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An ADHD diagnosis is conventionally determined by questionnaires, interviews and tests. In principle, several different instruments should be used. This means that a good diagnosis requires several questionnaires, several tests, and absolutely a personal interview by the diagnostician.
Inter-questionnaire and inter-test agreement is limited despite verification of the validity and reliability of the respective tests.
Symptoms of ADHD also occur in other disorders. A study of 10 disorders found that 60% of the symptoms occurred in at least half of all disorders and were assessed in the respective disorder-specific questionnaires and tests.1
The questionnaires are filled out by the affected persons themselves and reference persons (parents, teachers, friends).
Questionnaires are very subjective and contain the danger that the personal opinion of the person answering the question about ADHD itself influences the standard of answering. It happens that parents reject the diagnosis of ADHD in principle, even more so in the case of their own child. Likewise, subjective ideas of affected persons (perhaps that they “want” a diagnosis in the hope of finding a solution to their suffering, perhaps that they reject a diagnosis because they fundamentally dislike ADHD or in order to avoid stigmatization) or the change in assessment standards due to intensive prior involvement can distort the results (bias).
For example, in tests of elimination diets for ADHD, the results of parent surveys are always far more positive than the results of objective tests.2 Since this occurs even in double-blind studies, there is a significant bias of parents to report the subjectively desired outcome (that ADHD could be treated by diet rather than by critically considered medication).
However, it is also conceivable that the parents were already enthusiastic about the small improvements that an elimination diet can produce or that the placebo effect can produce on the affected child and were not even aware of the much better effect that could be achieved by medication or therapy, or at least were not aware of it at the time of assessment.
Youth Self-Report, YSR/11-18 (questionnaire for youth)7
Child Behavior Checklist, CBCL/1.5-5 (Parent Behavior Questionnaire
of preschool children between 1,5 and 5 years)84
Child Behavior Checklist, CBCL/6-18 (Parent Behavior Questionnaire
of children and adolescents from 4 to 18 years)94
Child and Adolescent Behavior Inventory (CABI)
CABI is a parent questionnaire with 75 questions.
CABI was more accurate than CBCL with respect to ADHD and anxiety, CBCL was more accurate with respect to conduct disorder (CD) and oppositional defiant behavior (ODD).10
Quantitative Behaviour Test (QbTest)
70% accuracy in adults 55 to 79 years of age. In combination with self-reported ADHD symptom severity, 91% accuracy.1314
Assessment sheet for parents, teachers and educators (FBB-HKS)15
“ADHD Screening for Adults (ADHD-E)” (including severity of expression compared to norm scores)
Screening test with self-report scale V1.1 for adults with ADHD (ASRS-V1.1) (global assessment, no quality criteria on German-speaking countries)
AD-H-D test system: attention and hyperactivity deficit disorder questionnaire test. Sponsel (2002)
CAPT: Continuous Attention Performance Test - German version. Nubel, Starzacher, Grohmann (2006)
BADD: Brown Attention Deficit Disorders Scale, a 40-item self-completion questionnaire assessing cognitive ADHD symptoms
A meta-study of 9 ADHD questionnaires found that only 37% asked about identical symptoms/behaviors.1 Most questionnaires for children were answered by parents, most questionnaires for adults were self-tests.
Behavioral symptoms was asked from 28% to 81% of the questions of the questionnaires
Cognitive symptoms were addressed by 9% to 44% of the questions
Emotional symptoms concerned between 0 % and 24 % of the questions
Physical symptoms were only asked about at all in 3 of the 9 instruments
In the case of questionnaires, a study showed considerable discrepancies in the assessments of parents, teachers and affected persons, with the exception of emotional dysregulation, which affected all existing symptoms, but even more so the frequency of their occurrence.17
Emotional dysregulation (also in ADHD) can be tested with the
Reactivity, Intensity, Polarity and Stability questionnaire (RIPoSt-40)18
Individual studies found that ADHD-affected children performed worse on tests with slow event rates, while their scores on exciting, challenging tasks were comparable to those of unaffected individuals1920
It fits in with this that the results of tests with ADHD sufferers change when rewards are promised.21 This also suggests that it is not the ability to concentrate or inhibit per se that is impaired, but rather the insufficient activation by “normally interesting” stimuli that is the real key.
