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What are the underlying basis/mechanism for inattentiveness in ADHD?

What are the underlying basis/mechanism for inattentiveness in ADHD?

I have been exploring inattentive ADHD and I am really struggling to understand the difference between clinically significant inattentiveness in people with ADHD versus non-clinically significant inattentiveness.

Are there good explanations and evidence of neurological differences that can help me understand the pathways?

I am not sure whether a discussion about the differences in brain structure would be helpful in elucidating and elaborating the differences. I could not find anything relevant in this SE, the brain structure differences in hyperactivity has been discussed in this question but nothing really about inattentiveness in ADHD - Which brain areas are linked to Hyperactivity in ADHD?


Neurodevelopment of cognitive control in autism: adolescence to young adulthood

Description:
This study examines the development of cognitive control across adolescence into young adulthood and its relationship to functional outcomes in individuals with autism spectrum disorders (ASD) using functional magnetic resonance imaging (fMRI) and behavioral measures.

Funding:
National Institutes of Health / National Institute of Mental Health

The department received nearly $24 million in National Institutes of Health research funding in 2020. Psychiatric research at UC Davis School of Medicine ranks 14th out of 88 academic psychiatry departments nationwide.


The Not-So-Hidden Cause Behind the A.D.H.D. Epidemic

Between the fall of 2011 and the spring of 2012, people across the United States suddenly found themselves unable to get their hands on A.D.H.D. medication. Low-dose generics were particularly in short supply. There were several factors contributing to the shortage, but the main cause was that supply was suddenly being outpaced by demand.

The number of diagnoses of Attention Deficit Hyperactivity Disorder has ballooned over the past few decades. Before the early 1990s, fewer than 5 percent of school-age kids were thought to have A.D.H.D. Earlier this year, data from the Centers for Disease Control and Prevention showed that 11 percent of children ages 4 to 17 had at some point received the diagnosis — and that doesn’t even include first-time diagnoses in adults. (Full disclosure: I’m one of them.)

That amounts to millions of extra people receiving regular doses of stimulant drugs to keep neurological symptoms in check. For a lot of us, the diagnosis and subsequent treatments — both behavioral and pharmaceutical — have proved helpful. But still: Where did we all come from? Were that many Americans always pathologically hyperactive and unable to focus, and only now are getting the treatment they need?

Probably not. Of the 6.4 million kids who have been given diagnoses of A.D.H.D., a large percentage are unlikely to have any kind of physiological difference that would make them more distractible than the average non-A.D.H.D. kid. It’s also doubtful that biological or environmental changes are making physiological differences more prevalent. Instead, the rapid increase in people with A.D.H.D. probably has more to do with sociological factors — changes in the way we school our children, in the way we interact with doctors and in what we expect from our kids.

Which is not to say that A.D.H.D. is a made-up disorder. In fact, there’s compelling evidence that it has a strong genetic basis. Scientists often study twins to examine whether certain behaviors and traits are inborn. They do this by comparing identical twins (who share almost 100 percent of the same genes) with fraternal twins (who share about half their genes). If a disorder has a genetic basis, then identical twins will be more likely to share it than fraternal twins. In 2010, researchers at Michigan State University analyzed 22 different studies of twins and found that the traits of hyperactivity and inattentiveness were highly inheritable. Numerous brain-imaging studies have also shown distinct differences between the brains of people given diagnoses of A.D.H.D. and those not — including evidence that some with A.D.H.D. may have fewer receptors in certain regions for the chemical messenger dopamine, which would impair the brain’s ability to function in top form.

None of that research yet translates into an objective diagnostic approach, however. Before I received my diagnosis, I spent multiple sessions with a psychologist who interviewed me and my husband, took a health history from my doctor and administered several intelligence tests. That’s not the norm, though, and not only because I was given my diagnosis as an adult. Most children are given the diagnosis on the basis of a short visit with their pediatrician. In fact, the diagnosis can be as simple as prescribing Ritalin to a child and telling the parents to see if it helps improve their school performance.

This lack of rigor leaves room for plenty of diagnoses that are based on something other than biology. Case in point: The beginning of A.D.H.D. as an “epidemic” corresponds with a couple of important policy changes that incentivized diagnosis. The incorporation of A.D.H.D. under the Individuals With Disabilities Education Act in 1991 — and a subsequent overhaul of the Food and Drug Administration in 1997 that allowed drug companies to more easily market directly to the public — were hugely influential, according to Adam Rafalovich, a sociologist at Pacific University in Oregon. For the first time, the diagnosis came with an upside — access to tutors, for instance, and time allowances on standardized tests. By the late 1990s, as more parents and teachers became aware that A.D.H.D. existed, and that there were drugs to treat it, the diagnosis became increasingly normalized, until it was viewed by many as just another part of the experience of childhood.

Stephen Hinshaw, a professor of psychology at University of California, Berkeley, has found another telling correlation. Hinshaw was struck by the disorder’s uneven geographical distribution. In 2007, 15.6 percent of kids between the ages of 4 and 17 in North Carolina had at some point received an A.D.H.D. diagnosis. In California, that number was 6.2 percent. This disparity between the two states is representative of big differences, generally speaking, in the rates of diagnosis between the South and West. Even after Hinshaw’s team accounted for differences like race and income, they still found that kids in North Carolina were nearly twice as likely to be given diagnoses of A.D.H.D. as those in California.

Hinshaw, as well as sociologists like Rafalovich and Peter Conrad of Brandeis University, argues that such numbers are evidence of sociological influences on the rise in A.D.H.D. diagnoses. In trying to narrow down what those influences might be, Hinshaw evaluated differences between diagnostic tools, types of health insurance, cultural values and public perceptions of mental illness. Nothing seemed to explain the difference — until he looked at educational policies.

The No Child Left Behind Act, signed into law by President George W. Bush, was the first federal effort to link school financing to standardized-test performance. But various states had been slowly rolling out similar policies for the last three decades. North Carolina was one of the first to adopt such a program California was one of the last. The correlations between the implementation of these laws and the rates of A.D.H.D. diagnosis matched on a regional scale as well. When Hinshaw compared the rollout of these school policies with incidences of A.D.H.D., he found that when a state passed laws punishing or rewarding schools for their standardized-test scores, A.D.H.D. diagnoses in that state would increase not long afterward. Nationwide, the rates of A.D.H.D. diagnosis increased by 22 percent in the first four years after No Child Left Behind was implemented.

To be clear: Those are correlations, not causal links. But A.D.H.D., education policies, disability protections and advertising freedoms all appear to wink suggestively at one another. From parents’ and teachers’ perspectives, the diagnosis is considered a success if the medication improves kids’ ability to perform on tests and calms them down enough so that they’re not a distraction to others. (In some school districts, an A.D.H.D. diagnosis also results in that child’s test score being removed from the school’s official average.) Writ large, Hinshaw says, these incentives conspire to boost the diagnosis of the disorder, regardless of its biological prevalence.

Rates of A.D.H.D. diagnosis also vary widely from country to country. In 2003, when nearly 8 percent of American kids had been given a diagnosis of A.D.H.D., only about 2 percent of children in Britain had. According to the British National Health Service, the estimate of kids affected by A.D.H.D. there is now as high as 5 percent. Why would Britain have such a comparatively low incidence of the disorder? But also, why is that incidence on the rise?

Conrad says both questions are linked to the different ways our societies define disorders. In the United States, we base those definitions on the Diagnostic and Statistical Manual of Mental Disorders (D.S.M.), while Europeans have historically used the International Classification of Diseases (I.C.D.). “The I.C.D. has much stricter guidelines for diagnosis,” Conrad says. “But, for a variety of reasons, the D.S.M. has become more widely used in more places.” Conrad, who’s currently researching the spread of A.D.H.D. diagnosis rates, believes that America is essentially exporting the D.S.M. definition and the medicalized response to it. A result, he says, is that “now we see higher and higher prevalence rates outside the United States.”

According to Joel Nigg, professor of psychiatry at Oregon Health and Science University, this is part of a broader trend in America: the medicalization of traits that previous generations might have dealt with in other ways. Schools used to punish kids who wouldn’t sit still. Today we tend to see those kids as needing therapy and medicine. When people don’t fit in, we react by giving their behavior a label, either medicalizing it, criminalizing it or moralizing it, Nigg says.

For some kids, getting medicine might be a better outcome than being labeled a troublemaker. But of course there are also downsides, especially when there are so many incentives encouraging overdiagnosis. Medicalization can hurt people just as much as moralizing can. Not so long ago, homosexuality was officially considered a mental illness. And in a remarkable bit of societal blindness, the diagnosis of drapetomania was used to explain why black slaves would want to escape to freedom.


What has ADHD to do with schizophrenia?

Attention deficit hyperactivity disorder and schizophrenia are two different disorders that can profoundly affect a person’s life. While they have many differences, they also share some characteristics.

For this reason, some scientists have been looking into a possible link between them.

Attention deficit hyperactivity disorder (ADHD) is a chronic condition that involves behavioral symptoms, including inattentiveness, hyperactivity, and impulsiveness.

It is a neurodevelopmental disorder, and diagnosis usually takes place before the age of 12 years. Although symptoms tend to improve with age, some people continue to have symptoms as adults.

During childhood, ADHD is more common in males than in females, but the prevalence becomes relatively even in adulthood. It is possible that fewer girls receive a diagnosis because they show symptoms differently, meaning that caregivers or teachers may not notice them.

The Centers for Disease Control and Prevention (CDC) estimate that, in 2016, about 6.1 million children living in the United States had received a diagnosis of ADHD.

Schizophrenia is a long-term mental health condition that affects how a person thinks, feels, and behaves. It involves psychosis and other symptoms, including inattention.

Schizophrenia is slightly more common in males than females. Symptoms often begin between the ages of 16 and 30 years, but it can sometimes appear during childhood.

Around 1 percent of people in the U.S. have schizophrenia, according to the National Alliance on Mental Illness (NAMI).

Share on Pinterest A lack of focus is common with ADHD and with schizophrenia.

Various studies have identified some similarities between ADHD and schizophrenia and a possible overlap.

The conclusions of researchers include the following:

  • People with schizophrenia often have symptoms of other psychiatric disorders, including ADHD, in early adolescence.
  • Children and teenagers with ADHD may be 4.3 times more likely to develop schizophrenia as adults than people without ADHD.
  • Close relatives of people with ADHD may be more likely than second-degree relatives to receive a diagnosis of schizophrenia, suggesting that it may have a genetic component.

In 2013, a team of geneticists looking at ADHD in children and schizophrenia in adults found evidence of a “small but significant shared genetic susceptibility.”

The exact causes of ADHD and schizophrenia are not clear, but a combination of genetic and environmental factors may increase the risk of both.

A person with specific genetic features may develop symptoms if they encounter certain triggers, whether this exposure occurs before birth or during childhood and adolescence.

Factors that may contribute to ADHD include:

  • Genetic features: ADHD can run in families.
  • Environmental factors: Exposure to toxic materials , including as a fetus, may increase the risk.
  • Developmental issues: Problems with the central nervous system at important stages of development may result in ADHD.

Schizophrenia

Factors that may increase a person’s likelihood of developing schizophrenia include:

  • Genetic features: Genetic factors appear to play a role. Having a close family member with schizophrenia may increase the risk.
  • Brain development: Research shows that some individuals with schizophrenia have subtle differences in their brain structure.
  • Neurotransmitters: An imbalance between dopamine and serotonin, the chemical messengers in the brain, may have a connection with schizophrenia. Drugs that alter the levels of these chemicals appear to relieve schizophrenia symptoms.
  • Pregnancy and birth complications: A low birth weight, premature labor, or insufficient oxygen during birth are more likely to have affected people with schizophrenia.

ADHD and schizophrenia

Both conditions involve neurodevelopmental changes and can run in families. However, researchers do not yet know whether the same changes relate to both conditions or to what extent these underlying features overlap.

The risk factors for ADHD and schizophrenia are not the same, but they may overlap. For both conditions, some risk factors may affect a person before birth, while others come into effect during childhood and adolescence.

  • a family history of ADHD or another mental health disorder
  • exposure to certain substances while in the womb
  • a lack of specific nutrients, such as folate, zinc, magnesium, and polyunsaturated acids
  • psychosocial factors
  • maternal alcohol and drug use during pregnancy
  • preterm birth or low birth weight
  • maternal stress and anxiety during pregnancy
  • maternal smoking during pregnancy

Schizophrenia

There is growing evidence that some environmental factors can lead to neurodevelopmental problems that result in schizophrenia.

Possible environmental factors include :

  • exposure to certain substances, such as cannabis or lead, before birth
  • nutritional deficits, including low levels of folic acid and iron
  • rubella or other maternal infections during pregnancy
  • maternal stress during pregnancy
  • infections during childhood and adolescence
  • deficiency in iron and vitamin D resulting in decreased choline during pregnancy
  • an increase in immune system activity due to inflammation or autoimmune disease
  • taking mind-altering drugs as teenagers or young adults

Some researchers have suggested that there may be a link between low birth weight and mental illness, possibly including schizophrenia. However, they have noted that more evidence is necessary to confirm this.

The authors of a 2011 review concluded:

“It appears increasingly likely that a large portion, if not the majority, of schizophrenia cases can be accounted for by interactions between environmental and genetic factors and by other mechanisms involving the subtle interplay between environments and genes.”

ADHD and schizophrenia

Scientists believe that there is an overlap in the factors that can lead to ADHD and schizophrenia.

Genetic factors: A person who has a close relative with schizophrenia may be more likely to develop ADHD. Researchers say that up to 80 percent of cases of schizophrenia and between 60 and 80 percent of cases of ADHD may result from inheritance.

Changes in underlying brain mechanisms: Some neurological factors are common to both conditions.

Environmental influences: Exposure to specific influences before birth and during childhood appears to increase the risk of both conditions.

Shared history: People who have schizophrenia are more likely to have had a diagnosis of ADHD during childhood.

Does ADHD medication lead to schizophrenia?

Some people who use stimulant medication to relieve the symptoms of ADHD go on to experience symptoms of psychosis.

However, it is unclear whether using stimulants to treat ADHD increases the risk of schizophrenia or schizophrenia-type symptoms, specifically psychosis. These symptoms may have appeared without the use of stimulant medication.

Exposure to psychostimulant drugs does appear to increase the risk of psychosis. Psychosis that appears at a younger age is more likely to result from the use of psychostimulant drugs.

However, it remains unclear whether psychosis results from the use of the drugs or whether these individuals were already susceptible to psychosis.

In addition, the type of psychosis that people with ADHD experience tends to be different from that in people with schizophrenia as it involves brief mental changes rather than full hallucinations.

The symptoms of ADHD and schizophrenia are different, but they overlap in the area of inattention.

There are three different types of ADHD:

  • inattentive ADHD
  • hyperactive and impulsive ADHD
  • combined inattentive and hyperactive ADHD

Symptoms of inattentiveness include:

  • having a short attention span and getting easily distracted
  • making careless mistakes during activities
  • appearing not to listen
  • being unable to follow instructions and complete tasks
  • having problems with organizing tasks
  • being forgetful or frequently losing things
  • avoiding tasks that require mental effort

Symptoms of hyperactivity and impulsiveness include:

  • fidgeting constantly and being unable to sit still
  • being unable to engage quietly in leisure activities
  • lacking concentration
  • talking excessively
  • interrupting other people’s conversations or intruding on their activities
  • being restless
  • running excessively or climbing in inappropriate situations
  • acting without thinking
  • having little or no sense of danger

Not everyone who has ADHD will have hyperactivity as a symptom.

Schizophrenia

Doctors categorize the symptoms of schizophrenia as either positive, negative, or cognitive.

Positive symptoms include:

  • hallucinations
  • delusions, such as believing that the government is pursuing them
  • paranoid thoughts
  • agitated or excessive body movements
  • agitated or inappropriate behavior

Negative symptoms include:

  • social withdrawal
  • not caring about appearance and personal hygiene
  • reduced emotional expression
  • losing interest and motivation
  • trouble concentrating
  • changes in sleep habits
  • feeling unable to leave the house
  • a decrease in conversation and speaking

Cognitive symptoms include:

  • having confused or disorganized thoughts
  • an inability to understand information and make decisions
  • a lack of focus and attention
  • difficulty using learned information immediately

ADHD and schizophrenia

ADHD and schizophrenia may share some symptoms.

For example, attention problems affect both people with ADHD and people with schizophrenia.

However, some researchers have suggested that the type of inattention involved in ADHD may be different from that in schizophrenia and that the underlying neurological features are also different.

Thought disorders and psychosis can also occur in both schizophrenia and ADHD. People with schizophrenia often experience psychotic episodes, which can involve hallucinations, delusions, and disturbed thoughts.

Psychosis is not typical of ADHD, but around 10 percent of people with this condition experience psychotic symptoms. One theory is that the stimulant drugs that doctors prescribe to treat ADHD may trigger these psychotic symptoms.

Research has shown that some people whose genetic makeup puts them at high risk of schizophrenia will meet the criteria for a diagnosis of ADHD.

Some people with ADHD also have hyperactivity, but this is not a symptom of schizophrenia.

Doctors use different criteria to diagnose ADHD and schizophrenia.

There is no specific test to diagnose ADHD. A doctor will ask the individual about their medical history and symptoms and then conduct a medical examination to rule out other causes. The doctor will compare the symptoms with ADHD criteria and rating scales to make a diagnosis.

Diagnosis usually happens in childhood, often before the age of 12 years.

Schizophrenia

A doctor will ask the individual about their medical history and the symptoms that they are experiencing. They will also ensure that the symptoms are not due to medication, substance abuse, or another medical condition.

The doctor may carry out alcohol and drug screening or imaging studies, such as an MRI or CT scan.

If a doctor or mental health professional suspects schizophrenia, they will perform a psychiatric evaluation and compare the symptoms with diagnostic criteria for schizophrenia.

According to the NAMI, schizophrenia usually presents in males who are in their late teenage years or early 20s, while the onset tends to occur in females aged about 25–35 years.

ADHD and schizophrenia

A doctor will diagnose both ADHD and schizophrenia by comparing symptoms to those on a list in the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).

The DSM-5 classifies schizophrenia and ADHD as completely different conditions. Schizophrenia is a psychotic disorder, while ADHD is a neurobehavioral disorder.

There is no cure for ADHD or schizophrenia, but treatment can help relieve symptoms.

Treatment options include:

  • stimulant drugs to boost and balance brain chemical levels
  • nonstimulant medicines, which take longer to work than stimulants but can improve attention, focus, and impulsiveness
  • behavioral therapy to help people manage and change their behavior

Schizophrenia

Treatment options for managing the symptoms of schizophrenia include medications and psychosocial therapy.

Antipsychotic drugs: These aim to manage symptoms by controlling levels of the brain chemical dopamine.

Psychosocial therapy: This combines psychotherapy and social training to provide support, education, and guidance to people with schizophrenia.

Hospitalization: This may be necessary when a person’s symptoms are severe.

Electroconvulsive therapy (ECT): People whose symptoms do not respond to medication may benefit from ECT.

Similarities and differences

The treatment options for ADHD and schizophrenia are different. In both cases, doctors aim to manage symptoms rather than cure the condition.

For ADHD, a doctor may prescribe stimulants that increase dopamine levels in the brain. In some people, this type of drug may trigger psychosis.

For schizophrenia, a doctor will prescribe antipsychotic drugs that block the effect of dopamine.

ADHD and schizophrenia are different conditions, but they can occur together, and there may be some overlap between them. Some researchers believe that they share some underlying features. However, exactly how they relate to each other remains unclear.

Both conditions involve inattention, for example, but it is not apparent if this is the same kind of inattention or if it has the same cause.

ADHD tends to start at a younger age, and symptoms often improve with time, although they can continue into adulthood. Some people with ADHD go on to develop symptoms of schizophrenia, including psychosis.

Schizophrenia is usually a long-term condition. Treatment can relieve symptoms and enable many people to live a normal life, but relapse is likely if they do not follow their treatment plan. A person with schizophrenia may also have symptoms of ADHD.

ADHD is far more common than schizophrenia. Many people have ADHD and never develop schizophrenia. There is no evidence that one condition causes the other.


Philosophical context

According to the scientific philosophy of Popper, a scientific hypothesis must be testable and therefore open to falsification [6]. If a scientist can specify in advance an experiment that can falsify the hypothesis, then and only then is the hypothesis scientific. Popper argued that whilst it was easy to obtain confirmations or verifications for nearly every theory when one looked for a confirmation, a 'good' scientific theory forbade certain things to occur. A genuine test of a theory should lead to an attempt to refute it [7]. Popper suggested Einstein's theory of gravitation as an example of a theory that clearly satisfied the criterion of falsifiability. In contrast, he proposed that the two psycho-analytic theories of Freud and Adler were examples of theories that were non-testable and irrefutable (p.37) [7]. As Chalmers writes, "Usually, potential falsifiers will involve the specification of an experimental set-up designed to test a theory together with the description of an outcome inconsistent with the prediction of the theory" (p.68) [8]. If a current theory is proved false, then new theories will be developed that take into account the discriminating case. For a hypothesis to be testable, it must be well-described and precise, so as to allow for falsification and replication [6].

Other philosophers have argued that in practice, when anomalous (non-predicted) results are reported and accepted as real data, rather than abandoning that theory, scientists are more likely to modify their existing hypotheses to align with the new findings (or alternatively ignore the new results) [9]. According to Lakatos, a scientific theory (or "research program") has a "hard core", a hypothesis central to that theory. The hard core is stubbornly defended against criticism and refutation by "auxiliary hypotheses", produced in the light of new findings. Research programs fall into two types: progressive and degenerative. A degenerative program is marked by a lack of new facts and by lack of growth. In comparison, the progressive program generates new facts, new hypotheses and is the subject of growth. Scientific progression occurs when the auxiliary hypotheses of the progressive program aid the discovery of new knowledge, whilst the degenerative program is abandoned [9]. It has also been argued that new scientific findings improve the current set of hypotheses until there comes a point in time where a fresh and new hypothesis comes into being that starts a paradigm shift in thinking about that scientific topic [10].

