disorders, and schizophrenia. These data suggest that inflammation is transdiagnostic in nature, occurring in subpopulations of patients within a number of psychiatric disorders. It is revealed that Yoga and alpha meditation increases parasympathetic outflow and consequently decrease inflammation.
    A physical health examination is helpful in the evaluation of a possible anxiety disorder.

Self Test for Anxiety

This Self-Assessment Test for Anxiety called the General Anxiety Disorders screening tool with the 7 questions (GAD-7). It can help you find out if you might have an anxiety disorder that needs treatment. It calculates how many common symptoms you have and, based on your answers, suggests where you might be on a scale, from mild to severe anxiety.

Hamilton Anxiety Rating Scale (HAM-A) for Rating by Clinicians

The Hamilton Anxiety Rating Scale (HAM-A) was one of the first rating scales developed to measure the severity of anxiety symptoms and is still widely used today in both clinical and research settings. The scale is intended for adults, adolescents, and children and should take approximately ten to fifteen minutes to administer.
The major value of HAM-A is to assess the patient’s response to a course of treatment, rather than as a diagnostic or screening tool. By administering the scale serially, a clinician can document the results of drug treatment, psychotherapy or neurofeedback.
The scale consists of 14 items; each defined by a series of symptoms, and measures both psychic anxiety (mental agitation and psychological distress) and somatic anxiety (physical complaints related to anxiety).

Brain Region and Anxiety Disorders from Neurofeedback Management Perspective

Normally, the brain manages our fear and anxiety without allowing them to interfere with our daily functioning. If there’s a nearby threat, different areas of the brain help us make sense of the threat by amplifying or quelling our anxiety and fear.
The various anxiety disorders involve many different areas of the brain. These areas reflect both the uniqueness of each of these disorders and the features that they have in common. Anxiety is the result of interaction between a number of different brain regions — a fear network. No one brain region drives anxiety on its own. Instead, interactions among many brain areas are all important for how we experience anxiety. Contemporary models of anxiety disorders have primarily focused on amygdala-cortical interactions. We only feel anxiety when signals from the amygdala overpower the cognitive brain, and into our consciousness. If you can rationalize that, then cognitive brain network overtakes and suppresses the emotional fear network.

Symptoms of anxiety disorders are thought to result in part from a disruption in the balance of activity in the emotional centers of the brain rather than in the higher cognitive centers.

The higher cognitive centers of the brain reside in the frontal lobe.

The prefrontal cortex (PFC) is responsible for executive functions such as planning, decision making, predicting consequences for potential behaviors, and understanding and moderating social behavior.

The orbitofrontal cortex (OFC) codes information, controls impulses and regulates mood. This region is crucial for the self-regulation of emotions and the relearning of stimulus-reinforcement associations.

Medial OFC is implicated in fear of extinction. Successful treatment of spider phobia is primarily accompanied by functional changes of the medial OFC.

In contrast to mOFC, anterolateral OFC (lOFC) has been associated with negative affects and obsessions and thus dysfunctional lOFC may underlie different aspects of certain anxiety disorders.

The ventromedial PFC (vmPFC) is involved in reward processing and in the visceral response to emotions.
In the healthy brain, these frontal cortical regions regulate impulses, emotions, and behavior via inhibitory top-down control of emotional-processing structures. Ventromedial prefrontal cortex to dampen the signals coming from the amygdala. Patients with damage to this brain region are more likely to experience anxiety since the brakes on the amygdala have been lifted.

The emotional-processing brain structures are referred to as the limbic cortex.
It includes the insular cortex and cingulate cortex. The limbic cortex integrates the sensory, affective, and cognitive components of pain and processes information regarding the internal bodily state. Dysfunction in the posterior cingulate cortex (PCC) may play an important role in anxiety psychopathology. 

A relative gray matter deficit was found in the right anterior cingulate cortex of patients with panic disorder (PD) compared with controls. Deactivation in PCC while listening to threat-related words alternating with emotionally neutral words. Dorsal anterior cingulate cortex (dACC), amplifies fearful signals coming from the amygdala. When anxious patients are shown pictures of fearful faces, the dACC, and amygdala ramp up their interaction, producing palpable anxiety. People without anxiety show little to no response.
A relative increase in gray matter volume was found also in the left insula of patients with panic disorder (PD) compared with controls.