Interviews are questionnaires that are filled out by the interviewing physician/therapist. These are usually very closely oriented to the DSM criteria.22 This narrows down the diagnosis unpleasantly, since DSM as well as ICD use only a very narrow catalog of symptoms.
Diagnostic Interview Schedule for Children (DISC-IV)23
Acquisition period 6 months
Diagnostic Interview for Children and Adolescents (DICA-R)24
Child and Adolescent Pschiatric Assessment (CAPA)25
Acquisition period 6 months
Schedule for Affective Disorders and Schizophrenia for School-Age Children (K-SADS)26
Childrens Interview for Psychiatric Syndromes (ChIPS)27
Swanson, Nolan and Pelham-IV (SNAP IV)
26 items across 18 ADHD and 9 ODD symptom criteria, aligned with DSM IV.
Free of charge for clinical use.28 Exists only in English language.29
Scale for the Assessment of Currently Present Symptoms of Attention Deficit/Hyperactivity Disorder and Oppositional Defiant Disorder According to DSM IV (ADHD-ODD Scale)30
According to Kiddie-Sads-Present and Lifetime Version, K-SADS-PL
Homburger ADHD Scales for Adults (HASE)
HASE consists of four individual procedures31
Wender Utah Rating Scale - German short form (WURS-K)
Objective: retrospective diagnosis of childhood ADHD-HI symptoms.
ADHD Self-Assessment Scale (ADHD-SB)
Measurement of the 18 diagnostic criteria of DSM-IV and ICD-10.
ADHD Diagnostic Checklist (ADHD-DC)
External assessment scale for experts based on DSM-IV and ICD-10 criteria
Wender Reimherr Interview (WRI)
structured interview with 28 psychopathological characteristics that are particularly relevant for ADHD diagnosis in adults
Attention tests are significantly more objective than questionnaires.
But even with them there is a risk that the result can be distorted. Influences can arise from training, hyperfocusing of an ADHDer, test anxiety of a non-affected person or high giftedness. Especially the latter points should therefore always be clarified by differential diagnosis.
Test battery for young professionals - concentration (START-K)
Frankfurt Adaptive Concentration Performance Test (FAKT-II)
BLAST (Bron/Lyon Attention Stability Test): Computerized test to identify task switching problems33
Cambridge Neuropsychological Test Automated Battery (CANTAB)
The CANTAB was not found to be useful in diagnosing ADHD in one study.34
Conners’ Continuous Performance Test 3rd Edition (CPT3)
Conners’ Continuous Auditory Test of Attention (CATA)
CPT3 plus CATA had higher sensitivity (82.6%), higher specificity (76%), higher positive predictive value (88.8%), higher negative predictive value (65.5%), and higher overall correct classification rate (80.6%) than CPT3 or CATA alone.35
One study found that Stroop Test, Stroop Plus Test, and Perceptual Selectivity Test did a good job of distinguishing ADHD in adults from non-affected individuals, with Stroop Test narrowly coming out on top. However, while Stroop Test and Stroop Plus Test differed according to the age of the subjects, Perceptual Selectivity Test showed little difference across age.36 Other studies also showed that subjects’ performance on the Stroop Test was age-dependent, with sometimes younger and sometimes older subjects performing better. In the study cited here, adult ADHD sufferers, like non-affected individuals, performed less well on the Stroop Test at older ages.
The Stroop test is designed to examine selective attention in particular.37
Study objective: selective attention in the dorsal anterior cingulate cortex (dACC) → striatum → thalamus → dACC network.37
Color word color interference test.