The strength and health of the field of ADHD behavioural research (and ADHD genetic research, as a concomitant), is dependent on proposed hypotheses being made testable and falsifiable. ADHD is currently a behavioural construct, defined by behavioural dysfunction rather than by a biological marker [11]. It is a complex, multifactorial disease entity and as such, it is important that testable hypotheses of dysfunction are produced [12].


Research support

The FDA provided marketing authorization for the prescription-only device to the biotechnology company NeuroSigma through its "de novo" premarket review pathway, which is used for new low- to moderate-risk devices with no existing market equivalent. Researchers from the Univer­sity of California, Los Angeles (UCLA), including one clinical and two educational psychologists, conducted the clinical trial with 62 children, ages 8 to 12, who had moderate to severe ADHD. Each participant received four weeks of at-home treatment using either the eTNS system or a placebo device.

Researchers administered two assessments on a weekly basis: the ADHD-IV Rating Scale (ADHD-RS), a parent questionnaire that evaluates a child’s behavior, and the Clinical Global Impressions (CGI) scale, which measures symptom severity.

Compared with the placebo group, children who used the eTNS device showed statistically significant improvements in ADHD symptoms, with average ADHD-RS scores dropping about 31 percent. Children in the placebo group experienced an average decrease of about 18 percent. Slightly over half of participants in the intervention group showed improvement that was clinically meaningful, defined as a score of "much improved" or "very much improved" on the CGI Improvement scale.

The research team also collected electroencephalography (EEG) data before and after administering treatment. Children who used the eTNS system displayed increased activity in the middle and right frontal regions of the brain, which help regulate attention and emotions.


In terms of treatment effect size, the behavioral changes observed are similar to those rendered by nonstimulant medications for ADHD, such as atomoxetine and guanfacine, but less pronounced than the effects of stimulant medications, says psychologist Sandra Loo, PhD, of UCLA’s Semel Institute for Neuroscience and Human Behavior, a co-author of the clinical trial.

"There’s a great demand for nonpharmacological ADHD treatments, so we’re excited about potentially offering empirically supported alternatives," she says, adding that around 30% of children taking stimulants for ADHD experience undesirable side effects—such as weight loss or insomnia—or do not respond to the drugs.

In the present study, more than half of the children using eTNS experienced side effects including fatigue, headache and increased appetite. Compared with the control group, these patients also showed significant changes in weight and pulse, with an average gain of about one kilogram and an increase of 10 beats per minute after four weeks, but no children withdrew from the study due to adverse side effects.

"This study shows that the eTNS device is relatively safe, efficacious and has a lot of promise," says Ronald T. Brown, PhD, a child psychologist and dean of the School of Health Sciences at the University of Nevada, Las Vegas, who was not involved in the clinical trial. "But these are preliminary results with a small number of participants that raise a number of additional questions."

For example, Brown, who was part of the AAP committee that developed the latest treatment guidelines for ADHD, says psychologists need more information about how the new device compares with traditional ADHD treatments, such as stimulant medications and behavior management. He also says it’s important to study the durability of the observed effects and whether improvements persist after a limited course of treatment.


Living With

What quick tips can be offered to help adults with ADHD Inattentive type cope with the day-to-day activities of life?

The following are tips for adults with ADHD, inattentive type, for self-regulating (controlling one’s behaviors, emotions and thoughts), and regaining control over many daily tasks:

To help cope with distractions:

  • Request a quiet or private work area move to an unused conference space or other area where there are few distractions or noise.
  • Wear earphones with soft music to cover up office noise.
  • Redirect phone calls to voice mail and return phone calls at set times throughout the day.

To help stay organized:

  • Set aside the first 10 to 20 minutes of your day to organize your tasks for the day.
  • Work on and complete one task at a time before moving on to the next one.
  • Keep a to-do list in a notebook or on your phone.
  • Put appointments in your phone and set up alarm reminders before the event.
  • Mark deadlines on calendars as a visible reminder tool.
  • Use daily planners or online task organizers to help keep track of tasks and events.
  • Use sticky pads to write important notes and place them in appropriate areas where they will be seen.
  • If a filing system is needed, use labels or color-coded folders or tabs.
  • Set up online automatic payment of bills so you don’t forget to pay them.

To prevent losing or misplacing important items:

  • Identify specific areas to place specific items and get into the routine of only placing items in these designated spots.

To help stay focused:

  • Take handwritten notes during meetings or tape record as a backup and to fill in details.
  • Break up larger tasks into smaller ones. Reward yourself when each task is completed.
  • Take short breaks to prevent boredom – take a short walk, do some stretches, drink some water.

Last reviewed by a Cleveland Clinic medical professional on 09/25/2019.

References

  • National Institute of Mental Health. Attention Deficit Hyperactivity Disorder. Accessed 10/4/2019.
  • Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD). Diagnosis of ADHD in Adults. Accessed 10/4/2019.
  • Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD). Cognitive-Behavioral Treatment. Accessed 10/4/2019.
  • Centers for Disease Control and Prevention. What is ADHD? Accessed 10/4/2019.
  • American Psychiatric Association. What is ADHD? Accessed 10/4/2019.
  • A.D.D. Resource Center. DSM-5 Criteria for ADHD. Accessed 10/4/2019.
  • Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD). Workplace issues. Accessed 10/4/2019.

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What dosage of phentermine is best for ADHD?

Due to the fact that phentermine hasn’t been formally evaluated for the treatment of ADHD, it is unknown as to what dosage would be optimal for this indication. Based on the fact that lower doses of phentermine (e.g. 20 mg) exert a modest central effect and don’t really alter dopaminergic transmission, it may be that a high dose is necessary for ADHD. In other words, if phentermine were to be used for ADHD, it is likely that a high dose such as 37.5 mg (or even greater) would be necessary to combat symptoms.

Compared to lower doses, administering phentermine at high doses should exert a more significant central effect, as well as noticeably modulate dopamine. In theory, this should help alleviate symptoms of ADHD caused by deficits in catecholaminergic signaling. The only problem with using a high dose (e.g. 37.5+) is that the peripheral effect will be potent enough to cause serious adverse effects.

Using a high dose of phentermine over an extended duration may significantly increase risk of a cardiac events, ischemic attack, and mortality. There are no formal dosing guidelines of phentermine for ADHD, and if the drug were to be utilized for ADHD, dosage optimization via guidance of a psychopharmacologist should be required. That said, extremely low doses are unlikely to have a significant effect upon ADHD symptoms unless peripheral dysfunction is heavily implicated as a causal underpinning.


Attention-Deficit/Hyperactivity Disorder (ADHD)

At Niagara Neuropsychology, we offer 3 levels of assessment for ADHD/ADD for those age 5 and up (including adults). These were developed in order to be able to provide the most comprehensive assessment possible and to ensure that even those with less financial means can obtain an adequate assessment and diagnosis.

Below are descriptions of each level of ADHD/ADD assessment from the top tier ADVANCED ADHD/ADD Assessment, middle tier INTERMEDIATE ADHD/ADD Assessment, and lowest tier BRIEF ADHD/ADD Assessment. Note that even the BRIEF ADHD/ADD Assessment is a more thorough assessment than what is obtained from most psychiatrists, pediatricians, and family physicians, and most psychologists.

TOP TIER—ADVANCED ADHD/ADD ASSESSMENT:

  • Most in-depth ADHD/ADD assessment available
  • A 60-minute intake interview with Dr. Friesen (charged separately at $195)
  • Parent/teacher/self-rating measures of executive functions (

MIDDLE TIER—INTERMEDIATE ADHD/ADD ASSESSMENT:

  • Detailed, thorough multimodal ADHD assessment
  • A 60-minute intake interview with Dr. Friesen (charged separately at $195)
  • Parent/teacher/self-rating measures of executive functions (

LOWEST TIER—BRIEF ADHD/ADD ASSESSMENT:

  • Although brief relative to the Intermediate and Full ADHD Assessments, this assessment is more thorough than ADHD assessments available via family physicians, pediatricians, psychiatrists, and most psychologists
  • A 60-minute intake interview with Dr. Friesen (charged separately at $195)
  • Parent/teacher/self-rating measures of executive functions (

Attention-Deficit/Hyperactivity Disorder (ADHD)

Attention-deficit hyperactivity disorder (ADHD) is the current term for a specific developmental disorder seen in both children and adults that is comprised of deficits in behavioural inhibition, sustained attention and resistance to distraction, and the regulation of one’s activity level to the demands of a situation (hyperactivity or restlessness). This disorder has had numerous different labels over the past century, including hyperactive child syndrome, hyperkinetic reaction of childhood, minimal brain dysfunction, and attention deficit disorder (with or without hyperactivity).

ADHD is one of the most common neurodevelopmental disorders of childhood and adolescence. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5: APA, 2013), ADHD is marked by “a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development…several inattentive or hyperactive-impulsive symptoms were present prior to age 12 years…clear evidence that the symptoms interfere with, or reduce the quality of, social, academic, or occupational functioning.” (APA, 2013, p. 59-60). According to the DSM-5, population surveys across most cultures find the prevalence of ADHD to be approximately 5% in children (and 2.5% in adults). ADHD is associated with numerous negative outcomes including reduced school performance/academic attainment, poor occupational attainment, social rejection, the development of conduct disorder/antisocial personality disorder, incarceration, substance abuse, physical injuries, traffic accidents/violations, obesity, and negative family relationships (APA, 2013). Thus, early and accurate identification and treatment of ADHD is of enormous societal importance.

How Is ADHD Diagnosed?

The FDA recently approved quantitative EEG (qEEG) for improving that accuracy of ADHD diagnoses (click here and here to learn more). At Niagara Neuropsychology we use qEEG in addition to clinical interviews, behavioural rating scales, and neuropsychological testing to provide the most up-to-date and accurate diagnostic process.

There are numerous reasons why a child, adolescent, or adult may have symptoms or behaviours consistent with ADHD. These include sleep disorders, bipolar disorder, depression, anxiety (e.g., Generalized Anxiety Disorder or GAD, Obsessive-Compulsive Disorder or OCD, Posttraumatic Stress Disorder or PTSD), head injuries (e.g., concussions or more significant traumatic brain injuries or TBI), Tourette’s syndrome, thyroid disease, nutritional deficiencies, and learning disorders.

When a patient does have ADHD, in addition to the subtypes based on behaviours outlined in the DSM-5, there are also a number of subtypes of ADHD based on qEEG. These include excessive slow wave (e.g., theta) activity in the front part of the brain (the vast majority of ADHD patients fall into this category) or excessive fast wave (beta) activity (a substantial but minority of ADHD patients fall into this category).

The effective treatment for these two subtypes is quite different. For example, the use of a stimulant (e.g., Ritalin or Adderall) for those with the high beta subtype may over activate the brain and lead to worsening of symptoms, including increased anxiety, appetite suppression, and insomnia. On the other hand, a stimulant is more likely to be effective in those patients with excessive slow wave activity (e.g., theta) in the frontal lobe. Similarly, the neurofeedback training for these two subtypes will be very different.

WHAT ABOUT TREATMENT?

Here is a brief clip from CNN on neurofeedback training for those with ADHD and anxiety:

*Partially adapted from ISRN.org

The International Society for Neuroregulation & Research (ISNR.org) regularly updates a comprehensive bibliography of neurofeedback research studies on various disorders including ADHD that can be accessed HERE.

Similarly, Applied Psychophysiology Education (APEd) has a comprehensive list of abstracts for neurofeedback research (including on ADHD) that you can access HERE.

EEG biofeedback or neurofeedback is a safe and effective treatment of ADHD that improves the core symptoms for patients diagnosed with ADHD. A meta-analysis by Arns et al. (2009) of ten well-controlled studies combined with an additional five prospective pre/post design studies. This meta-analysis concluded that “neurofeedback treatment for ADHD can be considered “Efficacious and specific” (the highest possible ranking) with a large effect size for inattention and impulsivity and a medium effect size for hyperactivity” [p. 180].

More recently, Narimani et al., (2018) published another meta-analysis of nine studies on the effectiveness of neurofeedback and ADHD symptoms in adults. They concluded “Based on the results of this meta-analysis, neurofeedback treatment was found to have a large effect in reducing ADHD symptoms in adults with attention deficit/hyperactivity disorder.” Click HERE for the article.

In October 2012, the company that maintains the Amer­i­can Academy of Pediatrics’ ranking of research support for psychosocial treatments awarded neurofeedback the highest level of evidence-based support for the treatment of ADHD [PracticeWise, 2012].

For a more layperson’s review of neurofeedback and ADHD, click HERE to read Dr. Vicent Monastra’s short article in ADDitude Magazine.

For a recent summary of one study that randomly assigned children and adolescents with ADHD to receive either 40 sessions of neurofeedback or computerized brain training, click HERE. Note they found the neurofeedback group had significantly more symptom reduction.

For another example of a randomized controlled trial that compared the effectiveness of neurofeedback to stimulant medication (i.e., methylphenidate or Ritalin), click HERE. This study found that neurofeedback was as effective as stimulant medication. The authors concluded “Neurofeedback was as effective as methylphenidate at treating the attentional and hyperactivity symptoms of ADHD, based on parental reports…This supports the use of neurofeedback as an alternative therapy for children and adolescents with ADHD“.

For a recent meta-analysis on the long-term effectiveness of neurofeedback for the treatment of ADHD, see the February 2018 issue of the journal European Child & Adolescent Psychiatry–Sustained Effects of Neurofeedback in ADHD: A Systematic Review and Meta-Analysis. The authors found the effects of neurofeedback were maintained for 6 to 12 months after training ended. They concluded, “Our meta-analytic results of NF treatment follow-up suggest that there are sustained symptom reductions over time in comparison with non-active control conditions. The improvements seen here are comparable to active treatments (including methylphenidate) at a short-term follow-up… As such, NF can be considered a non-pharmacological treatment option for ADHD with evidence of treatment effects that are sustained when treatment is completed and withdrawn.

Krepel et al., (2020) reported on a multi-centre effectiveness trial (across 5 clinics) of qEEG informed neurofeedback in ADHD patients. They found neurofeedback resulted in a 55% remission rate(i.e., no longer meeting diagnostic criteria for ADHD), compared to

33% remission rates in mutlicentre trials for ADHD medication. This study found that higher rates of hyperactivity predicted a poorer treatment response. 70% of ADHD patients had at least a 50% reduction in symptoms and 85% had a least a 25% reduction in symptoms. Click HERE for the article.

The International Society for Neurofeedback and Research (ISNR) recently commissioned a comprehensive review of NFB’s evidence-base for the treatment of ADHD. This review documents that not only has neurofeedback been found to be superior to a variety of experimental control group conditions, but also in three studies neurofeedback was found to be equivalent to stimulant medication in treating the core symptoms of ADHD [Pigott et al., 2013].

Furthermore, the review found five studies that assessed whether or not neurofeedback resulted in sustained benefits after treatment ended, including two studies with two-year follow-up assessments. In each of these follow-up assessments, the gains from neurofeedback were maintained after treatment had ended and in one study had increased further during the two-year follow-up such that half of the children no longer meet the diagnostic criteria for ADHD.

The MTA Cooperative Study’s follow-up results, the largest ever treatment effectiveness study for ADHD, documented that the commonly reimbursed treatments of stimulant medication and behaviour therapy failed to result in sustained benefit for the vast majority of ADHD children who received them. This multi-centered NIMH-funded study compared systematic medication management (SMM), multi-component behaviour therapy (BT), combined SMM/BT, and usual community care (CC) groups to evaluate their effectiveness in treating ADHD [Jensen et al., 2007 Molina et al., 2009]. Despite the initial superiority of SMM and combined SMM/BT treatments, these follow-up analyses found that after 2, 6, and 8 years the four treatment groups did not differ on any outcome measure. Most discouragingly, the researchers report that “the MTA participants fared worse than the local normative comparison group on 91% of the variables tested.” These researchers conclude by stating that “Innovative treatment approaches targeting specific areas of adolescent impairment are needed” [Molina et al., 2009, p. 484].

In contrast to the positive reports of sustained benefit following termination of neurofeedback treatment, stimulant medications’ beneficial effects commonly cease when the medication is stopped, and as found in the MTA study, the authors concluded that there was no evidence to support the “long-term advantage of medication treatment beyond 2 years for the majority of children” [Molina et al., 2009, p.497].

Finally, the recent published follow-up findings from the NIMH-funded Preschool Attention-Deficit/Hyperactivity Disorder Treatment Study (PATS) found results virtually identical to those from the MTA study. These researchers report that “medication status during follow-up, on versus off, did not predict symptom severity” and despite optimal parent training and systematic medication management at the study’s outset, the authors concluded that “ADHD in preschoolers is a relatively stable diagnosis over a 6-year period. The course is generally chronic, with high symptom severity and impairment, in very young children with moderate-to-severe ADHD, despite treatment with medication. Development of more effective ADHD intervention strategies is needed for this age group” [Riddle et al., 2013, p. 1].

Neurofeedback is one such “innovative” and “more effective” treatment for ADHD with proven effectiveness targeting the specific areas of impairment that are essential to its diagnosis: 1) inattention, 2) impulsivity, and 3) hyperactivity. Unlike the findings in both the MTA Cooperative and PATS studies, neurofeedback has been found to result in sustained improvement in ADHD’s core symptoms after the end of treatment.

For example, Van Doren et al., (2019) conducted a meta-analysis and found that while stimulant medication (e.g., Ritalin) resulted in somewhat stronger effects than neurofeedback while during treatment (i.e., large effect size), the neurofeedback effects lasted at least 6-months after the treatment ended and the effect of neurofeedback actually INCREASED after the treatment ended. For exampled, the strength of the neurofeedback training at reducing inattention was considered “medium” (i.e., a medium effect size) at the end of treatment. HOWEVER, the effect increased to “large” (i.e., a large effect size) at 2 to 12 months after treatment stopped. Click HERE to see the original study.

For a recent 2019 review of the evidence on neurofeedback in the treatment of ADHD, click HERE. The authors concluded:

Based on meta-analyses and (large multicenter) randomized controlled trials, three standard neurofeedback training protocols, namely theta/beta (TBR), sensori-motor rhythm (SMR), and slow cortical potential (SCP), turn out to be efficacious and specific. However, the practical implementation of neurofeedback as a clinical treatment is currently not regulated…We conclude that neurofeedback based on standard protocols in ADHD should be considered as a viable treatment alternative and suggest that further research is needed to understand how specific neurofeedback protocols work. Eventually, we emphasize the need for standard neurofeedback training for practitioners and binding standards for use in clinical practice.”

Below is a video by Dr. Ed Hamlin on the evidence for neurofeedback for ADHD:

*The following is partially adapted from Dr. Russell Barkley’s ADHD Factsheet:

MAJOR CHARACTERISTICS: The predominant features of this disorder include:

  • 1. Impaired response inhibition, impulse control, or the capacity to delay gratification. This is often noted in the individual’s inability to stop and think before acting to wait one’s turn while playing games, conversing with others, or having to wait in line to interrupt their responding quickly when it becomes evident that their actions are no longer effective to resist distractions while concentrating or working to work for larger, longer-term rewards rather than opting for smaller, more immediate ones and inhibiting the dominant or immediate reaction to an event, as the situation may demand.
  • 2. Excessive task-irrelevant activity or activity that is poorly regulated to the demands of a situation. Individuals with ADHD in many cases are noted to be excessively fidgety, restless, and “on the go.” They display excessive movement not required to complete a task, such as wriggling their feet and legs, tapping things, rocking while seated, or shifting their posture or position while performing relatively boring tasks. Younger children with the disorder may show excessive running, climbing, and other gross motor activity. While this tends to decline with age, even teenagers with ADHD are more restless and fidgety than their peers. In adults with the disorder, this restlessness may be more subjective than outwardly observable, although with some adults they remain outwardly restless as well and report a new to always be busy or doing something and being unable to sit still.
  • 3. Poor sustained attention or persistence of effort to tasks. This problem often arises when the individual is assigned boring, tedious, protracted, or repetitive activities that lack intrinsic appeal to the person. They often fail to show the same level of persistence, “stick-to-it-tiveness,” motivation, and willpower of others their age when uninteresting yet important tasks must be performed. They often report becoming easily bored with such tasks and consequently shift from one uncompleted activity to another without completing these activities. Loss of concentration during tedious, boring, or protracted tasks is commonplace, as is an inability to return to their task on which they were working should they be unexpectedly interrupted. Thus, they are easily distracted during periods when concentration is important to the task at hand. They may also have problems with completing routine assignments without direct supervision, being unable to stay on task during independent work.