The hippocampus is another limbic system structure. It has tonic inhibitory control over the hypothalamic stress-response system and plays a role in negative feedback for the hypothalamic–pituitary–adrenal (HPA) axis. Because all old memories depend on the hippocampus, this structure is involved in anxiety disorders that are generated by memories of painful experiences, such as post-traumatic stress disorder (PTSD). 

Studies do show that people who have suffered the stress of incest or military combat have a smaller hippocampus. This atrophy of the hippocampus might explain why such people experience explicit memory disturbances, flashbacks, and fragmentary memories of the traumatic events in question. Research shows that the hippocampus is also smaller in some depressed people. Stress, which plays a role in both anxiety and depression, may be a key factor here since there is some evidence that stress may suppress the production of new neurons (nerve cells) in the hippocampus.

The amygdala processes emotionally salient external stimuli and initiates the appropriate behavioral response. The amygdala is responsible for the expression of fear and aggression as well as species-specific defensive behavior, and it plays a role in the formation and retrieval of emotional and fear-related memories. The amygdala plays a central role in anxiety disorders. It warns us when danger is present in our environment and triggers the fear reaction and then the fight or flight reaction to get us out of it. 

Some studies have shown that monkeys with damage to the amygdala were unusually stoic in the face of scary stimulus, like a nearby snake.
The amygdala is implicated in generating fear responses, whereas cortical regions, specifically the mOFC and the vmPFC, are implicated in fear extinction. The central nucleus of the amygdala is heavily interconnected with cortical regions including the limbic cortex. It also receives input from the hippocampus, thalamus, and hypothalamus. It plays an important role in anxiety disorders that involve specific fears, such as phobias. Researchers have also observed that a group of very anxious children had a larger amygdala, on average than a group of normal children.

The amygdala act as a sensor of threats or a lack of control, communicating the need for a reaction to the hypothalamus. The hypothalamus, in turn, releases corticotropin-releasing hormone (CRH), which binds to the adenohypophysis that then produces the adrenocorticotrophic hormone (ACTH). ACTH binds to the adrenal cortex and adrenal medulla.

Researchers show that additional structures showing differential increases of gray matter were the left superior temporal gyrus, the midbrain, and the pons.

Additionally to the differences in the size of various brain structures, abnormally high or low activity in a particular region of the brain may be another kind of anomaly that results in anxiety disorders.

In addition to the activity of each brain region, it is also important to consider the neurotransmitters providing communication between these regions. 

Increased activity in emotion-processing brain regions in patients who have an anxiety disorder could result from decreased inhibitory signaling by gamma-amino-butyric-acid (GABA) or increased excitatory neurotransmission by glutamate. Well-documented anxiolytic and antidepressant properties of drugs that act primarily on monoaminergic systems have implicated serotonin, norepinephrine, and dopamine in the pathogenesis of mood and anxiety disorders.

Neurofeedback for Anxiety Disorders

Chronic anxiety and stress can increase catecholamine release, decrease growth hormones, and aberrantly activate immune and inflammatory cascades. As such, stress and anxiety can directly influence illness progression and can lead to irritable bowel syndrome exacerbations and increased cardiovascular risk. Increased frequency of general anxiety disorder has been found in people with asthma, cancer and chronic pain.

This comorbidity of anxiety with chronic illness can cause increased morbidity, mortality and decreased quality of life. Poorly controlled anxiety reduces the quality of life of many healthy individuals and is a key symptom of numerous neuropsychiatric and psychosomatic conditions.

For young children who perceive the world as a threatening place, a wide range of conditions can trigger anxious behaviors that then impair their ability to learn and to interact socially with others. Chronic and intense fear early in life affects the development of the stress response system and influences the processing of emotional memories.

Traditional treatment for anxiety includes psychological treatments such as cognitive therapy, cognitive behavioral therapy, exposure therapy, and self-help groups, as well as pharmacological modalities such as benzodiazepines and antidepressants. 