4 color words (green, red, blue, yellow) are visually displayed in different colors. The color word as well as the 4 non-color answer buttons on the right side of the screen below each other are always in the same position. The color words are displayed for 2 seconds, in between for 0.75 seconds a point to be fixed. In every fourth display, word and color match, in the others they do not. The subject is asked to name the visually displayed color of the displayed word as quickly as possible.
If the color word and the color are different, this is more difficult. ADHD sufferers have a higher error rate (in %) and a higher reaction time (in ms).36
Study objective: selective attention in the dorsal anterior cingulate cortex (dACC) → striatum → thalamus → dACC network.37
In the Stroop Plus Test, the structure of the Stroop Test is extended by four colored boxes that are arranged around the word. Along with the word, an arrow appears between the word and the boxes, pointing to one of the colored boxes. As in the Stroop test, the visually displayed color of the word and the color known by the word do not match in 3 out of 4 runs. Only in every ninth run do the color, word, and displayed color box match. The subject is asked to name the visually displayed color of the displayed word as quickly as possible.36
Study objective: selective attention in the dorsal anterior cingulate cortex (dACC) → striatum → thalamus → dACC network.37
In the center of the screen the Stroop test is presented. Around the word, four symbols (shape: circles or squares) are displayed in different colors (blue and yellow), 3 of which show one shape and one the other. In half of the runs, 3 symbols have the same color and one has the other color, in the other half, 2 each have one color and 2 have the other color.
In each of the shapes, a line is displayed that points (thought of as an hour hand) in at 12 o’clock, 13:30, 15 o’clock or 16:30. The subject should simply pay attention to the orientation of the line in the symbol that shows the individual shape (which here can be horizontal or vertical) and confirm it as quickly as possible with the assigned key.
This test is designed to measure what is known as perceptual selectivity, a subset of selective attention. This term refers to the discriminability of a stimulus, i.e., how effectively the participant can distinguish the target task when confronted with a single stimulus (shape change only) and with two stimuli (shape change and the presence of an irrelevant color).36
Study objective: sustained attention, working memory in the network dlPFC → striatum → thalamus → dlPFC.37
N is a variable.
In the 0-back visual test, the subject is shown a number on a screen and is asked to press the key corresponding to the number. In the 1-back variant, the subject is asked to press the key of the number that was shown before the one just displayed. In the 2-back variant, the subject is asked to press the penultimate number before the number shown. The higher N is, the higher the load on working memory.
The N-back test can also be queried by playing an acoustic number announcement. There is also a variant in which various fields light up one after the other on a square field and the respondent has to tap the field previously activated by N displays.
The stop signal task is used to measure impulsivity or inhibition.
The subject is to log results on visual signs that have two outcome alternatives. For example, a left or right key should be pressed as quickly as possible in response to arrow symbols pointing to the left or right. After a few unscored practice passes, the subject should not press a key when a simultaneous audio signal is heard, which sounds irregularly for about 25% of the passes. The stop signal sounds with a delay after the stimulus. This delay time can vary between 100 ms and 600 ms.38
The following are measured
Directional error count
Proportion of successful stops
Response time for Go - attempts
Stop signal response time (SSRT)
The stop signals vary in different passes to calibrate the test results of the stop signal response time to 50% error to obtain the most comparable measured value. Here is a Video of the stop signal task on Youtube.
The Stop Signal Task is part of the CANTAB. The CANTAB was not found to be suitable for the diagnosis of ADHD in one study.34
One study converted the stop-signal task to an application with mouse control instead of buttons, which showed several improvements in measurements:39
The SSRT shows a weak association with impulsivity, while the mouse movement measure shows a strong and significant association with impulsivity
A machine learning model (weak AI) was able to accurately predict impulsivity ratings of “unknown” participants using mouse movement data from “known” participants
Mouse movement characteristics such as maximum acceleration and maximum velocity are among the most important predictors of impulsivity
The use of preset stop signal delays leads to a behavior that better indexes impulsivity than adjusting the delay value to previous results (staircase model)
One study found evidence that performance on stop-signal tasks in ADHD reflected impairments in early attentional processes rather than inefficiencies in the stopping process.40
The Children’s Color Trail Test measures attention, divided attention, and speed of mental processing and is used to diagnose ADHD, among other conditions.4142
The Digit Span Test is a part of the Wechsler Adult Intelligence Scale- Revised (WAIS).