These are the three most common areas of difficulty associated with ADHD. However, research is suggesting that those with ADHD, particularly the subtypes associated with impulsive behavior (see below), may also have difficulties in the following areas of psychological functioning as well:

  • 1. Remembering to do things, or working memory. Working memory refers to the capacity to hold information in mind that will be used to guide one’s actions, either now, or at a later time. It is essential for remembering to do things in the near future. Those with ADHD often have difficulties with working memory and so are described as forgetful around doing things, unable to keep important information in mind that they will need to guide their actions later, and disorganized in their thinking and other activities as they often lose track of the goal of their activities. They may often be described as acting without hindsight or forethought, and being less able to anticipate and prepare for future events as well as others, all of which seem to be dependent on working memory. Recently, research suggests that those with ADHD cannot sense or use time as adequately as others in their daily activities, such that they are often late for appointments and deadlines, ill-prepared for upcoming activities, and less able to pursue long-term goals and plans as well as others. Problems with time management and organizing themselves for upcoming events are commonplace in older children and adults with the disorder.
  • 2. Delayed development of internal language (the mind’s voice) and rule-following. Research has lately been suggesting that children with ADHD are significantly delayed in the development of internal language, the private voice inside one’s mind that we employ to converse with ourselves, contemplate events, and direct or command our own behavior. This private speech is absolutely essential to the normal development of contemplation, reflection, and self-regulation. Its delay in those with ADHD contributes to significant problems with their ability to follow through on rules and instructions, to read and follow directions carefully, to follow through on their own plans, rules, and “dolists,” and even to act with legal or moral principles in mind. When combined with their difficulties with working memory, this problem with self-talk or private speech often results in significant interference with reading comprehension, especially of complex, uninteresting, or extended reading assignments.
  • 3. Difficulties with regulation of emotions, motivation, and arousal. Children and adults with ADHD often have problems inhibiting their emotional reactions to events as well as do others of their age. It is not that the emotions they experience are inappropriate, but that those with ADHD are more likely to publicly manifest the emotions they experience than would someone else. They seem less able to “internalize” their feelings, to keep them to themselves, and even to moderate them when they do so as others might do. Consequently, they are likely to appear to others as less emotionally mature, more reactive with their feelings, and more hot-headed, quick-tempered, and easily frustrated by events. Coupled with this problem with emotion regulation is the difficulty they have in generating intrinsic motivation for tasks that have no immediate payoff or appeal to them. This capacity to create private motivation, drive, or determination often makes them appear to lack willpower or self-discipline as they cannot stay with things that do not provide immediate reward, stimulation, or interest to them. Their motivation remains dependent on the immediate environment for how hard and how long they will work, whereas others develop a capacity for intrinsically motivating themselves in the absence of immediate rewards or other consequences. Also related to these difficulties with regulating emotion and motivation is that of regulating their general level of arousal to meet situational demands. Those with ADHD find it difficult to activate or arouse themselves to initiate work that must be done, often complain of being unable to stay alert or even awake in boring situations, and frequently seem to be daydreamy or “in a fog” when they should be more alert, focused, and actively engaged in a task.
  • 4. Diminished problem-solving ability, ingenuity, and flexibility in pursuing long-term goals. Often times, when we are engaged in goal-directed activities, problems are encountered that are obstacles to the goal’s attainment. At these times, individuals must be capable of quickly generating a variety of options to themselves, considering their respective outcomes, and selecting among them those which seem most likely to surmount the obstacle so they can continue toward their goal. Persons with ADHD find such hurdles to their goals to be more difficult to surmount often giving up their goals in the face of obstacles and not taking the time to think through other options that could help them succeed toward their goal. Thus they may appear as less flexible in approaching problem situations, more likely to respond automatically or on impulse, and so are less creative at overcoming the road-blocks to their goals than others are likely to be. These problems may even be evident in the speech and writing of those with the disorder, as they are less able to quickly assemble their ideas into a more organized, coherent explanation of their thoughts. And so they are less able to rapidly assemble their actions or ideas into a chain of responses that effectively accomplishes the goal given them, be it verbal or behavioral in nature.
  • 5. Greater than normal variability in their task or work performance. It is typical of those with ADHD, especially those subtypes associated with impulsive behavior, to show substantial variability across time in the performance of their work. These wide swings may be found in the quality, quantity, and even speed of their work, failing to maintain a relatively even pattern of productivity and accuracy in their work from moment to moment and day to day. Such variability is often puzzling to others who witness it as it is clear that at some times, the person with ADHD can complete their work quickly and correctly while at others times, their tasks are performed poorly, inaccurately, and quite erratically. Indeed, some researchers see this pattern of high variability in work-related activities to be as much a hallmark of the disorder as is the poor inhibition and inattention described above.

OTHER CHARACTERISTICS: Several other development characteristics are associated with the disorder:

  • 1. Early onset of the major characteristics. The symptoms of ADHD appear to arise, on average, between 3 and 6 years of age. This is particularly so for those subtypes of ADHD associated with hyperactive and impulsive behavior. Others may not develop their symptoms until somewhat later in childhood. But certainly the vast majority of those with the disorder have had some symptoms since before the age of 13 years. Those who have the Predominantly Inattentive Type of ADHD that is not associated with impulsiveness appear to develop their attention problems somewhat later than do the other subtypes, often in middle or later childhood. And so the disorder is believed to be one of childhood onset, regardless of the subtype, suggesting that should these symptoms develop for the first time in adulthood, other mental disorders rather than ADHD should be suspected.
  • 2. Situational variation of symptoms. The major symptoms of ADHD are likely to change markedly as a consequence of the nature of the situation the person happens to be in. Research suggests that those with ADHD behave better in one-to-one situations, when doing tasks that they enjoy or find interesting, when there is some immediate payoff for behaving well, when they are supervised, in their work done earlier in the day rather than later, and, for children, when they are with their fathers compared to their mothers. Conversely, those with ADHD may manifest more of their symptoms in group settings, when they must perform boring work, when they must work independently of supervision, when their work must be done later in the day, and when they are with their mothers. Sometimes or in some cases, these situational factors may have little effect on the person’s level of ADHD symptoms but they have been noted often enough in research to make such situational changes in their symptoms important to appreciate.
  • 3. Relatively chronic course. ADHD symptoms are often quite developmental stable. Although the absolute level of symptoms does decline with age, this is true of the inattentiveness, impulsiveness, and activity levels of normal individuals as well. And so those with ADHD may be improving in their behavior but not always catching up with their peer group in this regard. This seems to leave them chronically behind others of their age in their capacity to inhibit behavior, sustain attention, control distractibility, and regulate their activity level. Research suggests that among those children clinically diagnosed with the disorder in childhood, 50-80 percent will continue to meet the criteria for the diagnosis in adolescence, and 10-65 percent may continue to do so in adulthood. Whether or not they have the full syndrome in adulthood, at least 50-70 percent may continue to manifest some symptoms that are causing them some impairment in their adult life.

ADULT OUTCOME: It has been estimated that anywhere from 15 to 50 percent of those with ADHD ultimately outgrow the disorder. However, these figures come from follow-up studies in which the current and more rigorous diagnostic criteria for the disorder were not used. When more appropriate and modern criteria are employed, probably only 20-35 percent of children with the disorder no longer have any symptoms resulting in impairment in their adult life. Over the course of their lives, a significant minority of those with ADHD experience a greater risk for developing oppositional and defiant behavior (50%+), conduct problems and antisocial difficulties (25-45%), learning disabilities (25-40%), low self-esteem, and depression (25%). Approximately 5-10 percent of those with ADHD may develop more serious mental disorders, such as manic-depression or bipolar disorder. Between 10 and 20 percent may develop antisocial personality disorder by adulthood, most of whom will also have problems with substance abuse. Overall, approximately 10-25 percent develop difficulties with over-use, dependence upon, or even abuse of legal (i.e., alcohol, tobacco) or illegal substances (i.e., marijuana, cocaine, illicit use of prescription drugs, etc.), with this risk being greatest among those who had conduct disorder or delinquency as adolescents. Despite these risks, note should certainly be taken that upwards of half or more of those having ADHD do not develop these associated difficulties or disorders. However, the majority of those with ADHD certainly experienced problems with school performance, with as many as 30-50 percent having been retained in their school grade at least once, and 25-36 percent never completing high school.

As adults, those with ADHD are likely to be under-educated relative to their intellectual ability and family educational background. They are also likely to be experience difficulties with work adjustment, and may be under-employed in their occupations relative to their intelligence, and educational and family backgrounds. They tend to change their jobs more often than others do, sometimes out of boredom or because of interpersonal problems in the workplace. They also tend to have a greater turnover of friendships and dating relationships and seem more prone to marital discord and even divorce. Difficulties with speeding while driving are relatively commonplace, as are more traffic citations for this behavior, and, in some cases, more motor vehicle accidents than others are likely to experience in their driving careers. Thus, they are more likely to have had their driver’s license suspended or revoked.

SUBTYPES: Since 1980, it has become possible to place those with ADHD into several subtypes, depending upon the combinations of symptoms they experience. Those who have difficulties primarily with impulsive and hyperactive behavior and not with attention or concentration are now referred to as having the Predominantly HyperactiveImpulsive Type. Individuals with the opposite pattern, significant inattentiveness without being impulsive or hyperactive are called the Predominantly Inattentive Type. However, most individuals with the disorder will manifest both of these clinical features and so are referred to as the Combined Type of ADHD. Research on those with the Combined Type suggests that they are likely to develop their hyperactive and/or impulsive symptoms first and usually during the preschool years. At this age, then, they may be diagnosed as having the Predominantly HyperactiveImpulsive Type. However, in most of these cases, they will eventually progress to developing the difficulties with attention span, persistence, and distractibility within a few years of entering school such that they will now be diagnosed as having the Combined Type.

There is considerably less research on the Predominantly Inattentive Type of ADHD, or what used to be referred to as attention deficit disorder without hyperactivity. What research does exist suggests some qualitative differences between the attention problems these individuals experience and those with the other types of ADHD in which hyperactive or impulsive behavior is present. The Predominantly Inattentive Type of ADHD appears to be associated with more daydreaming, passiveness, sluggishness, difficulties with focused or selective attention (filtering important from unimportant information), slow processing of information, mental fogginess and confusion, social quietness or apprehensiveness, hypo-activity, and inconsistent retrieval of information from memory. It is also considerably less likely to be associated with impulsiveness (by definition) as well as oppositional/defiant behavior, conduct problems, or delinquency. Should further research continue to demonstrate such differences, there would be good reason to view this subtype as actually a separate and distinct disorder from that of ADHD.

PREVALENCE: ADHD occurs in approximately 3-7 percent of the childhood population and approximately 2-5 percent of the adult population. Among children the gender ratio is approximately 3:1 with boys more likely to have the disorder than girls. Among adults, the gender ratio falls to 2:1 or lower. The disorder has been found to exist in virtually every country in which it has been investigated, including North America, South America, Great Britain, Scandinavia, Europe, Japan, China, Turkey and the middle East. The disorder may not be referred to as ADHD in these countries and may not be treated in the same fashion as in North America but there is little doubt that the disorder is virtually universal among human populations. The disorder is more likely to be found in families in which others have the disorder or where depression is more common. It is also more likely to occur in those with conduct problems and delinquency, tic disorders or Tourette’s Syndrome, learning disabilities, or those with a history of prenatal alcohol or tobacco-smoke exposure, premature delivery or significantly low birth weight, or significant trauma to the frontal regions of the brain.

ETIOLOGIES: ADHD has very strong biological contributions to its occurrence. While precise causes have not yet been identified, there is little question that heredity/genetics makes the largest contribution to the expression of the disorder in the population. The heritability of ADHD averages approximately 80 percent, meaning that genetic factors account for 80 percent of the differences among individuals in this set of behavioral traits. For comparison, consider that this figure rivals that for the role of genetics in human height. Several genes associated with the disorder have been identified and undoubtedly more will be so given that ADHD represents a set of complex behavioral traits and so a single gene is unlikely to account for the disorder. In instances where heredity does not seem to be a factor, difficulties during pregnancy, prenatal exposure to alcohol and tobacco smoke, prematurity of delivery and significantly low birth weight, excessively high body lead levels, as well as post-natal injury to the prefrontal regions of the brain have all been found to contribute to the risk for the disorder in varying degrees. Research has not supported popularly held views that ADHD arises from excessive sugar intake, food additives, excessive viewing of television, or poor child management by parents. Some drugs used to treat seizure disorders in children may increase symptoms of ADHD in those children as side effects of these drugs but these effects are reversible.

Can an EEG Biomarker Aid in the Identification of ADHD? An Examination of the Theta/Beta Ratio (TBR) (by Dr. Chris Friesen, Ph.D., C.Psych., BCN)

Attention Deficit-Hyperactivity Disorder (ADHD) is one of the most common neurodevelopmental disorders of childhood and adolescence. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5: APA, 2013), ADHD is marked by “a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development…several inattentive or hyperactive-impulsive symptoms were present prior to age 12 years…clear evidence that the symptoms interfere with, or reduce the quality of, social, academic, or occupational functioning.” (APA, 2013, p. 59-60). According to the DSM-5, population surveys across most cultures find the prevalence of ADHD to be approximately 5% in children (and 2.5% in adults). ADHD is associated with numerous negative outcomes including reduced school performance/academic attainment, poor occupational attainment, social rejection, the development of conduct disorder/antisocial personality disorder, incarceration, substance abuse, physical injuries, traffic accidents/violations, obesity, and negative family relationships (APA, 2013). Thus, early and accurate identification and treatment of ADHD is of enormous societal importance.

At this point in time, the standard method of diagnosing ADHD is based solely on a clinical interview by a physician (e.g., pediatrician or psychiatrist) or psychologist. However, there are numerous problems with the use of clinical interviews for decision making regarding patient diagnoses, predictions, and treatment planning (e.g., various heuristics such as the availability, base-rate, and representativeness heuristics see Dawes, Faust, & Meehl, 1989) that are beyond the current paper to discuss in detail. The addition of standardized and normative-based behavior/symptom rating scales generally add useful information above and beyond what can be obtained from clinical interview alone. Although such measures are often used, they are not required to make a diagnosis of ADHD according to the DSM-5. However, these measures suffer some of the same flaws of clinical interviews in that they primarily rely on parent, teacher, and/or self-reported symptoms/behaviors. These methods can be problematic due to various biases of the person making the ratings. These can include lack of knowledge of base-rate behaviors, lack of insight, and impression management by those doing the ratings. They can also include teachers’ negative perceptions towards children who misbehave and/or parents’/teachers’ lack of knowledge of normative behaviors at particular ages. For example Elder (2010) found that approximately 8.4% of children who are diagnosed with ADHD are born in the month prior to their cutoff date for kindergarten eligibility (and are thus the youngest and most developmentally immature children within a grade). This is compared to 5.1% of children being diagnosed with ADHD when they are born in the month immediately afterward. This finding is consistent with the possibility that diagnoses/ratings may be being driven by teachers’ lack of knowledge of normative behaviors at particular ages and their perceptions of poor behavior among the youngest children in a classroom. Elder (2010) also found that the youngest children in fifth and eighth grades are nearly twice as likely as their older classmates to regularly use stimulants prescribed to treat ADHD. Thus, even ADHD rating scales that are standardized and normative–based are problematic when it comes to assessing for ADHD. The next level of assessment is the use of neuropsychological/cognitive testing to aid in the identification of ADHD. Although abnormal findings that are consistent with ADHD (e.g., impaired findings on continuous performance tests, inhibition tests such as the Stroop task, working memory, and other executive functioning measures) can be found, many children and adolescents with ADHD display no abnormalities on neuropsychological testing (see Nigg, 2006). In my own practice, it was not until relatively recently that I relied on a combination of the above measures (i.e., clinical interviews, rating scales, and neuropsychological testing) when I assessed for the presence of ADHD. Although this assessment battery is much more thorough than what a typical pediatrician or psychiatrist does, there is room for improvement.

As noted in the DSM-5, many of the symptoms and behaviors used to diagnose ADHD can be the result of factors other than ADHD including other psychiatric/psychological disorders/symptoms (e.g., anxiety, oppositional behavior, depression, bipolar disorder, disruptive mood dysregulation disorder, substance abuse, autism spectrum disorder, intermittent explosive disorder), medical/neurological conditions (e.g., Tourette’s disorder), or medications taken for other problems (e.g., thyroid medication, bronchodilators). Because of the above (and other) issues, ADHD tends to be over-diagnosed. For example, Bruchmüller, Margraf, and Schneider (2012) found that 16.7% of mental health professionals misdiagnosed ADHD when provided with case vignettes of children that would not meet DSM-IV diagnostic criteria for ADHD but instead met criteria for other diagnoses such an anxiety disorder. Similarly Chilakamarri and Filkowski (2011) found that in children/adolescents with major depressive disorder, 38% were misdiagnosed with ADHD. Similarly, these authors noted that 29% of children/adolescents with bipolar disorder were misdiagnosed with ADHD. Thus, there is evidence that with the standard methods currently being used to diagnose ADHD, many clinicians are not able to accurately do so.

Given that ADHD is considered to be a neurodevelopmental disorder and the various problems with properly assessing and diagnosing ADHD noted above, finding a reliable biomarker for this disorder is likely possible and of critical importance. Although there is research into various biomarkers for ADHD (e.g., the use of fMRI, PET/SPECT scans, blood tests, genetic testing etc.), many of these are of little clinical utility for various reasons (e.g., non-specificity, expensive equipment). The development of a valid biomarker could not only help properly diagnose children and adolescents, but also help determine the type of, or even whether, pharmacological and/or psychological treatments would be effective.

As noted by Monastra et al. (1999), most major ADHD theorists and researchers have found evidence of anatomical and biochemical abnormalities in the prefrontal cortex in those with ADHD. For example, older imaging studies have found evidence of hypoperfusion and low metabolic activity in the prefrontal and caudate nuclei regions (Monastra et al., 1999). One of the most promising potential biomarkers for aiding in the accurate identification of ADHD is the measurement of the theta/beta ratio (TBR) by use of quantitative electroencephalographs (qEEG). The TBR is essentially the ratio of slow-brain wave activity (theta) to fast-brain wave activity (beta). Higher ratios suggest cortical slowing (i.e., too much slow wave relative to fast wave brain activity). EEG equipment is relatively inexpensive to purchase and run (especially relative to other imaging modalities such as fMRI, PET, and SPECT). For this reason, if EEG indexes such as the TBR can be shown to reliably and accurate aid in the diagnosis of ADHD, it could become relatively easily implemented in hospitals, community clinics, and in private practices of specialist physicians (e.g., neurologists, psychiatrist, and pediatricians) and psychologists.

Although previous researchers have used EEG to look for abnormalities in the brains of those diagnosed with ADHD, it was the work of Joel Lubar (1991) with his use of more extensive EEG recording montages with simplified ratios that found abnormalities. More specifically, Lubar (1991) found increased frontal TBR in boys with attention problems without hyperactivity. It was Lubar and his colleagues (Monastra et al., 1999) who completed a pioneering initial validation study to determine whether the TBR could reliably identify children, adolescents, and young adults of both sexes with or without ADHD. In this study, the authors recruited 482 individuals, ages 6 to 30 years-old, to test the hypothesis that cortical slowing (as measured by via single-channel EEG at the vertex of the scalp) in the prefrontal region could serve as a basis for differentiating patients with ADHD from a nonclinical control group. The authors classified the participants into inattentive-ADHD, inattentive-hyperactive-impulsive combined ADHD, and control (i.e., those not meeting for any DSM-IV disorder and no evidence of ADHD via self-report, ratings scales, and on a continuous performance test) groups. Monastra et al. (1999) found that the TBR measurement revealed evidence of cortical slowing in both ADHD groups, regardless of age or sex. Amazingly, the sensitivity (i.e., the proportion of ADHD patients correctly classified as having ADHD) of the TBR was 86% while the specificity (i.e., the proportion of those without ADHD that were correctly classified as not having ADHD) was 98%.

Monastra et al.’s (1999) results were so promising that Monastra, Lubar, and Linden (2001) completed a series of studies using the qEEG-based TBR in the assessment of ADHD in 469 children and adolescents. They again found that the TBR could correctly classify inattentive-ADHD, inattentive-hyperactive-impulsive combined ADHD, and control participants with a high degree of accuracy. Of course, no measure can be valid without first being demonstrated to be reliable. One important question was whether the TBR readings were consistent over time (i.e., test-retest reliability). The authors found that the TBR was highly reliable (r = .96) when measured one week apart, suggesting that this is likely a stable characteristic of children and adolescents with ADHD. They also found that the TBR findings were consistent with results of rating scales and a continuous performance test (Test of Variables of Attention TOVA). Lastly, the TBR was found to be able to differentiate those with ADHD and those without ADHD with a sensitivity of 90% and specificity of 94% in their sample.

Since these pioneering studies were performed, many similar studies have been carried out. As will be seen below, despite positive findings, there are some researchers who have found inconsistent results or criticized the use of the TBR. For example Kitsune et al (2015) found that qEEG results varied as a function of the time/context in which they were obtained (i.e., at the beginning or the end of the evaluation). They found that at the start of the recording session, slow wave activity (i.e., delta and theta power) was elevated in their ADHD group only, while at the end of the recording session the ADHD group only demonstrated elevated fast wave activity (higher beta power) relative to controls. However, they did find that the ADHD participants had more slow-wave activity supporting theories of cortical hypoarousal in ADHD. However, Kitsune et al. (2015) did not find evidence for atypical TBR in their sample (n = 76) of adolescents and young adults with ADHD.

Similarly, Buyck and Wiersema (2014) found no evidence of an elevated TBR in their recent study. They concluded that “the findings indicate that it is unlikely that stable, univariate EEG abnormalities are implicated in all children with ADHD and that it is important to take into account state-dependent characteristics when evaluating EEG in ADHD. From a clinical perspective, this implies that cautiousness is warranted in using simple EEG measures as a supplementary diagnostic tool, as has been proposed by some researchers (Monastra, Lubar, & Linden, 2001 Snyder et al., 2008).” (Buyck & Wiersema, 2014, p. 3223). However, these authors only included 22 children with ADHD and 29 typically developing children between 7 and 14 years of age and thus the generalizability of their findings is questionable. Similarly, 50% (11) of the ADHD sample children were taking stimulant medication (although they were asked to abstain for 48 hours before the study). The authors concede that previous research had found that stimulant medication decreases slow wave theta and the TBR.

Once an area of study has matured enough, the gold-standard method of identifying the robustness of a finding is the use of meta-analyses. Snyder and Hall (2006) completed a meta-analysis examining qEEG studies that evaluated ADHD using DSM-IV criteria. Nine studies (n =1498) met their criteria and they found that the TBR had with a pooled effect size of 3.08 (95% confidence interval, 2.90, 3.26) for ADHD versus controls (normal children, adolescents, and adults). Snyder and Hall (2006) noted that on average, the studies included had sensitivity and specificity rates of 94% which was similar to the results of previous studies. They also noted that their literature search uncovered 32 studies that were carried out before the DSM-IV ADHD criteria were available and that 29 of the 32 studies had findings consistent with their meta-analytic results. They concluded that their meta-analysis supported the finding that higher TBR are commonly found ADHD relative to normal controls. However, they cautioned that high TBR may possibly occur in other conditions and that further research would be required to be sure that a high TBR is specific to ADHD.