The most common anxiety treatment is psychotherapy. Psychotherapy, specifically Cognitive Behavioral Therapy (CBT), has been shown through research to be very effective in addressing the symptoms associated with anxiety.

Although anxiety medication may temporarily help with anxiety relief, they usually don’t address the root cause, as well as negatively reinforce avoidant behaviors instead of learning how to deal with stress and uncomfortable feelings. Medications just treat the symptoms and do not correct the source of the problem in the brain. Besides, many anxiolytics may cause addictions.

Neurofeedback for Anxiety disorders management is almost such effective as medication and helps reduce or eliminate the use of these medications.

Neurofeedback is all about teaching the brain to self-regulate and reduce or completely eliminate symptoms of anxiety disorders. Neurofeedback works at the subconscious level, which is control 90 to 95% of the time. Through a process of measurement and reinforcement, you learn to regulate your brainwave activity. Quite simply, you are reinforced for changing brainwaves at a subconscious level through the use of computers. Almost any brain, regardless of its level of function (or dysfunction), can be trained to function better. Research has shown that the long-term effects of neurofeedback in anxiety disorders are stable over time, in difference with the anxiolytic medication that has an effect short period after discontinuation.

The first step in Neurofeedback for anxiety disorders treatment is to have an evaluation and measurement of brainwaves in different areas of the brain and reveal their functioning and activity. EEG shows any brain areas where there is too much or too little activity. It could also show which areas are not communicating well with other areas. Certain brainwave patterns are associated with certain neuropsychological functions and conditions. In this aspect, very precision results may be obtained by qEEG brain mapping.

The qEEG analysis allows specialists to see exactly excessive activation in part of the fear network in the brain in anxiety disorders. Once we see the source of the problem, we target that area for change through neurofeedback brain training. This allows you to reshape your brain, not just mask your symptoms.

People suffering from anxiety disorders often have over-activation in brain regions such as the right insula, hippocampus, and amygdala. Theory today suggests that anxiety disorders involve deficits in cognitive skills, such as the control of attention and these cognitive aspects of the disorders are the most likely targets for neurofeedback for anxiety disorders management, whose effects are thought to be mediated mostly by cognitive skill enhancement.

From a neurofeedback management perspective, alpha band (8-12 Hz) asymmetry with prevalence in the left frontal cortex has emerged as the most prominent electroencephalographic (EEG) correlate of both anxiety and depression in right-handed people, followed by excessive band power in beta 1 (12-20 Hz) and beta 2 waves (20-30 Hz) in the right parietal lobe. There is also research that shows the association of anxiety disorders with High-Beta in conjunction with a decrease of Low Beta activity in temporal lobes
Neurofeedback for anxiety disorders enables people to consciously control changed activation of the brain, reducing their anxiety levels. Anxiety disorders neurofeedback management since first studied has used a wide enough range of EEG target frequency-bands and protocols. This includes frequencies in the alpha, beta and theta ranges, comprising almost half the typically measured spectrum of frequencies.

Healthy alpha asymmetry and regulation of alpha powers bands with the Neurofeedback have been successfully used to treat anxiety disorders and depression. Whereas increasing the power of sensorimotor rhythm (SMR) bands (12-15 Hz) over the sensorimotor cortex – has been used successfully to improve memory and sleep qualityIncrease the alpha/beta3 ratio (9.5-12 Hz/23-38 Hz) at parietal lobe lead to improvement of anxiety, depression, and sleep quality, as well as some improvement in executive functions. 

The combination of both protocols the SMR followed by alpha/beta3 ratio leads to an overall improvement in the symptoms reported by patients with anxiety disorders. The neurofeedback training protocol usually lasts 20 sessions, during which the individual is trained to increase beta 1 (12-15 Hz) at C4 with eyes open, followed by closed-eyes training designed to increase the alpha/beta 3 ratio (9.5-12 Hz/23-38 Hz) at P4. Researches show marked improvement in anxiety, depression, and sleep quality, as well as some improvement in executive functions.