Arns, Conners, and Kraemer (2013) conducted a meta-analysis examining the accuracy of the TBR in correctly identifying ADHD. These authors did use a few of the studies used in the previous meta-analysis by Snyder and Hall (2006) if they met their inclusion criteria. Arns et al. (2013) included nine studies (n = 1253) using children/adolescents. They found effect sizes (ES) of 0.75 and 0.62 for 6-13 year-olds and 6-18 year-olds respectively with regard to the magnitude of differences in TBR relative to controls. Due to certain statistical assumptions not being met, they noted that the effect sizes may have been overestimated. These authors concluded that “excessive TBR cannot be considered a reliable diagnostic measure of ADHD, however a substantial sub-group of ADHD patients do deviate on this measure and TBR has prognostic value in this sub-group, warranting its use as a prognostic measure rather than a diagnostic measure.” (Arns et al., 2013, p. 374). They added that “…based on recent studies, this excess theta and TBR is found in a substantial subgroup of patients with ADHD (25%-40%) and has been demonstrated to be of prognostic value in predicting treatment outcome to stimulant medication and neurofeedback, warranting its use as a prognostic measure rather than a diagnostic measure.” (Arns et al., 2013, p. 381). The authors note that their less reliable findings were mainly related to the control groups TBRs increasing as the date of the studies became more recent as opposed to the ADHD group’s TBR decreasing. However, an examination of their graphed data (figure 3 in their published article) of this trend showed a variable trend towards increasing TBR in control subjects primarily due to two or three of the most recent of the included nine studies. They note that this was not due to changes in inclusion criteria for the control groups. Rather they hypothesize that the findings may have been due to differences in the EEG hardware and/or software used and the well-established finding that children are obtaining less sleep each year. In fact, this latter effect (i.e., poor sleep increasing the TBR) is well known in the neurofeedback community (based on my experiencing attending neurofeedback/EEG conferences and workshops). Arns et al. (2013) note that “a recent meta-analysis incorporating data from 35,936 healthy children reported that sleep duration is clearly positively associated with school performance and executive function, and negatively associated with internalizing and externalizing behavior problems.” (p. 380). They also noted that “A well-known EEG signature for fatigue or drowsiness is increased theta suggesting this would result in increased TBR.” (Arns et al., 2013, p. 380). Thus, as sleep duration was not controlled for, the perceived trend of the control groups’ TBRs increasing may have been an artifact of sleep deprivation and thus calls into question the findings of Arns et al. (2013).

To help answer the question of whether the TBR is specific to ADHD, Snyder, Quintana, Sexson, Knott, Haque, and Reynold (2008) conducted a blinded, prospective, multi-center study of a representative clinical sample examining the sensitivity and specificity of the TBR in accurately identifying ADHD relative to as non-ADHD children/adolescents (which included other childhood/adolescent disorders or no diagnosis). Snyder et al.’s (2008) ADHD sample had a number of comorbidities including mood, anxiety, disruptive, and learning disorders. Snyder et al. (2008) found that the TBR identified ADHD with 87% sensitivity and 94% specificity. In comparison, parent and teacher rating scales (the results of which were not available to the clinical team making the diagnosis) were found to have sensitivity ratings of 38% to 79% and specificity ratings of 13% to 61%. The rating scales were often not consistent with the clinical team’s diagnoses whereas the TBR findings were consistent with the team’s diagnoses. The authors cautioned that because TBR findings do not identify comorbidities or alternative diagnoses, the TBR should not be used as a stand-alone diagnostic tool. Rather, they recommended it be used to complement a thorough clinical evaluation. However, in a recent literature review of the clinical utility of EEG in the assessment and treatment of ADHD, Loo and Makeig (2012) examined Snyder et al.’s (2008) study and noted that although the findings suggest that an abnormally high TBR identifies almost all of the children with ADHD, 18% of those with a normal TBR also go on to receive an ADHD diagnosis and state that “for clinical purposes, a misdiagnosis rate of 18% is simply too high.” (Loo & Makeig, 2012, p. 575). However, the Snyder et al. (2008) found a specificity of 94% which suggests that only 6% of those without ADHD are misclassified (false-positive) as having ADHD by having a high TBR. Similarly, their findings found a sensitivity of 87% which suggests that 13% of patients diagnosed with ADHD by the assessment team had normal TBRs (false-negative). And of course, these ratings are assuming that a “team consensus” diagnosis is correct. Loo and Makeig (2012) concede that “the increases in both theta band activity and in the theta/beta power ratio are two of the most reliable EEG findings in ADHD to date.” (p. 572). They also note that Snyder et al.’s (2008) “…results are remarkably consistent with previous reported results using the ?/? power ratio, and suggest that this measure exhibits similar accuracy rates among diverse clinical samples and age ranges. However, an increased ?/? power ratio, as previously reviewed, is not ubiquitous in ADHD…” (p. 575). They add that “it is difficult to reconcile such disparate results regarding the reliability of the ?/? ratio marker. The Snyder et al. study in 2008 was scientifically sound and it provides class 1 evidence that EEG may indeed be useful in confirming a diagnosis of ADHD as part of a multimodal assessment that includes clinical interviews, behavior rating scales, and neuropsychological tests for identification of comorbid learning disabilities and co-occurring psychiatric disorders. The inconsistencies across studies may be due to methodological issues, such as sampling, instrumentation, and data processing and analysis differences or actual EEG heterogeneity within the ADHD population. In addition, a rarely mentioned fact is that there may be wide variation in EEG instrumentation that can make it extremely difficult to compare across datasets collected with different EEG hardware and software.” (Loo & Makeig, 2008, p. 575).

Bink, Van Boxtel, Popma, Bongers, Denissen, and van Nieuwenhuizen (2015) examined the EEG patterns of adolescents with diagnoses of ADHD only and adolescents with combined autism spectrum disorder (ASD) and ADHD. The authors found that the adolescents with ADHD had more slow (theta) brain-wave activity than adolescents with ASD and ADHD during the eyes open and task conditions. They also found that only the adolescents with ADHD showed a relationship between lowered attention test performance (as measured by the d2) and increased slow-wave activity (theta) in the eyes open condition. The authors interpreted the results as suggesting that the underlying psychophysiological mechanisms of ADHD and ASD-ADHD comorbid adolescents are different, despite there being similarities on a behavioral level as the ASD-ADHD comorbid adolescents demonstrated fewer EEG signs usually associated with ADHD.

A recent meta-analysis by Rudo-Hull (2015) found evidence in support of the cortical hypoarousal theory for externalizing behaviors/disorders in general (which includes ADHD, antisocial personality disorder, conduct disorder, substance abuse, oppositional defiant disorder, and psychopathy). Rudo-Hull (2015) combined the results of 62 studies (n = 4649) that examined qEEG in relationship to externalizing disorders/behaviors. Generally, the author found that for those diagnosed with an externalizing disorder, there was significantly more slow-wave brain activity (i.e., delta but primarily theta) and less fast-wave brain activity (i.e., beta) relative to controls. Rudo-Hull (2015) found that there was no relationship between slow-wave brain activity (i.e., delta and theta) and externalizing behaviors in antisocial or mixed samples. There was a positive relationship between slow-wave brain activity and externalizing behaviors in the ADHD samples however. She also found a negative relationship between fast wave activity (i.e., beta) and externalizing behaviors in both antisocial and ADHD samples. These results led the author to conclude that “…overall, while increased slow-wave activity appears to be more characteristic of ADHD samples, both antisocial and ADHD samples seem to display the decreased fast-wave activity” (Rudo-Hull, 2015, p. 13-14). However, the author noted that the antisocial groups were much more varied (e.g., from children with conduct problems to accused murderers) and there were fewer studies of slow-wave activity in the antisocial samples than in ADHD samples and thus the lack of finding of increased slow wave activity in the antisocial groups may have been due to lack of statistical power. The author added that the TBR, although widely researched within the ADHD field, has not “…been tested in the antisocial behavior field.” (p. 14). The author concluded that “it is therefore possible that these measures (e.g., TBR) may differentiate ADHD from antisocial populations, and future research with these measures may help clarify whether ADHD should continue to be studied largely on its own or in conjunction with other externalizing behaviors.” (p. 14). Thus, the results from the Snyder et al. (2008), Bink et al. (2015), and Rudo-Hull (2015) studies suggests that the TBR ratio may be relatively specific to ADHD but more research is required.

In one of the best designed studies examining how the TBR will likely be used in a clinical setting (i.e., not as a standalone measure but rather in combination with a clinical assessment) was published by Snyder, Rugino, Hornig, and Stein (2015). The authors investigated the predictive accuracy of adding the TBR to a clinician’s typical assessment procedures via a prospective, triple-blinded, multi-site (13 sites), clinical cohort study (275 children and adolescents presenting to clinics with attentional and behavioral problems) with a diagnosis reference standard based on an independent multidisciplinary team (psychiatrist, psychologist, and neurodevelopmental pediatrician). The authors chose to integrate the clinical assessment with the TBR to help improve certainty with regard to the DSM-5 criterion E (i.e., whether symptoms are better explained by another condition). Similar to what was found in previous studies outlined in the current paper, Snyder et al. (2015) found that the site clinicians likely over-diagnosed ADHD in 34% (93/275) of cases (when compared to the multidisciplinary team’s diagnoses). Of those 34% (93), 91% were found to have lower TBR. The authors also found that when the clinician was uncertain about the diagnosis and was able to integrate their assessment with the TBR, there was 97% agreement with the multidisciplinary team. Generally, Snyder et al. (2015) found that children and adolescents with relatively lower TBR were more likely to have other conditions that could affect criterion E (e.g., anger issues or medical or neurological conditions that mimic ADHD such as brain injuries, headaches, auditory processing disorders, substance abuse, cerebral palsy, vision or hearing problems). They found that integration of TBR with a clinician’s ADHD evaluation could help to improve diagnostic accuracy from 61% to 88%.

In summary, the early and accurate identification and treatment of ADHD is of enormous societal importance due to the numerous possible negative outcomes for those children and adolescents that are undiagnosed and/or undertreated. Similarly, misdiagnosing children and adolescents with ADHD can also have significant negative psychological consequences (e.g., self-fulfilling prophesies, social ridicule, etc.) in addition to the problems of incorrectly medicating children and adolescents with stimulants that directly affect the brain’s dopamine system at a time when the brain is still developing. The current paper attempted to demonstrate that the assessment and diagnosis of ADHD has traditionally been problematic. Only a clinical interview is required for diagnosing ADHD as outlined by the DSM-5. There are numerous problems with the use of clinical interviews for decision making regarding patient diagnoses, predictions, and treatment planning. The addition of standardized and normative-based behavior/symptom rating scales generally add useful information above and beyond what can be obtained from clinical interviews alone but can also be problematic. Although the addition of neuropsychological/cognitive testing to aid in the identification of ADHD can be helpful when there are findings of deficits, many children and adolescents with ADHD display no abnormalities on neuropsychological/cognitive testing. Thus, finding a biomarker for the disorder is of critical importance.

Although basic research has repeatedly found evidence of cortical hypoactivation in children and adolescents with ADHD, the methods used were traditionally of little clinical utility for various reasons (e.g., non-specificity, expensive equipment). However, through the original work of Lubar and Monastra (see Lubar, 1991 Monatra et al., 1999), a relatively cheap and accurate EEG-based measure that can be used to aid in the identification of ADHD appears to have been discovered. This measure is known as the theta-beta ratio (TBR) and is essentially the ratio of slow-brain wave activity (theta) to fast-brain wave activity (beta) with higher ratios suggesting cortical slowing. The current paper attempted to summarize some of the research with regard to the clinical utility of the TBR in the identification of ADHD. Although not all research has supported the finding of higher TBRs in ADHD children and adolescents relative to controls, the majority of the research has found the TBR to be highly sensitive to ADHD. Although more research should be conducted to insure this finding is robust, the research available to date does suggest that the TBR is also relatively specific to ADHD.

These findings have been convincing enough to cause me to change my clinical practice when it comes to the assessment of ADHD. Although I have always performed relatively comprehensive assessments which have included clinical interviews, rating scales and neuropsychological/cognitive testing, I have very recently added the measurement the TBR via EEG. I do not believe it is wise to use only the TBR when determining the presence or absence of ADHD. All the assessment methods I use are required for a proper differential diagnosis and for treatment planning. Measuring the TBR is especially helpful when trying to confirm an ADHD diagnosis when the other data suggest its presence. For example, if a patient (or patient’s parent/teacher) complains of symptoms and behaviors suggestive of ADHD but there is no indication of an elevated TBR, I will now look at the case much more thoroughly to determine if there is some other explanation for the symptoms other than ADHD. Similarly, I would also make sure the patient has had adequate sleep in the days prior to the assessment due to the fact that poor sleep can potentially affect the TBR. I believe that the incorporation of the TBR in my assessments has allowed me to improve the accuracy of my assessment and hence treatment of ADHD.

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Bink, M., van Boxtel, G.J.M., Popma, A., Bongers, I.L., Denissen, A.J.M., van Nieuwenhuizen, C. (2015). EEG theta and beta power spectra in adolescents with ADHD versus adolescents with ASD + ADHD. European Child and Adolescent Psychiatry, 24, 873–886.

Bruchmüller, K. & Margraf, J., & Schneider, S. (2012). Is ADHD diagnosed in accord with diagnostic criteria? Overdiagnosis and influence of client gender on diagnosis. Journal of Consulting Clinical Psychology, 80(1), 128-138.

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Monastra, V. J., Lubar, J. F., & Linden, M. (2001). The development of a quantitative electroencephalographic scanning process for attention deficit-hyperactivity disorder: Reliability and validity studies. Neuropsychology, 15, 136–144.

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Snyder, S.M., Quintana, H., Sexson, S.B., Knott, P., Haque, A.F.M., & Reynolds, D.A. (2008). Blinded, multi-center validation of EEG and rating scales in identifying ADHD within a clinical sample. Psychiatry Research, 159, 346–358

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Featured Studies

Featured studies include only those currently recruiting participants. Studies with the most recent start date appear first.

Helping Toddlers and Parents Together

Using stakeholder feedback (i.e., behavioral health providers & caregivers), the goal of this study is to develop a behavioral parenting program that focuses on both parent mental health and parenting for parents of toddlers (12-35 months old). Using a deployment focused intervention model, this study will : (1) develop an early parenting intervention for parents of at-risk toddlers which integrates a focus on parent mental health with evidence-based behavioral parenting strategies, and (2) examine context-specific factors related to the intervention, including feasibility and acceptability to design a more practice-ready intervention.

Treating Parents With ADHD and Their Young Children Via Telehealth: A Hybrid Type I Effectiveness-Implementation Trial

This study will compare the effectiveness of combined parental stimulant medication and behavioral parent training (BPT) versus BPT alone on child ADHD-related impairment (primary outcome), child ADHD and externalizing symptoms, time to child stimulant prescription (secondary child outcomes) and parental ADHD impairment, parental ADHD symptoms, parenting, and BPT engagement (parental outcomes/target mechanisms). This study will also assess the care delivery context and develop an implementation approach for treatment of families with a parent with ADHD and a child with elevated ADHD symptoms via telehealth in primary care sites providing pediatric care.

School Health Implementation Network: Eastern Mediterranean

An estimated 10-20% of children globally are affected by a mental health problem. Child mental health has been identified as a priority issue by the World Health Organization's Eastern Mediterranean Regional Office (WHO EMRO). Following consultations with international and regional experts and stakeholders, WHO EMRO developed an evidence-based School Mental Health Program (SMHP), endorsed by WHO EMRO member countries, including Pakistan. The federal and provincial health departments in Pakistan made recommendations for a phased implementation of the SMHP in a pilot district. In the formative phase of this program, a number of implementation challenges were identified by the stakeholders. Broadly, these included the need to operationalize and adapt the existing components of the intervention to the local context and to develop sustainable mechanisms for delivery of quality training and supervision.

Informed by the results of a formative phase investigations, the SHINE scale-up research team adapted the SMHP (henceforth called Conventional SMHP or cSMHP) to address these implementation challenges. The enhanced version of the intervention is called Enhanced School Mental Health Program (eSMHP). Enhancements to cSMHP have occurred at two levels: A) Content enhancements, such as a collaborative care model for engaging parents/primary caregivers, strategies for teacher's wellbeing, and adaptation and operationalization of particular clinical intervention strategies and B) Technological enhancements which include adaptation of the training manual for delivery using an online training platform, and a 'Chat-bot' to aid the implementation of intervention strategies in classroom settings.

The primary objective of the study is to evaluate the effectiveness of eSMHP in reducing socio-emotional difficulties in school-going children, aged 8-13, compared to cSMHP in Gujar Khan, a rural sub-district of Rawalpindi, Pakistan.

The secondary objectives are to compare the cost-effectiveness, acceptability, adoption, appropriateness (including cultural appropriateness), feasibility, penetration and sustainability of scaled-up implementation of eSMHP and cSMHP. It is hypothesized that eSMHP will prove to be both more effective and more scalable than cSMHP.

The research is embedded within the phased district level implementation of the cSMHP in Rawalpindi, Pakistan. The study population will consist of children of both genders, aged 8-13 (n=960) with socio-emotional difficulties, studying in rural public schools of sub-district Gujar Khan in Rawalpindi.

The proposed study design is a cluster randomized controlled trial (cRCT), embedded within the conventional implementation of the SMHP. Following relevant ethics committees and regulatory approvals, 80 eligible schools, stratified by gender, will be randomized into intervention and control arms with a 1:1 allocation ratio. Following informed consent from the parent/ primary caregiver, children will be screened for socio-emotional difficulties using Strengths and Difficulties Questionnaire (SDQ). 960 children scoring > 12 on the teacher-rated SDQ total difficulty scores and > 14 on the parent-rated SDQ total difficulty scores will be recruited and equally randomized into intervention and control arms (480 in each arm).

Teachers in the intervention arm will receive training in eSMHP, whereas teachers in the active control will be trained in cSMHP. Trained teachers will deliver the program to children in their respective arms.

Primary Outcome: The primary outcome is reduction in socio-emotional total difficulties scores, measured with the parent-rated SDQ, 9 months after commencing intervention delivery.

Secondary Outcomes: Implementation data on acceptability, adoption, appropriateness (including cultural appropriateness), feasibility, penetration and sustainability outcomes will be collected from children, parents/primary caregivers, head teachers and teachers. In addition, data will be collected on self-reported Psychological Outcome Profiles (PSYCHLOPS)-KIDS to measure progress on psycho-social problems and wellbeing annual academic performance classroom absenteeism, stigmatizing experiences and parent-teacher interaction. Data on teachers' sense of efficacy and subjective well-being, and on the schools' psychosocial environment profile will be collected. All secondary outcome data will be collected at baseline and 9 months after commencing intervention delivery.

Outcomes will be analyzed on an intention to treat basis. The role of various factors as potential mediators and moderators eSMHP effectiveness will be explored.

Cost-effectiveness evaluation of SMHP shall be evaluated in terms of costs associated with implementation of eSMHP compared with cSMHP.

Brain Plasticity Underlying Acquisition of New Organizational Skills in Children

Organizational, time management and planning (OTMP) skills deficits are impairing features of developmental disorders, such as Attention Deficit Hyperactive Disorder (ADHD), which compromise school performance and family relations. The manualized Organizational Skills Training program (OST) was designed to target children's specific OTMP deficits. However, the brain mechanisms of treatment-induced changes remain unknown. The current study combines a training intervention (OST) with non-invasive MRI imaging in a pre-/post-design in a randomized two-arm (treatment vs. waitlist) trial to address this question.

A Novel fNIRS Neurofeedback Intervention for Enhancement of Working Memory in Attention Deficit Hyperactivity Disorder (ADHD)

The proposed study is to test and validate a novel intervention that integrates computerized cognitive training with real-time neuromonitoring and neurofeedback to enhance working memory by probing the individualized neural systems underlying working memory. We will test the proposed intervention on children with ADHD with working memory deficits. The R61 proof-of-concept phase will assess the target engagement, effective dose and feasibility.

School-Based Depression Prevention for Adolescents With ADHD

The purpose of this study is to develop a modified behavioral activation program in adolescents with ADHD to be implemented by school mental health providers in an urban, low-income school district. Subsequently we will examine its effectiveness in reducing depressive symptoms and improving emotion regulation and reward responsivity, compared to usual care.

Sleep Dysfunction and Neurocognitive Outcomes in Adolescent ADHD

This study seeks to characterize sleep physiology in adolescents with and without Attention deficit hyperactivity disorder (ADHD) and its relationship to differential neurocognitive and clinical outcomes within these groups.

Ventral Tegmental Area (VTA) Self-Activation in Attention Deficit Hyperactivity Disorder (ADHD)

The purpose of this study is to see if a non-medication intervention can increase motivation in individuals with ADHD by observing brain activity using magnetic resonance imaging (MRI).

Virtual Reality Attention Management

Problems with distraction are widespread in the 21st century, but for people with developmental delays or behavioral challenges they can have more damaging effects. For example, susceptibility to distraction is associated with worse school and social performance, lower high school graduation rates, and increased incidence of serious accidents. The investigators' goal is to improve understanding of distractibility and develop a targeted treatment. The proposed intervention is based on models of habituation, which is a term that means reduced physiological and emotional response to a stimulus (e.g. moving object, or loud noise, etc.) as it is seen repeatedly. The investigators use virtual reality technology to show study participants distracting stimuli repeatedly in a virtual classroom setting, and their hypothesis states that participants will improve attention in the face of distraction by training with this technology intervention. The virtual classroom setting is especially relevant for children who have significant challenges with distractibility, such as children with ADHD. This intervention will likely be effective in helping individuals with other clinical disorders and perhaps the general population as well.

Brain Imaging of Childhood Onset Psychiatric Disorders, Endocrine Disorders and Healthy Volunteers

Magnetic Resonance Imaging (MRI) unlike X-rays and CT-scans does not use radiation to create a picture. MRI use as the name implies, magnetism to create pictures with excellent anatomical resolution. Functional MRIs are diagnostic tests that allow doctors to not only view anatomy, but physiology and function. It is for these reasons that MRIs are excellent methods for studying the brain.

In this study, researchers will use MRI to assess brain anatomy and function in X and Y chromosome variation, healthy volunteers, and patients with a variety of childhood onset psychiatric disorders. The disorders include attention deficit disorder, autism, congenital adrenal hyperplasia, childhood-onset schizophrenia, dyslexia, obsessive compulsive disorder, Sydenham's chorea, and Tourette's syndrome.

Results of the MRIs showing the anatomy of the brain and brain function will be compared across age, sex (gender), and diagnostic groups. Correlations between brain and behavioral measures will be examined for normal and clinical populations.


Research support

The FDA provided marketing authorization for the prescription-only device to the biotechnology company NeuroSigma through its "de novo" premarket review pathway, which is used for new low- to moderate-risk devices with no existing market equivalent. Researchers from the Univer­sity of California, Los Angeles (UCLA), including one clinical and two educational psychologists, conducted the clinical trial with 62 children, ages 8 to 12, who had moderate to severe ADHD. Each participant received four weeks of at-home treatment using either the eTNS system or a placebo device.

Researchers administered two assessments on a weekly basis: the ADHD-IV Rating Scale (ADHD-RS), a parent questionnaire that evaluates a child’s behavior, and the Clinical Global Impressions (CGI) scale, which measures symptom severity.

Compared with the placebo group, children who used the eTNS device showed statistically significant improvements in ADHD symptoms, with average ADHD-RS scores dropping about 31 percent. Children in the placebo group experienced an average decrease of about 18 percent. Slightly over half of participants in the intervention group showed improvement that was clinically meaningful, defined as a score of "much improved" or "very much improved" on the CGI Improvement scale.

The research team also collected electroencephalography (EEG) data before and after administering treatment. Children who used the eTNS system displayed increased activity in the middle and right frontal regions of the brain, which help regulate attention and emotions.


In terms of treatment effect size, the behavioral changes observed are similar to those rendered by nonstimulant medications for ADHD, such as atomoxetine and guanfacine, but less pronounced than the effects of stimulant medications, says psychologist Sandra Loo, PhD, of UCLA’s Semel Institute for Neuroscience and Human Behavior, a co-author of the clinical trial.

"There’s a great demand for nonpharmacological ADHD treatments, so we’re excited about potentially offering empirically supported alternatives," she says, adding that around 30% of children taking stimulants for ADHD experience undesirable side effects—such as weight loss or insomnia—or do not respond to the drugs.

In the present study, more than half of the children using eTNS experienced side effects including fatigue, headache and increased appetite. Compared with the control group, these patients also showed significant changes in weight and pulse, with an average gain of about one kilogram and an increase of 10 beats per minute after four weeks, but no children withdrew from the study due to adverse side effects.

"This study shows that the eTNS device is relatively safe, efficacious and has a lot of promise," says Ronald T. Brown, PhD, a child psychologist and dean of the School of Health Sciences at the University of Nevada, Las Vegas, who was not involved in the clinical trial. "But these are preliminary results with a small number of participants that raise a number of additional questions."

For example, Brown, who was part of the AAP committee that developed the latest treatment guidelines for ADHD, says psychologists need more information about how the new device compares with traditional ADHD treatments, such as stimulant medications and behavior management. He also says it’s important to study the durability of the observed effects and whether improvements persist after a limited course of treatment.


Philosophical context

According to the scientific philosophy of Popper, a scientific hypothesis must be testable and therefore open to falsification [6]. If a scientist can specify in advance an experiment that can falsify the hypothesis, then and only then is the hypothesis scientific. Popper argued that whilst it was easy to obtain confirmations or verifications for nearly every theory when one looked for a confirmation, a 'good' scientific theory forbade certain things to occur. A genuine test of a theory should lead to an attempt to refute it [7]. Popper suggested Einstein's theory of gravitation as an example of a theory that clearly satisfied the criterion of falsifiability. In contrast, he proposed that the two psycho-analytic theories of Freud and Adler were examples of theories that were non-testable and irrefutable (p.37) [7]. As Chalmers writes, "Usually, potential falsifiers will involve the specification of an experimental set-up designed to test a theory together with the description of an outcome inconsistent with the prediction of the theory" (p.68) [8]. If a current theory is proved false, then new theories will be developed that take into account the discriminating case. For a hypothesis to be testable, it must be well-described and precise, so as to allow for falsification and replication [6].

Other philosophers have argued that in practice, when anomalous (non-predicted) results are reported and accepted as real data, rather than abandoning that theory, scientists are more likely to modify their existing hypotheses to align with the new findings (or alternatively ignore the new results) [9]. According to Lakatos, a scientific theory (or "research program") has a "hard core", a hypothesis central to that theory. The hard core is stubbornly defended against criticism and refutation by "auxiliary hypotheses", produced in the light of new findings. Research programs fall into two types: progressive and degenerative. A degenerative program is marked by a lack of new facts and by lack of growth. In comparison, the progressive program generates new facts, new hypotheses and is the subject of growth. Scientific progression occurs when the auxiliary hypotheses of the progressive program aid the discovery of new knowledge, whilst the degenerative program is abandoned [9]. It has also been argued that new scientific findings improve the current set of hypotheses until there comes a point in time where a fresh and new hypothesis comes into being that starts a paradigm shift in thinking about that scientific topic [10].

The strength and health of the field of ADHD behavioural research (and ADHD genetic research, as a concomitant), is dependent on proposed hypotheses being made testable and falsifiable. ADHD is currently a behavioural construct, defined by behavioural dysfunction rather than by a biological marker [11]. It is a complex, multifactorial disease entity and as such, it is important that testable hypotheses of dysfunction are produced [12].


Neurodevelopment of cognitive control in autism: adolescence to young adulthood

Description:
This study examines the development of cognitive control across adolescence into young adulthood and its relationship to functional outcomes in individuals with autism spectrum disorders (ASD) using functional magnetic resonance imaging (fMRI) and behavioral measures.

Funding:
National Institutes of Health / National Institute of Mental Health

The department received nearly $24 million in National Institutes of Health research funding in 2020. Psychiatric research at UC Davis School of Medicine ranks 14th out of 88 academic psychiatry departments nationwide.


Living With

What quick tips can be offered to help adults with ADHD Inattentive type cope with the day-to-day activities of life?

The following are tips for adults with ADHD, inattentive type, for self-regulating (controlling one’s behaviors, emotions and thoughts), and regaining control over many daily tasks:

To help cope with distractions:

  • Request a quiet or private work area move to an unused conference space or other area where there are few distractions or noise.
  • Wear earphones with soft music to cover up office noise.
  • Redirect phone calls to voice mail and return phone calls at set times throughout the day.

To help stay organized:

  • Set aside the first 10 to 20 minutes of your day to organize your tasks for the day.
  • Work on and complete one task at a time before moving on to the next one.
  • Keep a to-do list in a notebook or on your phone.
  • Put appointments in your phone and set up alarm reminders before the event.
  • Mark deadlines on calendars as a visible reminder tool.
  • Use daily planners or online task organizers to help keep track of tasks and events.
  • Use sticky pads to write important notes and place them in appropriate areas where they will be seen.
  • If a filing system is needed, use labels or color-coded folders or tabs.
  • Set up online automatic payment of bills so you don’t forget to pay them.

To prevent losing or misplacing important items:

  • Identify specific areas to place specific items and get into the routine of only placing items in these designated spots.

To help stay focused:

  • Take handwritten notes during meetings or tape record as a backup and to fill in details.
  • Break up larger tasks into smaller ones. Reward yourself when each task is completed.
  • Take short breaks to prevent boredom – take a short walk, do some stretches, drink some water.

Last reviewed by a Cleveland Clinic medical professional on 09/25/2019.

References

  • National Institute of Mental Health. Attention Deficit Hyperactivity Disorder. Accessed 10/4/2019.
  • Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD). Diagnosis of ADHD in Adults. Accessed 10/4/2019.
  • Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD). Cognitive-Behavioral Treatment. Accessed 10/4/2019.
  • Centers for Disease Control and Prevention. What is ADHD? Accessed 10/4/2019.
  • American Psychiatric Association. What is ADHD? Accessed 10/4/2019.
  • A.D.D. Resource Center. DSM-5 Criteria for ADHD. Accessed 10/4/2019.
  • Children and Adults with Attention-Deficit/Hyperactivity Disorder (CHADD). Workplace issues. Accessed 10/4/2019.

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What has ADHD to do with schizophrenia?

Attention deficit hyperactivity disorder and schizophrenia are two different disorders that can profoundly affect a person’s life. While they have many differences, they also share some characteristics.

For this reason, some scientists have been looking into a possible link between them.

Attention deficit hyperactivity disorder (ADHD) is a chronic condition that involves behavioral symptoms, including inattentiveness, hyperactivity, and impulsiveness.

It is a neurodevelopmental disorder, and diagnosis usually takes place before the age of 12 years. Although symptoms tend to improve with age, some people continue to have symptoms as adults.

During childhood, ADHD is more common in males than in females, but the prevalence becomes relatively even in adulthood. It is possible that fewer girls receive a diagnosis because they show symptoms differently, meaning that caregivers or teachers may not notice them.

The Centers for Disease Control and Prevention (CDC) estimate that, in 2016, about 6.1 million children living in the United States had received a diagnosis of ADHD.

Schizophrenia is a long-term mental health condition that affects how a person thinks, feels, and behaves. It involves psychosis and other symptoms, including inattention.

Schizophrenia is slightly more common in males than females. Symptoms often begin between the ages of 16 and 30 years, but it can sometimes appear during childhood.

Around 1 percent of people in the U.S. have schizophrenia, according to the National Alliance on Mental Illness (NAMI).

Share on Pinterest A lack of focus is common with ADHD and with schizophrenia.

Various studies have identified some similarities between ADHD and schizophrenia and a possible overlap.

The conclusions of researchers include the following:

  • People with schizophrenia often have symptoms of other psychiatric disorders, including ADHD, in early adolescence.
  • Children and teenagers with ADHD may be 4.3 times more likely to develop schizophrenia as adults than people without ADHD.
  • Close relatives of people with ADHD may be more likely than second-degree relatives to receive a diagnosis of schizophrenia, suggesting that it may have a genetic component.

In 2013, a team of geneticists looking at ADHD in children and schizophrenia in adults found evidence of a “small but significant shared genetic susceptibility.”

The exact causes of ADHD and schizophrenia are not clear, but a combination of genetic and environmental factors may increase the risk of both.

A person with specific genetic features may develop symptoms if they encounter certain triggers, whether this exposure occurs before birth or during childhood and adolescence.

Factors that may contribute to ADHD include:

  • Genetic features: ADHD can run in families.
  • Environmental factors: Exposure to toxic materials , including as a fetus, may increase the risk.
  • Developmental issues: Problems with the central nervous system at important stages of development may result in ADHD.

Schizophrenia

Factors that may increase a person’s likelihood of developing schizophrenia include:

  • Genetic features: Genetic factors appear to play a role. Having a close family member with schizophrenia may increase the risk.
  • Brain development: Research shows that some individuals with schizophrenia have subtle differences in their brain structure.
  • Neurotransmitters: An imbalance between dopamine and serotonin, the chemical messengers in the brain, may have a connection with schizophrenia. Drugs that alter the levels of these chemicals appear to relieve schizophrenia symptoms.
  • Pregnancy and birth complications: A low birth weight, premature labor, or insufficient oxygen during birth are more likely to have affected people with schizophrenia.

ADHD and schizophrenia

Both conditions involve neurodevelopmental changes and can run in families. However, researchers do not yet know whether the same changes relate to both conditions or to what extent these underlying features overlap.

The risk factors for ADHD and schizophrenia are not the same, but they may overlap. For both conditions, some risk factors may affect a person before birth, while others come into effect during childhood and adolescence.

  • a family history of ADHD or another mental health disorder
  • exposure to certain substances while in the womb
  • a lack of specific nutrients, such as folate, zinc, magnesium, and polyunsaturated acids
  • psychosocial factors
  • maternal alcohol and drug use during pregnancy
  • preterm birth or low birth weight
  • maternal stress and anxiety during pregnancy
  • maternal smoking during pregnancy

Schizophrenia

There is growing evidence that some environmental factors can lead to neurodevelopmental problems that result in schizophrenia.

Possible environmental factors include :

  • exposure to certain substances, such as cannabis or lead, before birth
  • nutritional deficits, including low levels of folic acid and iron
  • rubella or other maternal infections during pregnancy
  • maternal stress during pregnancy
  • infections during childhood and adolescence
  • deficiency in iron and vitamin D resulting in decreased choline during pregnancy
  • an increase in immune system activity due to inflammation or autoimmune disease
  • taking mind-altering drugs as teenagers or young adults

Some researchers have suggested that there may be a link between low birth weight and mental illness, possibly including schizophrenia. However, they have noted that more evidence is necessary to confirm this.

The authors of a 2011 review concluded:

“It appears increasingly likely that a large portion, if not the majority, of schizophrenia cases can be accounted for by interactions between environmental and genetic factors and by other mechanisms involving the subtle interplay between environments and genes.”

ADHD and schizophrenia

Scientists believe that there is an overlap in the factors that can lead to ADHD and schizophrenia.

Genetic factors: A person who has a close relative with schizophrenia may be more likely to develop ADHD. Researchers say that up to 80 percent of cases of schizophrenia and between 60 and 80 percent of cases of ADHD may result from inheritance.

Changes in underlying brain mechanisms: Some neurological factors are common to both conditions.

Environmental influences: Exposure to specific influences before birth and during childhood appears to increase the risk of both conditions.

Shared history: People who have schizophrenia are more likely to have had a diagnosis of ADHD during childhood.

Does ADHD medication lead to schizophrenia?

Some people who use stimulant medication to relieve the symptoms of ADHD go on to experience symptoms of psychosis.

However, it is unclear whether using stimulants to treat ADHD increases the risk of schizophrenia or schizophrenia-type symptoms, specifically psychosis. These symptoms may have appeared without the use of stimulant medication.

Exposure to psychostimulant drugs does appear to increase the risk of psychosis. Psychosis that appears at a younger age is more likely to result from the use of psychostimulant drugs.

However, it remains unclear whether psychosis results from the use of the drugs or whether these individuals were already susceptible to psychosis.

In addition, the type of psychosis that people with ADHD experience tends to be different from that in people with schizophrenia as it involves brief mental changes rather than full hallucinations.

The symptoms of ADHD and schizophrenia are different, but they overlap in the area of inattention.

There are three different types of ADHD:

  • inattentive ADHD
  • hyperactive and impulsive ADHD
  • combined inattentive and hyperactive ADHD

Symptoms of inattentiveness include:

  • having a short attention span and getting easily distracted
  • making careless mistakes during activities
  • appearing not to listen
  • being unable to follow instructions and complete tasks
  • having problems with organizing tasks
  • being forgetful or frequently losing things
  • avoiding tasks that require mental effort

Symptoms of hyperactivity and impulsiveness include:

  • fidgeting constantly and being unable to sit still
  • being unable to engage quietly in leisure activities
  • lacking concentration
  • talking excessively
  • interrupting other people’s conversations or intruding on their activities
  • being restless
  • running excessively or climbing in inappropriate situations
  • acting without thinking
  • having little or no sense of danger

Not everyone who has ADHD will have hyperactivity as a symptom.

Schizophrenia

Doctors categorize the symptoms of schizophrenia as either positive, negative, or cognitive.

Positive symptoms include:

  • hallucinations
  • delusions, such as believing that the government is pursuing them
  • paranoid thoughts
  • agitated or excessive body movements
  • agitated or inappropriate behavior

Negative symptoms include:

  • social withdrawal
  • not caring about appearance and personal hygiene
  • reduced emotional expression
  • losing interest and motivation
  • trouble concentrating
  • changes in sleep habits
  • feeling unable to leave the house
  • a decrease in conversation and speaking

Cognitive symptoms include:

  • having confused or disorganized thoughts
  • an inability to understand information and make decisions
  • a lack of focus and attention
  • difficulty using learned information immediately

ADHD and schizophrenia

ADHD and schizophrenia may share some symptoms.

For example, attention problems affect both people with ADHD and people with schizophrenia.

However, some researchers have suggested that the type of inattention involved in ADHD may be different from that in schizophrenia and that the underlying neurological features are also different.

Thought disorders and psychosis can also occur in both schizophrenia and ADHD. People with schizophrenia often experience psychotic episodes, which can involve hallucinations, delusions, and disturbed thoughts.

Psychosis is not typical of ADHD, but around 10 percent of people with this condition experience psychotic symptoms. One theory is that the stimulant drugs that doctors prescribe to treat ADHD may trigger these psychotic symptoms.

Research has shown that some people whose genetic makeup puts them at high risk of schizophrenia will meet the criteria for a diagnosis of ADHD.

Some people with ADHD also have hyperactivity, but this is not a symptom of schizophrenia.

Doctors use different criteria to diagnose ADHD and schizophrenia.

There is no specific test to diagnose ADHD. A doctor will ask the individual about their medical history and symptoms and then conduct a medical examination to rule out other causes. The doctor will compare the symptoms with ADHD criteria and rating scales to make a diagnosis.

Diagnosis usually happens in childhood, often before the age of 12 years.

Schizophrenia

A doctor will ask the individual about their medical history and the symptoms that they are experiencing. They will also ensure that the symptoms are not due to medication, substance abuse, or another medical condition.

The doctor may carry out alcohol and drug screening or imaging studies, such as an MRI or CT scan.

If a doctor or mental health professional suspects schizophrenia, they will perform a psychiatric evaluation and compare the symptoms with diagnostic criteria for schizophrenia.

According to the NAMI, schizophrenia usually presents in males who are in their late teenage years or early 20s, while the onset tends to occur in females aged about 25–35 years.

ADHD and schizophrenia

A doctor will diagnose both ADHD and schizophrenia by comparing symptoms to those on a list in the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).

The DSM-5 classifies schizophrenia and ADHD as completely different conditions. Schizophrenia is a psychotic disorder, while ADHD is a neurobehavioral disorder.

There is no cure for ADHD or schizophrenia, but treatment can help relieve symptoms.

Treatment options include:

  • stimulant drugs to boost and balance brain chemical levels
  • nonstimulant medicines, which take longer to work than stimulants but can improve attention, focus, and impulsiveness
  • behavioral therapy to help people manage and change their behavior

Schizophrenia

Treatment options for managing the symptoms of schizophrenia include medications and psychosocial therapy.

Antipsychotic drugs: These aim to manage symptoms by controlling levels of the brain chemical dopamine.

Psychosocial therapy: This combines psychotherapy and social training to provide support, education, and guidance to people with schizophrenia.

Hospitalization: This may be necessary when a person’s symptoms are severe.

Electroconvulsive therapy (ECT): People whose symptoms do not respond to medication may benefit from ECT.

Similarities and differences

The treatment options for ADHD and schizophrenia are different. In both cases, doctors aim to manage symptoms rather than cure the condition.

For ADHD, a doctor may prescribe stimulants that increase dopamine levels in the brain. In some people, this type of drug may trigger psychosis.

For schizophrenia, a doctor will prescribe antipsychotic drugs that block the effect of dopamine.

ADHD and schizophrenia are different conditions, but they can occur together, and there may be some overlap between them. Some researchers believe that they share some underlying features. However, exactly how they relate to each other remains unclear.

Both conditions involve inattention, for example, but it is not apparent if this is the same kind of inattention or if it has the same cause.

ADHD tends to start at a younger age, and symptoms often improve with time, although they can continue into adulthood. Some people with ADHD go on to develop symptoms of schizophrenia, including psychosis.

Schizophrenia is usually a long-term condition. Treatment can relieve symptoms and enable many people to live a normal life, but relapse is likely if they do not follow their treatment plan. A person with schizophrenia may also have symptoms of ADHD.

ADHD is far more common than schizophrenia. Many people have ADHD and never develop schizophrenia. There is no evidence that one condition causes the other.


Featured Studies

Featured studies include only those currently recruiting participants. Studies with the most recent start date appear first.

Helping Toddlers and Parents Together

Using stakeholder feedback (i.e., behavioral health providers & caregivers), the goal of this study is to develop a behavioral parenting program that focuses on both parent mental health and parenting for parents of toddlers (12-35 months old). Using a deployment focused intervention model, this study will : (1) develop an early parenting intervention for parents of at-risk toddlers which integrates a focus on parent mental health with evidence-based behavioral parenting strategies, and (2) examine context-specific factors related to the intervention, including feasibility and acceptability to design a more practice-ready intervention.

Treating Parents With ADHD and Their Young Children Via Telehealth: A Hybrid Type I Effectiveness-Implementation Trial

This study will compare the effectiveness of combined parental stimulant medication and behavioral parent training (BPT) versus BPT alone on child ADHD-related impairment (primary outcome), child ADHD and externalizing symptoms, time to child stimulant prescription (secondary child outcomes) and parental ADHD impairment, parental ADHD symptoms, parenting, and BPT engagement (parental outcomes/target mechanisms). This study will also assess the care delivery context and develop an implementation approach for treatment of families with a parent with ADHD and a child with elevated ADHD symptoms via telehealth in primary care sites providing pediatric care.

School Health Implementation Network: Eastern Mediterranean

An estimated 10-20% of children globally are affected by a mental health problem. Child mental health has been identified as a priority issue by the World Health Organization's Eastern Mediterranean Regional Office (WHO EMRO). Following consultations with international and regional experts and stakeholders, WHO EMRO developed an evidence-based School Mental Health Program (SMHP), endorsed by WHO EMRO member countries, including Pakistan. The federal and provincial health departments in Pakistan made recommendations for a phased implementation of the SMHP in a pilot district. In the formative phase of this program, a number of implementation challenges were identified by the stakeholders. Broadly, these included the need to operationalize and adapt the existing components of the intervention to the local context and to develop sustainable mechanisms for delivery of quality training and supervision.

Informed by the results of a formative phase investigations, the SHINE scale-up research team adapted the SMHP (henceforth called Conventional SMHP or cSMHP) to address these implementation challenges. The enhanced version of the intervention is called Enhanced School Mental Health Program (eSMHP). Enhancements to cSMHP have occurred at two levels: A) Content enhancements, such as a collaborative care model for engaging parents/primary caregivers, strategies for teacher's wellbeing, and adaptation and operationalization of particular clinical intervention strategies and B) Technological enhancements which include adaptation of the training manual for delivery using an online training platform, and a 'Chat-bot' to aid the implementation of intervention strategies in classroom settings.

The primary objective of the study is to evaluate the effectiveness of eSMHP in reducing socio-emotional difficulties in school-going children, aged 8-13, compared to cSMHP in Gujar Khan, a rural sub-district of Rawalpindi, Pakistan.