EEG biofeedback protocols for the treatment of anxiety disorders have included alpha enhancement (e.g., Hardt & Kamiya, 1978), theta enhancement (e.g., Sittenfield et al., 1976), and alpha-theta enhancement (Peniston & Kulkosky, 1991) paradigms. Information regarding the location of sensors, frequency bands to be reinforced/inhibited, and type of feedback is provided below. 

Fp1 (Left Prefrontal Cortex):

Location: Frontal pole, 10% of the distance from the nasion (bridge of the nose).
Relevance: Involved in cognitive control and emotional regulation. Increasing alpha activity here can promote relaxation.

Fp2 (Right Prefrontal Cortex):

Location: Frontal pole, 10% of the distance from the Nasion.
Relevance: Associated with stress and anxiety responses. Training can help balance activity and reduce anxiety symptoms.

F3 (Left Dorsolateral Prefrontal Cortex – DLPFC):

Location: Frontal lobe, 30% of the distance from the nasion to the inion and 20% from the midline.
Relevance: Involved in cognitive control and emotional regulation. Enhancing alpha or SMR activity here can reduce anxiety.

F4 (Right Dorsolateral Prefrontal Cortex – DLPFC):

Location: Frontal lobe, analogous to F3 on the right side.
Relevance: Balancing activity with F3 can help regulate anxiety-related imbalances.

Cz (Central Midline):

Location: The scalp vertex, halfway between the nasion and inion and equally spaced between the left and right preauricular points (just above the ears).
Relevance: Often used as a reference or ground electrode in neurofeedback sessions, also involved in general arousal and relaxation.

Alpha enhancement protocol

  • Sensor location – O1, Oz (most common); C3, C4 (less common). 
  • Reinforced frequencies – 8-13 Hz.
  • Reinforced EEG pattern – Percentage of time patient produces alpha amplitudes above a threshold
    (e.g., 10 microvolts), or patient pro¬duction of alpha amplitudes above a set point
    (e.g., 19-21 microvolts).
  • Feedback modality – Auditory (tones and/or verbal feedback); eyes are typically closed during training.
  • Timing of sessions – Ranges from daily to weekly.

Theta enhancement protocol

  • Sensor location – Oz or C4.
  • Reinforced frequencies – Maintaining 3.5- to 7.5-Hz activity above a preset microvolt threshold, while suppressing 8- to 12-Hz pro-duction below a specified microvolt threshold
  • Feedback modality – Primarily auditory with eyes closed; visual feedback has been provided in instances where surface electromyographic (EMG) feedback is also provided.
  • Timing of sessions – Daily to weekly.

During the Neurofeedback procedure, the computer measures brainwave activity through the electrodes that placed on the scalp (watch video). When input falls into acceptable and healthy parameters, the system generates pleasant stimuli (audio or video feedback) to reinforce the change. Typically a movie plays consistently with a ding for each time a pre-set goal is achieved. This process is very pleasant, and since the brain craves this simple reinforcement, it typically begins changing within a few seconds of the commencement of the session. This operant conditioning is continued over numerous sessions of neurofeedback to reinforce transient changes in brain function using the patient’s own input as a guide. Through this process of reinforcement, the brain begins to regulate, and you see symptom reduction. With neurofeedback, it is possible to break open subconscious fears or worries and thus treat them. This is often the only way to gain access to the origin of anxiety/panic attacks.

Most people require two Neurofeedback sessions a week and the number of sessions varies based on the person and particular issue. While some people notice a reduction of symptoms after the first session, others may experience a gradual reduction of symptoms over time. The effects are often felt within the first few sessions; further training allows these to become permanent. Neurofeedback management of anxiety disorders calms the CNS so that a child, teen, or individual with anxiety can learn to manage stress in healthy ways.

Electrode Application Sites for Anxiety Neurofeedback Management

After obtaining stable results with the help of neurofeedback specialists people with anxiety can continue to perform neurofeedback management of anxiety disorders upon their needs with the help of home use neurofeedback devices. They are very simple to use and adapted for alpha and beta neurofeedback training, i.e. for relaxation and concentration. Additionally, the constant use of these devices will improve short-term and long-term memory, quality of sleep, and stress resistance.

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