The secondary objectives are to compare the cost-effectiveness, acceptability, adoption, appropriateness (including cultural appropriateness), feasibility, penetration and sustainability of scaled-up implementation of eSMHP and cSMHP. It is hypothesized that eSMHP will prove to be both more effective and more scalable than cSMHP.

The research is embedded within the phased district level implementation of the cSMHP in Rawalpindi, Pakistan. The study population will consist of children of both genders, aged 8-13 (n=960) with socio-emotional difficulties, studying in rural public schools of sub-district Gujar Khan in Rawalpindi.

The proposed study design is a cluster randomized controlled trial (cRCT), embedded within the conventional implementation of the SMHP. Following relevant ethics committees and regulatory approvals, 80 eligible schools, stratified by gender, will be randomized into intervention and control arms with a 1:1 allocation ratio. Following informed consent from the parent/ primary caregiver, children will be screened for socio-emotional difficulties using Strengths and Difficulties Questionnaire (SDQ). 960 children scoring > 12 on the teacher-rated SDQ total difficulty scores and > 14 on the parent-rated SDQ total difficulty scores will be recruited and equally randomized into intervention and control arms (480 in each arm).

Teachers in the intervention arm will receive training in eSMHP, whereas teachers in the active control will be trained in cSMHP. Trained teachers will deliver the program to children in their respective arms.

Primary Outcome: The primary outcome is reduction in socio-emotional total difficulties scores, measured with the parent-rated SDQ, 9 months after commencing intervention delivery.

Secondary Outcomes: Implementation data on acceptability, adoption, appropriateness (including cultural appropriateness), feasibility, penetration and sustainability outcomes will be collected from children, parents/primary caregivers, head teachers and teachers. In addition, data will be collected on self-reported Psychological Outcome Profiles (PSYCHLOPS)-KIDS to measure progress on psycho-social problems and wellbeing annual academic performance classroom absenteeism, stigmatizing experiences and parent-teacher interaction. Data on teachers' sense of efficacy and subjective well-being, and on the schools' psychosocial environment profile will be collected. All secondary outcome data will be collected at baseline and 9 months after commencing intervention delivery.

Outcomes will be analyzed on an intention to treat basis. The role of various factors as potential mediators and moderators eSMHP effectiveness will be explored.

Cost-effectiveness evaluation of SMHP shall be evaluated in terms of costs associated with implementation of eSMHP compared with cSMHP.

Brain Plasticity Underlying Acquisition of New Organizational Skills in Children

Organizational, time management and planning (OTMP) skills deficits are impairing features of developmental disorders, such as Attention Deficit Hyperactive Disorder (ADHD), which compromise school performance and family relations. The manualized Organizational Skills Training program (OST) was designed to target children's specific OTMP deficits. However, the brain mechanisms of treatment-induced changes remain unknown. The current study combines a training intervention (OST) with non-invasive MRI imaging in a pre-/post-design in a randomized two-arm (treatment vs. waitlist) trial to address this question.

A Novel fNIRS Neurofeedback Intervention for Enhancement of Working Memory in Attention Deficit Hyperactivity Disorder (ADHD)

The proposed study is to test and validate a novel intervention that integrates computerized cognitive training with real-time neuromonitoring and neurofeedback to enhance working memory by probing the individualized neural systems underlying working memory. We will test the proposed intervention on children with ADHD with working memory deficits. The R61 proof-of-concept phase will assess the target engagement, effective dose and feasibility.

School-Based Depression Prevention for Adolescents With ADHD

The purpose of this study is to develop a modified behavioral activation program in adolescents with ADHD to be implemented by school mental health providers in an urban, low-income school district. Subsequently we will examine its effectiveness in reducing depressive symptoms and improving emotion regulation and reward responsivity, compared to usual care.

Sleep Dysfunction and Neurocognitive Outcomes in Adolescent ADHD

This study seeks to characterize sleep physiology in adolescents with and without Attention deficit hyperactivity disorder (ADHD) and its relationship to differential neurocognitive and clinical outcomes within these groups.

Ventral Tegmental Area (VTA) Self-Activation in Attention Deficit Hyperactivity Disorder (ADHD)

The purpose of this study is to see if a non-medication intervention can increase motivation in individuals with ADHD by observing brain activity using magnetic resonance imaging (MRI).

Virtual Reality Attention Management

Problems with distraction are widespread in the 21st century, but for people with developmental delays or behavioral challenges they can have more damaging effects. For example, susceptibility to distraction is associated with worse school and social performance, lower high school graduation rates, and increased incidence of serious accidents. The investigators' goal is to improve understanding of distractibility and develop a targeted treatment. The proposed intervention is based on models of habituation, which is a term that means reduced physiological and emotional response to a stimulus (e.g. moving object, or loud noise, etc.) as it is seen repeatedly. The investigators use virtual reality technology to show study participants distracting stimuli repeatedly in a virtual classroom setting, and their hypothesis states that participants will improve attention in the face of distraction by training with this technology intervention. The virtual classroom setting is especially relevant for children who have significant challenges with distractibility, such as children with ADHD. This intervention will likely be effective in helping individuals with other clinical disorders and perhaps the general population as well.

Brain Imaging of Childhood Onset Psychiatric Disorders, Endocrine Disorders and Healthy Volunteers

Magnetic Resonance Imaging (MRI) unlike X-rays and CT-scans does not use radiation to create a picture. MRI use as the name implies, magnetism to create pictures with excellent anatomical resolution. Functional MRIs are diagnostic tests that allow doctors to not only view anatomy, but physiology and function. It is for these reasons that MRIs are excellent methods for studying the brain.

In this study, researchers will use MRI to assess brain anatomy and function in X and Y chromosome variation, healthy volunteers, and patients with a variety of childhood onset psychiatric disorders. The disorders include attention deficit disorder, autism, congenital adrenal hyperplasia, childhood-onset schizophrenia, dyslexia, obsessive compulsive disorder, Sydenham's chorea, and Tourette's syndrome.

Results of the MRIs showing the anatomy of the brain and brain function will be compared across age, sex (gender), and diagnostic groups. Correlations between brain and behavioral measures will be examined for normal and clinical populations.


What dosage of phentermine is best for ADHD?

Due to the fact that phentermine hasn’t been formally evaluated for the treatment of ADHD, it is unknown as to what dosage would be optimal for this indication. Based on the fact that lower doses of phentermine (e.g. 20 mg) exert a modest central effect and don’t really alter dopaminergic transmission, it may be that a high dose is necessary for ADHD. In other words, if phentermine were to be used for ADHD, it is likely that a high dose such as 37.5 mg (or even greater) would be necessary to combat symptoms.

Compared to lower doses, administering phentermine at high doses should exert a more significant central effect, as well as noticeably modulate dopamine. In theory, this should help alleviate symptoms of ADHD caused by deficits in catecholaminergic signaling. The only problem with using a high dose (e.g. 37.5+) is that the peripheral effect will be potent enough to cause serious adverse effects.

Using a high dose of phentermine over an extended duration may significantly increase risk of a cardiac events, ischemic attack, and mortality. There are no formal dosing guidelines of phentermine for ADHD, and if the drug were to be utilized for ADHD, dosage optimization via guidance of a psychopharmacologist should be required. That said, extremely low doses are unlikely to have a significant effect upon ADHD symptoms unless peripheral dysfunction is heavily implicated as a causal underpinning.


The Not-So-Hidden Cause Behind the A.D.H.D. Epidemic

Between the fall of 2011 and the spring of 2012, people across the United States suddenly found themselves unable to get their hands on A.D.H.D. medication. Low-dose generics were particularly in short supply. There were several factors contributing to the shortage, but the main cause was that supply was suddenly being outpaced by demand.

The number of diagnoses of Attention Deficit Hyperactivity Disorder has ballooned over the past few decades. Before the early 1990s, fewer than 5 percent of school-age kids were thought to have A.D.H.D. Earlier this year, data from the Centers for Disease Control and Prevention showed that 11 percent of children ages 4 to 17 had at some point received the diagnosis — and that doesn’t even include first-time diagnoses in adults. (Full disclosure: I’m one of them.)

That amounts to millions of extra people receiving regular doses of stimulant drugs to keep neurological symptoms in check. For a lot of us, the diagnosis and subsequent treatments — both behavioral and pharmaceutical — have proved helpful. But still: Where did we all come from? Were that many Americans always pathologically hyperactive and unable to focus, and only now are getting the treatment they need?

Probably not. Of the 6.4 million kids who have been given diagnoses of A.D.H.D., a large percentage are unlikely to have any kind of physiological difference that would make them more distractible than the average non-A.D.H.D. kid. It’s also doubtful that biological or environmental changes are making physiological differences more prevalent. Instead, the rapid increase in people with A.D.H.D. probably has more to do with sociological factors — changes in the way we school our children, in the way we interact with doctors and in what we expect from our kids.

Which is not to say that A.D.H.D. is a made-up disorder. In fact, there’s compelling evidence that it has a strong genetic basis. Scientists often study twins to examine whether certain behaviors and traits are inborn. They do this by comparing identical twins (who share almost 100 percent of the same genes) with fraternal twins (who share about half their genes). If a disorder has a genetic basis, then identical twins will be more likely to share it than fraternal twins. In 2010, researchers at Michigan State University analyzed 22 different studies of twins and found that the traits of hyperactivity and inattentiveness were highly inheritable. Numerous brain-imaging studies have also shown distinct differences between the brains of people given diagnoses of A.D.H.D. and those not — including evidence that some with A.D.H.D. may have fewer receptors in certain regions for the chemical messenger dopamine, which would impair the brain’s ability to function in top form.

None of that research yet translates into an objective diagnostic approach, however. Before I received my diagnosis, I spent multiple sessions with a psychologist who interviewed me and my husband, took a health history from my doctor and administered several intelligence tests. That’s not the norm, though, and not only because I was given my diagnosis as an adult. Most children are given the diagnosis on the basis of a short visit with their pediatrician. In fact, the diagnosis can be as simple as prescribing Ritalin to a child and telling the parents to see if it helps improve their school performance.

This lack of rigor leaves room for plenty of diagnoses that are based on something other than biology. Case in point: The beginning of A.D.H.D. as an “epidemic” corresponds with a couple of important policy changes that incentivized diagnosis. The incorporation of A.D.H.D. under the Individuals With Disabilities Education Act in 1991 — and a subsequent overhaul of the Food and Drug Administration in 1997 that allowed drug companies to more easily market directly to the public — were hugely influential, according to Adam Rafalovich, a sociologist at Pacific University in Oregon. For the first time, the diagnosis came with an upside — access to tutors, for instance, and time allowances on standardized tests. By the late 1990s, as more parents and teachers became aware that A.D.H.D. existed, and that there were drugs to treat it, the diagnosis became increasingly normalized, until it was viewed by many as just another part of the experience of childhood.

Stephen Hinshaw, a professor of psychology at University of California, Berkeley, has found another telling correlation. Hinshaw was struck by the disorder’s uneven geographical distribution. In 2007, 15.6 percent of kids between the ages of 4 and 17 in North Carolina had at some point received an A.D.H.D. diagnosis. In California, that number was 6.2 percent. This disparity between the two states is representative of big differences, generally speaking, in the rates of diagnosis between the South and West. Even after Hinshaw’s team accounted for differences like race and income, they still found that kids in North Carolina were nearly twice as likely to be given diagnoses of A.D.H.D. as those in California.

Hinshaw, as well as sociologists like Rafalovich and Peter Conrad of Brandeis University, argues that such numbers are evidence of sociological influences on the rise in A.D.H.D. diagnoses. In trying to narrow down what those influences might be, Hinshaw evaluated differences between diagnostic tools, types of health insurance, cultural values and public perceptions of mental illness. Nothing seemed to explain the difference — until he looked at educational policies.

The No Child Left Behind Act, signed into law by President George W. Bush, was the first federal effort to link school financing to standardized-test performance. But various states had been slowly rolling out similar policies for the last three decades. North Carolina was one of the first to adopt such a program California was one of the last. The correlations between the implementation of these laws and the rates of A.D.H.D. diagnosis matched on a regional scale as well. When Hinshaw compared the rollout of these school policies with incidences of A.D.H.D., he found that when a state passed laws punishing or rewarding schools for their standardized-test scores, A.D.H.D. diagnoses in that state would increase not long afterward. Nationwide, the rates of A.D.H.D. diagnosis increased by 22 percent in the first four years after No Child Left Behind was implemented.

To be clear: Those are correlations, not causal links. But A.D.H.D., education policies, disability protections and advertising freedoms all appear to wink suggestively at one another. From parents’ and teachers’ perspectives, the diagnosis is considered a success if the medication improves kids’ ability to perform on tests and calms them down enough so that they’re not a distraction to others. (In some school districts, an A.D.H.D. diagnosis also results in that child’s test score being removed from the school’s official average.) Writ large, Hinshaw says, these incentives conspire to boost the diagnosis of the disorder, regardless of its biological prevalence.

Rates of A.D.H.D. diagnosis also vary widely from country to country. In 2003, when nearly 8 percent of American kids had been given a diagnosis of A.D.H.D., only about 2 percent of children in Britain had. According to the British National Health Service, the estimate of kids affected by A.D.H.D. there is now as high as 5 percent. Why would Britain have such a comparatively low incidence of the disorder? But also, why is that incidence on the rise?

Conrad says both questions are linked to the different ways our societies define disorders. In the United States, we base those definitions on the Diagnostic and Statistical Manual of Mental Disorders (D.S.M.), while Europeans have historically used the International Classification of Diseases (I.C.D.). “The I.C.D. has much stricter guidelines for diagnosis,” Conrad says. “But, for a variety of reasons, the D.S.M. has become more widely used in more places.” Conrad, who’s currently researching the spread of A.D.H.D. diagnosis rates, believes that America is essentially exporting the D.S.M. definition and the medicalized response to it. A result, he says, is that “now we see higher and higher prevalence rates outside the United States.”

According to Joel Nigg, professor of psychiatry at Oregon Health and Science University, this is part of a broader trend in America: the medicalization of traits that previous generations might have dealt with in other ways. Schools used to punish kids who wouldn’t sit still. Today we tend to see those kids as needing therapy and medicine. When people don’t fit in, we react by giving their behavior a label, either medicalizing it, criminalizing it or moralizing it, Nigg says.

For some kids, getting medicine might be a better outcome than being labeled a troublemaker. But of course there are also downsides, especially when there are so many incentives encouraging overdiagnosis. Medicalization can hurt people just as much as moralizing can. Not so long ago, homosexuality was officially considered a mental illness. And in a remarkable bit of societal blindness, the diagnosis of drapetomania was used to explain why black slaves would want to escape to freedom.


Attention-Deficit/Hyperactivity Disorder (ADHD)

At Niagara Neuropsychology, we offer 3 levels of assessment for ADHD/ADD for those age 5 and up (including adults). These were developed in order to be able to provide the most comprehensive assessment possible and to ensure that even those with less financial means can obtain an adequate assessment and diagnosis.

Below are descriptions of each level of ADHD/ADD assessment from the top tier ADVANCED ADHD/ADD Assessment, middle tier INTERMEDIATE ADHD/ADD Assessment, and lowest tier BRIEF ADHD/ADD Assessment. Note that even the BRIEF ADHD/ADD Assessment is a more thorough assessment than what is obtained from most psychiatrists, pediatricians, and family physicians, and most psychologists.

TOP TIER—ADVANCED ADHD/ADD ASSESSMENT:

  • Most in-depth ADHD/ADD assessment available
  • A 60-minute intake interview with Dr. Friesen (charged separately at $195)
  • Parent/teacher/self-rating measures of executive functions (

MIDDLE TIER—INTERMEDIATE ADHD/ADD ASSESSMENT:

  • Detailed, thorough multimodal ADHD assessment
  • A 60-minute intake interview with Dr. Friesen (charged separately at $195)
  • Parent/teacher/self-rating measures of executive functions (

LOWEST TIER—BRIEF ADHD/ADD ASSESSMENT:

  • Although brief relative to the Intermediate and Full ADHD Assessments, this assessment is more thorough than ADHD assessments available via family physicians, pediatricians, psychiatrists, and most psychologists
  • A 60-minute intake interview with Dr. Friesen (charged separately at $195)
  • Parent/teacher/self-rating measures of executive functions (

Attention-Deficit/Hyperactivity Disorder (ADHD)

Attention-deficit hyperactivity disorder (ADHD) is the current term for a specific developmental disorder seen in both children and adults that is comprised of deficits in behavioural inhibition, sustained attention and resistance to distraction, and the regulation of one’s activity level to the demands of a situation (hyperactivity or restlessness). This disorder has had numerous different labels over the past century, including hyperactive child syndrome, hyperkinetic reaction of childhood, minimal brain dysfunction, and attention deficit disorder (with or without hyperactivity).

ADHD is one of the most common neurodevelopmental disorders of childhood and adolescence. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5: APA, 2013), ADHD is marked by “a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development…several inattentive or hyperactive-impulsive symptoms were present prior to age 12 years…clear evidence that the symptoms interfere with, or reduce the quality of, social, academic, or occupational functioning.” (APA, 2013, p. 59-60). According to the DSM-5, population surveys across most cultures find the prevalence of ADHD to be approximately 5% in children (and 2.5% in adults). ADHD is associated with numerous negative outcomes including reduced school performance/academic attainment, poor occupational attainment, social rejection, the development of conduct disorder/antisocial personality disorder, incarceration, substance abuse, physical injuries, traffic accidents/violations, obesity, and negative family relationships (APA, 2013). Thus, early and accurate identification and treatment of ADHD is of enormous societal importance.

How Is ADHD Diagnosed?

The FDA recently approved quantitative EEG (qEEG) for improving that accuracy of ADHD diagnoses (click here and here to learn more). At Niagara Neuropsychology we use qEEG in addition to clinical interviews, behavioural rating scales, and neuropsychological testing to provide the most up-to-date and accurate diagnostic process.

There are numerous reasons why a child, adolescent, or adult may have symptoms or behaviours consistent with ADHD. These include sleep disorders, bipolar disorder, depression, anxiety (e.g., Generalized Anxiety Disorder or GAD, Obsessive-Compulsive Disorder or OCD, Posttraumatic Stress Disorder or PTSD), head injuries (e.g., concussions or more significant traumatic brain injuries or TBI), Tourette’s syndrome, thyroid disease, nutritional deficiencies, and learning disorders.

When a patient does have ADHD, in addition to the subtypes based on behaviours outlined in the DSM-5, there are also a number of subtypes of ADHD based on qEEG. These include excessive slow wave (e.g., theta) activity in the front part of the brain (the vast majority of ADHD patients fall into this category) or excessive fast wave (beta) activity (a substantial but minority of ADHD patients fall into this category).

The effective treatment for these two subtypes is quite different. For example, the use of a stimulant (e.g., Ritalin or Adderall) for those with the high beta subtype may over activate the brain and lead to worsening of symptoms, including increased anxiety, appetite suppression, and insomnia. On the other hand, a stimulant is more likely to be effective in those patients with excessive slow wave activity (e.g., theta) in the frontal lobe. Similarly, the neurofeedback training for these two subtypes will be very different.

WHAT ABOUT TREATMENT?

Here is a brief clip from CNN on neurofeedback training for those with ADHD and anxiety:

*Partially adapted from ISRN.org

The International Society for Neuroregulation & Research (ISNR.org) regularly updates a comprehensive bibliography of neurofeedback research studies on various disorders including ADHD that can be accessed HERE.

Similarly, Applied Psychophysiology Education (APEd) has a comprehensive list of abstracts for neurofeedback research (including on ADHD) that you can access HERE.

EEG biofeedback or neurofeedback is a safe and effective treatment of ADHD that improves the core symptoms for patients diagnosed with ADHD. A meta-analysis by Arns et al. (2009) of ten well-controlled studies combined with an additional five prospective pre/post design studies. This meta-analysis concluded that “neurofeedback treatment for ADHD can be considered “Efficacious and specific” (the highest possible ranking) with a large effect size for inattention and impulsivity and a medium effect size for hyperactivity” [p. 180].

More recently, Narimani et al., (2018) published another meta-analysis of nine studies on the effectiveness of neurofeedback and ADHD symptoms in adults. They concluded “Based on the results of this meta-analysis, neurofeedback treatment was found to have a large effect in reducing ADHD symptoms in adults with attention deficit/hyperactivity disorder.” Click HERE for the article.

In October 2012, the company that maintains the Amer­i­can Academy of Pediatrics’ ranking of research support for psychosocial treatments awarded neurofeedback the highest level of evidence-based support for the treatment of ADHD [PracticeWise, 2012].

For a more layperson’s review of neurofeedback and ADHD, click HERE to read Dr. Vicent Monastra’s short article in ADDitude Magazine.

For a recent summary of one study that randomly assigned children and adolescents with ADHD to receive either 40 sessions of neurofeedback or computerized brain training, click HERE. Note they found the neurofeedback group had significantly more symptom reduction.

For another example of a randomized controlled trial that compared the effectiveness of neurofeedback to stimulant medication (i.e., methylphenidate or Ritalin), click HERE. This study found that neurofeedback was as effective as stimulant medication. The authors concluded “Neurofeedback was as effective as methylphenidate at treating the attentional and hyperactivity symptoms of ADHD, based on parental reports…This supports the use of neurofeedback as an alternative therapy for children and adolescents with ADHD“.

For a recent meta-analysis on the long-term effectiveness of neurofeedback for the treatment of ADHD, see the February 2018 issue of the journal European Child & Adolescent Psychiatry–Sustained Effects of Neurofeedback in ADHD: A Systematic Review and Meta-Analysis. The authors found the effects of neurofeedback were maintained for 6 to 12 months after training ended. They concluded, “Our meta-analytic results of NF treatment follow-up suggest that there are sustained symptom reductions over time in comparison with non-active control conditions. The improvements seen here are comparable to active treatments (including methylphenidate) at a short-term follow-up… As such, NF can be considered a non-pharmacological treatment option for ADHD with evidence of treatment effects that are sustained when treatment is completed and withdrawn.

Krepel et al., (2020) reported on a multi-centre effectiveness trial (across 5 clinics) of qEEG informed neurofeedback in ADHD patients. They found neurofeedback resulted in a 55% remission rate(i.e., no longer meeting diagnostic criteria for ADHD), compared to

33% remission rates in mutlicentre trials for ADHD medication. This study found that higher rates of hyperactivity predicted a poorer treatment response. 70% of ADHD patients had at least a 50% reduction in symptoms and 85% had a least a 25% reduction in symptoms. Click HERE for the article.

The International Society for Neurofeedback and Research (ISNR) recently commissioned a comprehensive review of NFB’s evidence-base for the treatment of ADHD. This review documents that not only has neurofeedback been found to be superior to a variety of experimental control group conditions, but also in three studies neurofeedback was found to be equivalent to stimulant medication in treating the core symptoms of ADHD [Pigott et al., 2013].

Furthermore, the review found five studies that assessed whether or not neurofeedback resulted in sustained benefits after treatment ended, including two studies with two-year follow-up assessments. In each of these follow-up assessments, the gains from neurofeedback were maintained after treatment had ended and in one study had increased further during the two-year follow-up such that half of the children no longer meet the diagnostic criteria for ADHD.

The MTA Cooperative Study’s follow-up results, the largest ever treatment effectiveness study for ADHD, documented that the commonly reimbursed treatments of stimulant medication and behaviour therapy failed to result in sustained benefit for the vast majority of ADHD children who received them. This multi-centered NIMH-funded study compared systematic medication management (SMM), multi-component behaviour therapy (BT), combined SMM/BT, and usual community care (CC) groups to evaluate their effectiveness in treating ADHD [Jensen et al., 2007 Molina et al., 2009]. Despite the initial superiority of SMM and combined SMM/BT treatments, these follow-up analyses found that after 2, 6, and 8 years the four treatment groups did not differ on any outcome measure. Most discouragingly, the researchers report that “the MTA participants fared worse than the local normative comparison group on 91% of the variables tested.” These researchers conclude by stating that “Innovative treatment approaches targeting specific areas of adolescent impairment are needed” [Molina et al., 2009, p. 484].

In contrast to the positive reports of sustained benefit following termination of neurofeedback treatment, stimulant medications’ beneficial effects commonly cease when the medication is stopped, and as found in the MTA study, the authors concluded that there was no evidence to support the “long-term advantage of medication treatment beyond 2 years for the majority of children” [Molina et al., 2009, p.497].

Finally, the recent published follow-up findings from the NIMH-funded Preschool Attention-Deficit/Hyperactivity Disorder Treatment Study (PATS) found results virtually identical to those from the MTA study. These researchers report that “medication status during follow-up, on versus off, did not predict symptom severity” and despite optimal parent training and systematic medication management at the study’s outset, the authors concluded that “ADHD in preschoolers is a relatively stable diagnosis over a 6-year period. The course is generally chronic, with high symptom severity and impairment, in very young children with moderate-to-severe ADHD, despite treatment with medication. Development of more effective ADHD intervention strategies is needed for this age group” [Riddle et al., 2013, p. 1].

Neurofeedback is one such “innovative” and “more effective” treatment for ADHD with proven effectiveness targeting the specific areas of impairment that are essential to its diagnosis: 1) inattention, 2) impulsivity, and 3) hyperactivity. Unlike the findings in both the MTA Cooperative and PATS studies, neurofeedback has been found to result in sustained improvement in ADHD’s core symptoms after the end of treatment.

For example, Van Doren et al., (2019) conducted a meta-analysis and found that while stimulant medication (e.g., Ritalin) resulted in somewhat stronger effects than neurofeedback while during treatment (i.e., large effect size), the neurofeedback effects lasted at least 6-months after the treatment ended and the effect of neurofeedback actually INCREASED after the treatment ended. For exampled, the strength of the neurofeedback training at reducing inattention was considered “medium” (i.e., a medium effect size) at the end of treatment. HOWEVER, the effect increased to “large” (i.e., a large effect size) at 2 to 12 months after treatment stopped. Click HERE to see the original study.

For a recent 2019 review of the evidence on neurofeedback in the treatment of ADHD, click HERE. The authors concluded:

Based on meta-analyses and (large multicenter) randomized controlled trials, three standard neurofeedback training protocols, namely theta/beta (TBR), sensori-motor rhythm (SMR), and slow cortical potential (SCP), turn out to be efficacious and specific. However, the practical implementation of neurofeedback as a clinical treatment is currently not regulated…We conclude that neurofeedback based on standard protocols in ADHD should be considered as a viable treatment alternative and suggest that further research is needed to understand how specific neurofeedback protocols work. Eventually, we emphasize the need for standard neurofeedback training for practitioners and binding standards for use in clinical practice.”

Below is a video by Dr. Ed Hamlin on the evidence for neurofeedback for ADHD:

*The following is partially adapted from Dr. Russell Barkley’s ADHD Factsheet:

MAJOR CHARACTERISTICS: The predominant features of this disorder include:

  • 1. Impaired response inhibition, impulse control, or the capacity to delay gratification. This is often noted in the individual’s inability to stop and think before acting to wait one’s turn while playing games, conversing with others, or having to wait in line to interrupt their responding quickly when it becomes evident that their actions are no longer effective to resist distractions while concentrating or working to work for larger, longer-term rewards rather than opting for smaller, more immediate ones and inhibiting the dominant or immediate reaction to an event, as the situation may demand.
  • 2. Excessive task-irrelevant activity or activity that is poorly regulated to the demands of a situation. Individuals with ADHD in many cases are noted to be excessively fidgety, restless, and “on the go.” They display excessive movement not required to complete a task, such as wriggling their feet and legs, tapping things, rocking while seated, or shifting their posture or position while performing relatively boring tasks. Younger children with the disorder may show excessive running, climbing, and other gross motor activity. While this tends to decline with age, even teenagers with ADHD are more restless and fidgety than their peers. In adults with the disorder, this restlessness may be more subjective than outwardly observable, although with some adults they remain outwardly restless as well and report a new to always be busy or doing something and being unable to sit still.
  • 3. Poor sustained attention or persistence of effort to tasks. This problem often arises when the individual is assigned boring, tedious, protracted, or repetitive activities that lack intrinsic appeal to the person. They often fail to show the same level of persistence, “stick-to-it-tiveness,” motivation, and willpower of others their age when uninteresting yet important tasks must be performed. They often report becoming easily bored with such tasks and consequently shift from one uncompleted activity to another without completing these activities. Loss of concentration during tedious, boring, or protracted tasks is commonplace, as is an inability to return to their task on which they were working should they be unexpectedly interrupted. Thus, they are easily distracted during periods when concentration is important to the task at hand. They may also have problems with completing routine assignments without direct supervision, being unable to stay on task during independent work.

These are the three most common areas of difficulty associated with ADHD. However, research is suggesting that those with ADHD, particularly the subtypes associated with impulsive behavior (see below), may also have difficulties in the following areas of psychological functioning as well:

  • 1. Remembering to do things, or working memory. Working memory refers to the capacity to hold information in mind that will be used to guide one’s actions, either now, or at a later time. It is essential for remembering to do things in the near future. Those with ADHD often have difficulties with working memory and so are described as forgetful around doing things, unable to keep important information in mind that they will need to guide their actions later, and disorganized in their thinking and other activities as they often lose track of the goal of their activities. They may often be described as acting without hindsight or forethought, and being less able to anticipate and prepare for future events as well as others, all of which seem to be dependent on working memory. Recently, research suggests that those with ADHD cannot sense or use time as adequately as others in their daily activities, such that they are often late for appointments and deadlines, ill-prepared for upcoming activities, and less able to pursue long-term goals and plans as well as others. Problems with time management and organizing themselves for upcoming events are commonplace in older children and adults with the disorder.
  • 2. Delayed development of internal language (the mind’s voice) and rule-following. Research has lately been suggesting that children with ADHD are significantly delayed in the development of internal language, the private voice inside one’s mind that we employ to converse with ourselves, contemplate events, and direct or command our own behavior. This private speech is absolutely essential to the normal development of contemplation, reflection, and self-regulation. Its delay in those with ADHD contributes to significant problems with their ability to follow through on rules and instructions, to read and follow directions carefully, to follow through on their own plans, rules, and “dolists,” and even to act with legal or moral principles in mind. When combined with their difficulties with working memory, this problem with self-talk or private speech often results in significant interference with reading comprehension, especially of complex, uninteresting, or extended reading assignments.
  • 3. Difficulties with regulation of emotions, motivation, and arousal. Children and adults with ADHD often have problems inhibiting their emotional reactions to events as well as do others of their age. It is not that the emotions they experience are inappropriate, but that those with ADHD are more likely to publicly manifest the emotions they experience than would someone else. They seem less able to “internalize” their feelings, to keep them to themselves, and even to moderate them when they do so as others might do. Consequently, they are likely to appear to others as less emotionally mature, more reactive with their feelings, and more hot-headed, quick-tempered, and easily frustrated by events. Coupled with this problem with emotion regulation is the difficulty they have in generating intrinsic motivation for tasks that have no immediate payoff or appeal to them. This capacity to create private motivation, drive, or determination often makes them appear to lack willpower or self-discipline as they cannot stay with things that do not provide immediate reward, stimulation, or interest to them. Their motivation remains dependent on the immediate environment for how hard and how long they will work, whereas others develop a capacity for intrinsically motivating themselves in the absence of immediate rewards or other consequences. Also related to these difficulties with regulating emotion and motivation is that of regulating their general level of arousal to meet situational demands. Those with ADHD find it difficult to activate or arouse themselves to initiate work that must be done, often complain of being unable to stay alert or even awake in boring situations, and frequently seem to be daydreamy or “in a fog” when they should be more alert, focused, and actively engaged in a task.
  • 4. Diminished problem-solving ability, ingenuity, and flexibility in pursuing long-term goals. Often times, when we are engaged in goal-directed activities, problems are encountered that are obstacles to the goal’s attainment. At these times, individuals must be capable of quickly generating a variety of options to themselves, considering their respective outcomes, and selecting among them those which seem most likely to surmount the obstacle so they can continue toward their goal. Persons with ADHD find such hurdles to their goals to be more difficult to surmount often giving up their goals in the face of obstacles and not taking the time to think through other options that could help them succeed toward their goal. Thus they may appear as less flexible in approaching problem situations, more likely to respond automatically or on impulse, and so are less creative at overcoming the road-blocks to their goals than others are likely to be. These problems may even be evident in the speech and writing of those with the disorder, as they are less able to quickly assemble their ideas into a more organized, coherent explanation of their thoughts. And so they are less able to rapidly assemble their actions or ideas into a chain of responses that effectively accomplishes the goal given them, be it verbal or behavioral in nature.
  • 5. Greater than normal variability in their task or work performance. It is typical of those with ADHD, especially those subtypes associated with impulsive behavior, to show substantial variability across time in the performance of their work. These wide swings may be found in the quality, quantity, and even speed of their work, failing to maintain a relatively even pattern of productivity and accuracy in their work from moment to moment and day to day. Such variability is often puzzling to others who witness it as it is clear that at some times, the person with ADHD can complete their work quickly and correctly while at others times, their tasks are performed poorly, inaccurately, and quite erratically. Indeed, some researchers see this pattern of high variability in work-related activities to be as much a hallmark of the disorder as is the poor inhibition and inattention described above.

OTHER CHARACTERISTICS: Several other development characteristics are associated with the disorder:

  • 1. Early onset of the major characteristics. The symptoms of ADHD appear to arise, on average, between 3 and 6 years of age. This is particularly so for those subtypes of ADHD associated with hyperactive and impulsive behavior. Others may not develop their symptoms until somewhat later in childhood. But certainly the vast majority of those with the disorder have had some symptoms since before the age of 13 years. Those who have the Predominantly Inattentive Type of ADHD that is not associated with impulsiveness appear to develop their attention problems somewhat later than do the other subtypes, often in middle or later childhood. And so the disorder is believed to be one of childhood onset, regardless of the subtype, suggesting that should these symptoms develop for the first time in adulthood, other mental disorders rather than ADHD should be suspected.
  • 2. Situational variation of symptoms. The major symptoms of ADHD are likely to change markedly as a consequence of the nature of the situation the person happens to be in. Research suggests that those with ADHD behave better in one-to-one situations, when doing tasks that they enjoy or find interesting, when there is some immediate payoff for behaving well, when they are supervised, in their work done earlier in the day rather than later, and, for children, when they are with their fathers compared to their mothers. Conversely, those with ADHD may manifest more of their symptoms in group settings, when they must perform boring work, when they must work independently of supervision, when their work must be done later in the day, and when they are with their mothers. Sometimes or in some cases, these situational factors may have little effect on the person’s level of ADHD symptoms but they have been noted often enough in research to make such situational changes in their symptoms important to appreciate.
  • 3. Relatively chronic course. ADHD symptoms are often quite developmental stable. Although the absolute level of symptoms does decline with age, this is true of the inattentiveness, impulsiveness, and activity levels of normal individuals as well. And so those with ADHD may be improving in their behavior but not always catching up with their peer group in this regard. This seems to leave them chronically behind others of their age in their capacity to inhibit behavior, sustain attention, control distractibility, and regulate their activity level. Research suggests that among those children clinically diagnosed with the disorder in childhood, 50-80 percent will continue to meet the criteria for the diagnosis in adolescence, and 10-65 percent may continue to do so in adulthood. Whether or not they have the full syndrome in adulthood, at least 50-70 percent may continue to manifest some symptoms that are causing them some impairment in their adult life.

ADULT OUTCOME: It has been estimated that anywhere from 15 to 50 percent of those with ADHD ultimately outgrow the disorder. However, these figures come from follow-up studies in which the current and more rigorous diagnostic criteria for the disorder were not used. When more appropriate and modern criteria are employed, probably only 20-35 percent of children with the disorder no longer have any symptoms resulting in impairment in their adult life. Over the course of their lives, a significant minority of those with ADHD experience a greater risk for developing oppositional and defiant behavior (50%+), conduct problems and antisocial difficulties (25-45%), learning disabilities (25-40%), low self-esteem, and depression (25%). Approximately 5-10 percent of those with ADHD may develop more serious mental disorders, such as manic-depression or bipolar disorder. Between 10 and 20 percent may develop antisocial personality disorder by adulthood, most of whom will also have problems with substance abuse. Overall, approximately 10-25 percent develop difficulties with over-use, dependence upon, or even abuse of legal (i.e., alcohol, tobacco) or illegal substances (i.e., marijuana, cocaine, illicit use of prescription drugs, etc.), with this risk being greatest among those who had conduct disorder or delinquency as adolescents. Despite these risks, note should certainly be taken that upwards of half or more of those having ADHD do not develop these associated difficulties or disorders. However, the majority of those with ADHD certainly experienced problems with school performance, with as many as 30-50 percent having been retained in their school grade at least once, and 25-36 percent never completing high school.

As adults, those with ADHD are likely to be under-educated relative to their intellectual ability and family educational background. They are also likely to be experience difficulties with work adjustment, and may be under-employed in their occupations relative to their intelligence, and educational and family backgrounds. They tend to change their jobs more often than others do, sometimes out of boredom or because of interpersonal problems in the workplace. They also tend to have a greater turnover of friendships and dating relationships and seem more prone to marital discord and even divorce. Difficulties with speeding while driving are relatively commonplace, as are more traffic citations for this behavior, and, in some cases, more motor vehicle accidents than others are likely to experience in their driving careers. Thus, they are more likely to have had their driver’s license suspended or revoked.

SUBTYPES: Since 1980, it has become possible to place those with ADHD into several subtypes, depending upon the combinations of symptoms they experience. Those who have difficulties primarily with impulsive and hyperactive behavior and not with attention or concentration are now referred to as having the Predominantly HyperactiveImpulsive Type. Individuals with the opposite pattern, significant inattentiveness without being impulsive or hyperactive are called the Predominantly Inattentive Type. However, most individuals with the disorder will manifest both of these clinical features and so are referred to as the Combined Type of ADHD. Research on those with the Combined Type suggests that they are likely to develop their hyperactive and/or impulsive symptoms first and usually during the preschool years. At this age, then, they may be diagnosed as having the Predominantly HyperactiveImpulsive Type. However, in most of these cases, they will eventually progress to developing the difficulties with attention span, persistence, and distractibility within a few years of entering school such that they will now be diagnosed as having the Combined Type.

There is considerably less research on the Predominantly Inattentive Type of ADHD, or what used to be referred to as attention deficit disorder without hyperactivity. What research does exist suggests some qualitative differences between the attention problems these individuals experience and those with the other types of ADHD in which hyperactive or impulsive behavior is present. The Predominantly Inattentive Type of ADHD appears to be associated with more daydreaming, passiveness, sluggishness, difficulties with focused or selective attention (filtering important from unimportant information), slow processing of information, mental fogginess and confusion, social quietness or apprehensiveness, hypo-activity, and inconsistent retrieval of information from memory. It is also considerably less likely to be associated with impulsiveness (by definition) as well as oppositional/defiant behavior, conduct problems, or delinquency. Should further research continue to demonstrate such differences, there would be good reason to view this subtype as actually a separate and distinct disorder from that of ADHD.

PREVALENCE: ADHD occurs in approximately 3-7 percent of the childhood population and approximately 2-5 percent of the adult population. Among children the gender ratio is approximately 3:1 with boys more likely to have the disorder than girls. Among adults, the gender ratio falls to 2:1 or lower. The disorder has been found to exist in virtually every country in which it has been investigated, including North America, South America, Great Britain, Scandinavia, Europe, Japan, China, Turkey and the middle East. The disorder may not be referred to as ADHD in these countries and may not be treated in the same fashion as in North America but there is little doubt that the disorder is virtually universal among human populations. The disorder is more likely to be found in families in which others have the disorder or where depression is more common. It is also more likely to occur in those with conduct problems and delinquency, tic disorders or Tourette’s Syndrome, learning disabilities, or those with a history of prenatal alcohol or tobacco-smoke exposure, premature delivery or significantly low birth weight, or significant trauma to the frontal regions of the brain.

ETIOLOGIES: ADHD has very strong biological contributions to its occurrence. While precise causes have not yet been identified, there is little question that heredity/genetics makes the largest contribution to the expression of the disorder in the population. The heritability of ADHD averages approximately 80 percent, meaning that genetic factors account for 80 percent of the differences among individuals in this set of behavioral traits. For comparison, consider that this figure rivals that for the role of genetics in human height. Several genes associated with the disorder have been identified and undoubtedly more will be so given that ADHD represents a set of complex behavioral traits and so a single gene is unlikely to account for the disorder. In instances where heredity does not seem to be a factor, difficulties during pregnancy, prenatal exposure to alcohol and tobacco smoke, prematurity of delivery and significantly low birth weight, excessively high body lead levels, as well as post-natal injury to the prefrontal regions of the brain have all been found to contribute to the risk for the disorder in varying degrees. Research has not supported popularly held views that ADHD arises from excessive sugar intake, food additives, excessive viewing of television, or poor child management by parents. Some drugs used to treat seizure disorders in children may increase symptoms of ADHD in those children as side effects of these drugs but these effects are reversible.

Can an EEG Biomarker Aid in the Identification of ADHD? An Examination of the Theta/Beta Ratio (TBR) (by Dr. Chris Friesen, Ph.D., C.Psych., BCN)

Attention Deficit-Hyperactivity Disorder (ADHD) is one of the most common neurodevelopmental disorders of childhood and adolescence. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5: APA, 2013), ADHD is marked by “a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development…several inattentive or hyperactive-impulsive symptoms were present prior to age 12 years…clear evidence that the symptoms interfere with, or reduce the quality of, social, academic, or occupational functioning.” (APA, 2013, p. 59-60). According to the DSM-5, population surveys across most cultures find the prevalence of ADHD to be approximately 5% in children (and 2.5% in adults). ADHD is associated with numerous negative outcomes including reduced school performance/academic attainment, poor occupational attainment, social rejection, the development of conduct disorder/antisocial personality disorder, incarceration, substance abuse, physical injuries, traffic accidents/violations, obesity, and negative family relationships (APA, 2013). Thus, early and accurate identification and treatment of ADHD is of enormous societal importance.

At this point in time, the standard method of diagnosing ADHD is based solely on a clinical interview by a physician (e.g., pediatrician or psychiatrist) or psychologist. However, there are numerous problems with the use of clinical interviews for decision making regarding patient diagnoses, predictions, and treatment planning (e.g., various heuristics such as the availability, base-rate, and representativeness heuristics see Dawes, Faust, & Meehl, 1989) that are beyond the current paper to discuss in detail. The addition of standardized and normative-based behavior/symptom rating scales generally add useful information above and beyond what can be obtained from clinical interview alone. Although such measures are often used, they are not required to make a diagnosis of ADHD according to the DSM-5. However, these measures suffer some of the same flaws of clinical interviews in that they primarily rely on parent, teacher, and/or self-reported symptoms/behaviors. These methods can be problematic due to various biases of the person making the ratings. These can include lack of knowledge of base-rate behaviors, lack of insight, and impression management by those doing the ratings. They can also include teachers’ negative perceptions towards children who misbehave and/or parents’/teachers’ lack of knowledge of normative behaviors at particular ages. For example Elder (2010) found that approximately 8.4% of children who are diagnosed with ADHD are born in the month prior to their cutoff date for kindergarten eligibility (and are thus the youngest and most developmentally immature children within a grade). This is compared to 5.1% of children being diagnosed with ADHD when they are born in the month immediately afterward. This finding is consistent with the possibility that diagnoses/ratings may be being driven by teachers’ lack of knowledge of normative behaviors at particular ages and their perceptions of poor behavior among the youngest children in a classroom. Elder (2010) also found that the youngest children in fifth and eighth grades are nearly twice as likely as their older classmates to regularly use stimulants prescribed to treat ADHD. Thus, even ADHD rating scales that are standardized and normative–based are problematic when it comes to assessing for ADHD. The next level of assessment is the use of neuropsychological/cognitive testing to aid in the identification of ADHD. Although abnormal findings that are consistent with ADHD (e.g., impaired findings on continuous performance tests, inhibition tests such as the Stroop task, working memory, and other executive functioning measures) can be found, many children and adolescents with ADHD display no abnormalities on neuropsychological testing (see Nigg, 2006). In my own practice, it was not until relatively recently that I relied on a combination of the above measures (i.e., clinical interviews, rating scales, and neuropsychological testing) when I assessed for the presence of ADHD. Although this assessment battery is much more thorough than what a typical pediatrician or psychiatrist does, there is room for improvement.

As noted in the DSM-5, many of the symptoms and behaviors used to diagnose ADHD can be the result of factors other than ADHD including other psychiatric/psychological disorders/symptoms (e.g., anxiety, oppositional behavior, depression, bipolar disorder, disruptive mood dysregulation disorder, substance abuse, autism spectrum disorder, intermittent explosive disorder), medical/neurological conditions (e.g., Tourette’s disorder), or medications taken for other problems (e.g., thyroid medication, bronchodilators). Because of the above (and other) issues, ADHD tends to be over-diagnosed. For example, Bruchmüller, Margraf, and Schneider (2012) found that 16.7% of mental health professionals misdiagnosed ADHD when provided with case vignettes of children that would not meet DSM-IV diagnostic criteria for ADHD but instead met criteria for other diagnoses such an anxiety disorder. Similarly Chilakamarri and Filkowski (2011) found that in children/adolescents with major depressive disorder, 38% were misdiagnosed with ADHD. Similarly, these authors noted that 29% of children/adolescents with bipolar disorder were misdiagnosed with ADHD. Thus, there is evidence that with the standard methods currently being used to diagnose ADHD, many clinicians are not able to accurately do so.

Given that ADHD is considered to be a neurodevelopmental disorder and the various problems with properly assessing and diagnosing ADHD noted above, finding a reliable biomarker for this disorder is likely possible and of critical importance. Although there is research into various biomarkers for ADHD (e.g., the use of fMRI, PET/SPECT scans, blood tests, genetic testing etc.), many of these are of little clinical utility for various reasons (e.g., non-specificity, expensive equipment). The development of a valid biomarker could not only help properly diagnose children and adolescents, but also help determine the type of, or even whether, pharmacological and/or psychological treatments would be effective.

As noted by Monastra et al. (1999), most major ADHD theorists and researchers have found evidence of anatomical and biochemical abnormalities in the prefrontal cortex in those with ADHD. For example, older imaging studies have found evidence of hypoperfusion and low metabolic activity in the prefrontal and caudate nuclei regions (Monastra et al., 1999). One of the most promising potential biomarkers for aiding in the accurate identification of ADHD is the measurement of the theta/beta ratio (TBR) by use of quantitative electroencephalographs (qEEG). The TBR is essentially the ratio of slow-brain wave activity (theta) to fast-brain wave activity (beta). Higher ratios suggest cortical slowing (i.e., too much slow wave relative to fast wave brain activity). EEG equipment is relatively inexpensive to purchase and run (especially relative to other imaging modalities such as fMRI, PET, and SPECT). For this reason, if EEG indexes such as the TBR can be shown to reliably and accurate aid in the diagnosis of ADHD, it could become relatively easily implemented in hospitals, community clinics, and in private practices of specialist physicians (e.g., neurologists, psychiatrist, and pediatricians) and psychologists.

Although previous researchers have used EEG to look for abnormalities in the brains of those diagnosed with ADHD, it was the work of Joel Lubar (1991) with his use of more extensive EEG recording montages with simplified ratios that found abnormalities. More specifically, Lubar (1991) found increased frontal TBR in boys with attention problems without hyperactivity. It was Lubar and his colleagues (Monastra et al., 1999) who completed a pioneering initial validation study to determine whether the TBR could reliably identify children, adolescents, and young adults of both sexes with or without ADHD. In this study, the authors recruited 482 individuals, ages 6 to 30 years-old, to test the hypothesis that cortical slowing (as measured by via single-channel EEG at the vertex of the scalp) in the prefrontal region could serve as a basis for differentiating patients with ADHD from a nonclinical control group. The authors classified the participants into inattentive-ADHD, inattentive-hyperactive-impulsive combined ADHD, and control (i.e., those not meeting for any DSM-IV disorder and no evidence of ADHD via self-report, ratings scales, and on a continuous performance test) groups. Monastra et al. (1999) found that the TBR measurement revealed evidence of cortical slowing in both ADHD groups, regardless of age or sex. Amazingly, the sensitivity (i.e., the proportion of ADHD patients correctly classified as having ADHD) of the TBR was 86% while the specificity (i.e., the proportion of those without ADHD that were correctly classified as not having ADHD) was 98%.

Monastra et al.’s (1999) results were so promising that Monastra, Lubar, and Linden (2001) completed a series of studies using the qEEG-based TBR in the assessment of ADHD in 469 children and adolescents. They again found that the TBR could correctly classify inattentive-ADHD, inattentive-hyperactive-impulsive combined ADHD, and control participants with a high degree of accuracy. Of course, no measure can be valid without first being demonstrated to be reliable. One important question was whether the TBR readings were consistent over time (i.e., test-retest reliability). The authors found that the TBR was highly reliable (r = .96) when measured one week apart, suggesting that this is likely a stable characteristic of children and adolescents with ADHD. They also found that the TBR findings were consistent with results of rating scales and a continuous performance test (Test of Variables of Attention TOVA). Lastly, the TBR was found to be able to differentiate those with ADHD and those without ADHD with a sensitivity of 90% and specificity of 94% in their sample.

Since these pioneering studies were performed, many similar studies have been carried out. As will be seen below, despite positive findings, there are some researchers who have found inconsistent results or criticized the use of the TBR. For example Kitsune et al (2015) found that qEEG results varied as a function of the time/context in which they were obtained (i.e., at the beginning or the end of the evaluation). They found that at the start of the recording session, slow wave activity (i.e., delta and theta power) was elevated in their ADHD group only, while at the end of the recording session the ADHD group only demonstrated elevated fast wave activity (higher beta power) relative to controls. However, they did find that the ADHD participants had more slow-wave activity supporting theories of cortical hypoarousal in ADHD. However, Kitsune et al. (2015) did not find evidence for atypical TBR in their sample (n = 76) of adolescents and young adults with ADHD.

Similarly, Buyck and Wiersema (2014) found no evidence of an elevated TBR in their recent study. They concluded that “the findings indicate that it is unlikely that stable, univariate EEG abnormalities are implicated in all children with ADHD and that it is important to take into account state-dependent characteristics when evaluating EEG in ADHD. From a clinical perspective, this implies that cautiousness is warranted in using simple EEG measures as a supplementary diagnostic tool, as has been proposed by some researchers (Monastra, Lubar, & Linden, 2001 Snyder et al., 2008).” (Buyck & Wiersema, 2014, p. 3223). However, these authors only included 22 children with ADHD and 29 typically developing children between 7 and 14 years of age and thus the generalizability of their findings is questionable. Similarly, 50% (11) of the ADHD sample children were taking stimulant medication (although they were asked to abstain for 48 hours before the study). The authors concede that previous research had found that stimulant medication decreases slow wave theta and the TBR.

Once an area of study has matured enough, the gold-standard method of identifying the robustness of a finding is the use of meta-analyses. Snyder and Hall (2006) completed a meta-analysis examining qEEG studies that evaluated ADHD using DSM-IV criteria. Nine studies (n =1498) met their criteria and they found that the TBR had with a pooled effect size of 3.08 (95% confidence interval, 2.90, 3.26) for ADHD versus controls (normal children, adolescents, and adults). Snyder and Hall (2006) noted that on average, the studies included had sensitivity and specificity rates of 94% which was similar to the results of previous studies. They also noted that their literature search uncovered 32 studies that were carried out before the DSM-IV ADHD criteria were available and that 29 of the 32 studies had findings consistent with their meta-analytic results. They concluded that their meta-analysis supported the finding that higher TBR are commonly found ADHD relative to normal controls. However, they cautioned that high TBR may possibly occur in other conditions and that further research would be required to be sure that a high TBR is specific to ADHD.

Arns, Conners, and Kraemer (2013) conducted a meta-analysis examining the accuracy of the TBR in correctly identifying ADHD. These authors did use a few of the studies used in the previous meta-analysis by Snyder and Hall (2006) if they met their inclusion criteria. Arns et al. (2013) included nine studies (n = 1253) using children/adolescents. They found effect sizes (ES) of 0.75 and 0.62 for 6-13 year-olds and 6-18 year-olds respectively with regard to the magnitude of differences in TBR relative to controls. Due to certain statistical assumptions not being met, they noted that the effect sizes may have been overestimated. These authors concluded that “excessive TBR cannot be considered a reliable diagnostic measure of ADHD, however a substantial sub-group of ADHD patients do deviate on this measure and TBR has prognostic value in this sub-group, warranting its use as a prognostic measure rather than a diagnostic measure.” (Arns et al., 2013, p. 374). They added that “…based on recent studies, this excess theta and TBR is found in a substantial subgroup of patients with ADHD (25%-40%) and has been demonstrated to be of prognostic value in predicting treatment outcome to stimulant medication and neurofeedback, warranting its use as a prognostic measure rather than a diagnostic measure.” (Arns et al., 2013, p. 381). The authors note that their less reliable findings were mainly related to the control groups TBRs increasing as the date of the studies became more recent as opposed to the ADHD group’s TBR decreasing. However, an examination of their graphed data (figure 3 in their published article) of this trend showed a variable trend towards increasing TBR in control subjects primarily due to two or three of the most recent of the included nine studies. They note that this was not due to changes in inclusion criteria for the control groups. Rather they hypothesize that the findings may have been due to differences in the EEG hardware and/or software used and the well-established finding that children are obtaining less sleep each year. In fact, this latter effect (i.e., poor sleep increasing the TBR) is well known in the neurofeedback community (based on my experiencing attending neurofeedback/EEG conferences and workshops). Arns et al. (2013) note that “a recent meta-analysis incorporating data from 35,936 healthy children reported that sleep duration is clearly positively associated with school performance and executive function, and negatively associated with internalizing and externalizing behavior problems.” (p. 380). They also noted that “A well-known EEG signature for fatigue or drowsiness is increased theta suggesting this would result in increased TBR.” (Arns et al., 2013, p. 380). Thus, as sleep duration was not controlled for, the perceived trend of the control groups’ TBRs increasing may have been an artifact of sleep deprivation and thus calls into question the findings of Arns et al. (2013).

To help answer the question of whether the TBR is specific to ADHD, Snyder, Quintana, Sexson, Knott, Haque, and Reynold (2008) conducted a blinded, prospective, multi-center study of a representative clinical sample examining the sensitivity and specificity of the TBR in accurately identifying ADHD relative to as non-ADHD children/adolescents (which included other childhood/adolescent disorders or no diagnosis). Snyder et al.’s (2008) ADHD sample had a number of comorbidities including mood, anxiety, disruptive, and learning disorders. Snyder et al. (2008) found that the TBR identified ADHD with 87% sensitivity and 94% specificity. In comparison, parent and teacher rating scales (the results of which were not available to the clinical team making the diagnosis) were found to have sensitivity ratings of 38% to 79% and specificity ratings of 13% to 61%. The rating scales were often not consistent with the clinical team’s diagnoses whereas the TBR findings were consistent with the team’s diagnoses. The authors cautioned that because TBR findings do not identify comorbidities or alternative diagnoses, the TBR should not be used as a stand-alone diagnostic tool. Rather, they recommended it be used to complement a thorough clinical evaluation. However, in a recent literature review of the clinical utility of EEG in the assessment and treatment of ADHD, Loo and Makeig (2012) examined Snyder et al.’s (2008) study and noted that although the findings suggest that an abnormally high TBR identifies almost all of the children with ADHD, 18% of those with a normal TBR also go on to receive an ADHD diagnosis and state that “for clinical purposes, a misdiagnosis rate of 18% is simply too high.” (Loo & Makeig, 2012, p. 575). However, the Snyder et al. (2008) found a specificity of 94% which suggests that only 6% of those without ADHD are misclassified (false-positive) as having ADHD by having a high TBR. Similarly, their findings found a sensitivity of 87% which suggests that 13% of patients diagnosed with ADHD by the assessment team had normal TBRs (false-negative). And of course, these ratings are assuming that a “team consensus” diagnosis is correct. Loo and Makeig (2012) concede that “the increases in both theta band activity and in the theta/beta power ratio are two of the most reliable EEG findings in ADHD to date.” (p. 572). They also note that Snyder et al.’s (2008) “…results are remarkably consistent with previous reported results using the ?/? power ratio, and suggest that this measure exhibits similar accuracy rates among diverse clinical samples and age ranges. However, an increased ?/? power ratio, as previously reviewed, is not ubiquitous in ADHD…” (p. 575). They add that “it is difficult to reconcile such disparate results regarding the reliability of the ?/? ratio marker. The Snyder et al. study in 2008 was scientifically sound and it provides class 1 evidence that EEG may indeed be useful in confirming a diagnosis of ADHD as part of a multimodal assessment that includes clinical interviews, behavior rating scales, and neuropsychological tests for identification of comorbid learning disabilities and co-occurring psychiatric disorders. The inconsistencies across studies may be due to methodological issues, such as sampling, instrumentation, and data processing and analysis differences or actual EEG heterogeneity within the ADHD population. In addition, a rarely mentioned fact is that there may be wide variation in EEG instrumentation that can make it extremely difficult to compare across datasets collected with different EEG hardware and software.” (Loo & Makeig, 2008, p. 575).

Bink, Van Boxtel, Popma, Bongers, Denissen, and van Nieuwenhuizen (2015) examined the EEG patterns of adolescents with diagnoses of ADHD only and adolescents with combined autism spectrum disorder (ASD) and ADHD. The authors found that the adolescents with ADHD had more slow (theta) brain-wave activity than adolescents with ASD and ADHD during the eyes open and task conditions. They also found that only the adolescents with ADHD showed a relationship between lowered attention test performance (as measured by the d2) and increased slow-wave activity (theta) in the eyes open condition. The authors interpreted the results as suggesting that the underlying psychophysiological mechanisms of ADHD and ASD-ADHD comorbid adolescents are different, despite there being similarities on a behavioral level as the ASD-ADHD comorbid adolescents demonstrated fewer EEG signs usually associated with ADHD.

A recent meta-analysis by Rudo-Hull (2015) found evidence in support of the cortical hypoarousal theory for externalizing behaviors/disorders in general (which includes ADHD, antisocial personality disorder, conduct disorder, substance abuse, oppositional defiant disorder, and psychopathy). Rudo-Hull (2015) combined the results of 62 studies (n = 4649) that examined qEEG in relationship to externalizing disorders/behaviors. Generally, the author found that for those diagnosed with an externalizing disorder, there was significantly more slow-wave brain activity (i.e., delta but primarily theta) and less fast-wave brain activity (i.e., beta) relative to controls. Rudo-Hull (2015) found that there was no relationship between slow-wave brain activity (i.e., delta and theta) and externalizing behaviors in antisocial or mixed samples. There was a positive relationship between slow-wave brain activity and externalizing behaviors in the ADHD samples however. She also found a negative relationship between fast wave activity (i.e., beta) and externalizing behaviors in both antisocial and ADHD samples. These results led the author to conclude that “…overall, while increased slow-wave activity appears to be more characteristic of ADHD samples, both antisocial and ADHD samples seem to display the decreased fast-wave activity” (Rudo-Hull, 2015, p. 13-14). However, the author noted that the antisocial groups were much more varied (e.g., from children with conduct problems to accused murderers) and there were fewer studies of slow-wave activity in the antisocial samples than in ADHD samples and thus the lack of finding of increased slow wave activity in the antisocial groups may have been due to lack of statistical power. The author added that the TBR, although widely researched within the ADHD field, has not “…been tested in the antisocial behavior field.” (p. 14). The author concluded that “it is therefore possible that these measures (e.g., TBR) may differentiate ADHD from antisocial populations, and future research with these measures may help clarify whether ADHD should continue to be studied largely on its own or in conjunction with other externalizing behaviors.” (p. 14). Thus, the results from the Snyder et al. (2008), Bink et al. (2015), and Rudo-Hull (2015) studies suggests that the TBR ratio may be relatively specific to ADHD but more research is required.

In one of the best designed studies examining how the TBR will likely be used in a clinical setting (i.e., not as a standalone measure but rather in combination with a clinical assessment) was published by Snyder, Rugino, Hornig, and Stein (2015). The authors investigated the predictive accuracy of adding the TBR to a clinician’s typical assessment procedures via a prospective, triple-blinded, multi-site (13 sites), clinical cohort study (275 children and adolescents presenting to clinics with attentional and behavioral problems) with a diagnosis reference standard based on an independent multidisciplinary team (psychiatrist, psychologist, and neurodevelopmental pediatrician). The authors chose to integrate the clinical assessment with the TBR to help improve certainty with regard to the DSM-5 criterion E (i.e., whether symptoms are better explained by another condition). Similar to what was found in previous studies outlined in the current paper, Snyder et al. (2015) found that the site clinicians likely over-diagnosed ADHD in 34% (93/275) of cases (when compared to the multidisciplinary team’s diagnoses). Of those 34% (93), 91% were found to have lower TBR. The authors also found that when the clinician was uncertain about the diagnosis and was able to integrate their assessment with the TBR, there was 97% agreement with the multidisciplinary team. Generally, Snyder et al. (2015) found that children and adolescents with relatively lower TBR were more likely to have other conditions that could affect criterion E (e.g., anger issues or medical or neurological conditions that mimic ADHD such as brain injuries, headaches, auditory processing disorders, substance abuse, cerebral palsy, vision or hearing problems). They found that integration of TBR with a clinician’s ADHD evaluation could help to improve diagnostic accuracy from 61% to 88%.

In summary, the early and accurate identification and treatment of ADHD is of enormous societal importance due to the numerous possible negative outcomes for those children and adolescents that are undiagnosed and/or undertreated. Similarly, misdiagnosing children and adolescents with ADHD can also have significant negative psychological consequences (e.g., self-fulfilling prophesies, social ridicule, etc.) in addition to the problems of incorrectly medicating children and adolescents with stimulants that directly affect the brain’s dopamine system at a time when the brain is still developing. The current paper attempted to demonstrate that the assessment and diagnosis of ADHD has traditionally been problematic. Only a clinical interview is required for diagnosing ADHD as outlined by the DSM-5. There are numerous problems with the use of clinical interviews for decision making regarding patient diagnoses, predictions, and treatment planning. The addition of standardized and normative-based behavior/symptom rating scales generally add useful information above and beyond what can be obtained from clinical interviews alone but can also be problematic. Although the addition of neuropsychological/cognitive testing to aid in the identification of ADHD can be helpful when there are findings of deficits, many children and adolescents with ADHD display no abnormalities on neuropsychological/cognitive testing. Thus, finding a biomarker for the disorder is of critical importance.

Although basic research has repeatedly found evidence of cortical hypoactivation in children and adolescents with ADHD, the methods used were traditionally of little clinical utility for various reasons (e.g., non-specificity, expensive equipment). However, through the original work of Lubar and Monastra (see Lubar, 1991 Monatra et al., 1999), a relatively cheap and accurate EEG-based measure that can be used to aid in the identification of ADHD appears to have been discovered. This measure is known as the theta-beta ratio (TBR) and is essentially the ratio of slow-brain wave activity (theta) to fast-brain wave activity (beta) with higher ratios suggesting cortical slowing. The current paper attempted to summarize some of the research with regard to the clinical utility of the TBR in the identification of ADHD. Although not all research has supported the finding of higher TBRs in ADHD children and adolescents relative to controls, the majority of the research has found the TBR to be highly sensitive to ADHD. Although more research should be conducted to insure this finding is robust, the research available to date does suggest that the TBR is also relatively specific to ADHD.

These findings have been convincing enough to cause me to change my clinical practice when it comes to the assessment of ADHD. Although I have always performed relatively comprehensive assessments which have included clinical interviews, rating scales and neuropsychological/cognitive testing, I have very recently added the measurement the TBR via EEG. I do not believe it is wise to use only the TBR when determining the presence or absence of ADHD. All the assessment methods I use are required for a proper differential diagnosis and for treatment planning. Measuring the TBR is especially helpful when trying to confirm an ADHD diagnosis when the other data suggest its presence. For example, if a patient (or patient’s parent/teacher) complains of symptoms and behaviors suggestive of ADHD but there is no indication of an elevated TBR, I will now look at the case much more thoroughly to determine if there is some other explanation for the symptoms other than ADHD. Similarly, I would also make sure the patient has had adequate sleep in the days prior to the assessment due to the fact that poor sleep can potentially affect the TBR. I believe that the incorporation of the TBR in my assessments has allowed me to improve the accuracy of my assessment and hence treatment of ADHD.

Select References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC.

Arns, M., Conners, K., & Kraemer, H.C. (2013). A decade of EEG Theta/Beta Ratio research in ADHD: A meta-analysis. Journal of Attention Disorders, 17(5), 374-383.

Bink, M., van Boxtel, G.J.M., Popma, A., Bongers, I.L., Denissen, A.J.M., van Nieuwenhuizen, C. (2015). EEG theta and beta power spectra in adolescents with ADHD versus adolescents with ASD + ADHD. European Child and Adolescent Psychiatry, 24, 873–886.

Bruchmüller, K. & Margraf, J., & Schneider, S. (2012). Is ADHD diagnosed in accord with diagnostic criteria? Overdiagnosis and influence of client gender on diagnosis. Journal of Consulting Clinical Psychology, 80(1), 128-138.

Dawes, R. M., Faust, D, & Meehl, P.E. (1989). Clinical versus actuarial judgment. Science, 243 (4899), 1668-1674.

Elder, T. E. (2010). The importance of relative standards in ADHD diagnoses: Evidence based on exact birth dates. Journal of Health Economics, 29, 641–656.

Kitsune, G.L., Cheung, C.H.M., Brandeis, D., Banaschewski, T., Asherson, P., McLoughlin, G., & Kuntsi, J. (2015). A matter of time: The influence of recording context on EEG spectral power in adolescents and young adults with ADHD. Brain Topography, 28, 580–590.

Loo, S.K. & Makeig, S. (2012). Clinical utility of EEG in Attention-Deficit/Hyperactivity Disorder: A research update. Neurotherapeutics, 9, 569–587.

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