The memory capacity of the working memory for numbers is measured. The subjects see or hear a sequence of digits and are asked to reproduce it correctly (forwards or backwards). During the test, the length of the digit sequences is increased. The subject’s number span is the longest number of digits that he or she can correctly reproduce.
At https://tools.timodenk.com/digit-span-test a Digit Span test can be taken online.
Nesplora aquarium
Virtual reality game / test, experimental. It is designed to predict ADHD symptoms in adults and adolescents based on current and retrospective self-reports.45
In another approach, artificial intelligence/machine learning was able to correctly diagnose ADHD with 81% probability in players of an online role-playing game (PlayerUnknown’s Battlegrounds).46 Generalized anxiety disorder was detected with 84.9 %.
Most online self-tests freely available on the Internet allow a rough initial assessment. However, preliminary exposure to such tests distorts the test results of subsequent tests (bias).
We have developed our own - quite comprehensive - online self-test, which shows an agreement of around 93% with existing ADHD diagnoses and around 96% with the CAARS-L. Nevertheless, like any online self-test, it is only an indication and can in no way replace a medical diagnosis. ⇒ ADHD online tests
One study found that live interviews and interviews via video showed no difference in outcomes.47
3.2. Problems with ADHD testing: measurement of ADHD symptoms does not occur consistently¶
When testing ADHD sufferers, it must always be kept in mind that the symptoms being measured are not always and consistently present in ADHD sufferers. Rewards change the symptom pattern in ADHD.21 In particular, high motivation of the affected person to participate in the test (intrinsically or through high extrinsic incentives) can distort the test results. This can go so far that the test is negative, although ADHD is present.
3.2.1. ADHD sufferers perform as well as non-affected individuals on tests when properly motivated¶
In ADHD, motivation is altered. Extrinsic incentives must be higher than in non-affected persons to trigger the same motivation.
This is consistent with our hypothesis that ADHD mediates its symptoms in the same way as certain severe chronic stress (dopamine and norepinephrine deficiency), with one benefit of chronic stress being a shift in motivation toward personal self-interest. This results in a shift toward intrinsic motivation and an attenuation of motivability by extrinsic incentives, while also explaining why, in chronic stress like ADHD, many symptoms diminish or even disappear when personal interest is high.
Against this background, computer games that aim to measure ADHD may face the problem that test results lose significance the more the computer game is fun. One study found nonsignificantly higher levels of flow and intrinsic motivation in a stop-signal game than in a non-game stop-signal test.48
3.2.1.1. No / fewer ADHD symptoms in tests with high motivation¶
In ADHD, it is not the technical ability to pay attention or to direct attention that is impaired, but the execution of attention direction is subject to different criteria than in non-affected persons. In ADHD, attentional control is subject to a deviant control, which is much more dependent on the satisfaction of one’s own needs than in non-affected persons. However, this is not egoism, but an altered control of motivation, over which the affected person has no influence.
Anyone who knows enough ADHD sufferers knows how much they wish they could just be like others - how much easier their lives would be. What looks from the outside like a “you can if you want to” is actually a “I can’t direct my want to as I should”.
If personal needs are addressed by intrinsic interest or by rewards (which must be higher on average than for nonaffected individuals), the attention performance of ADHD sufferers improves more than that of nonaffected individuals.49 A typical example is described by Ryffel-Rawak.50
A meta-study confirms that in ADHD, high rewards greatly improve test scores.51
In ADHD, deactivation of the default mode network (DMN), as occurs with attention to the environment, is markedly reduced. Personal motivation elicited by high rewards equalized DMN deactivation in ADHD, making it equivalent to that of unaffected individuals. MPH showed the same effect.52
The fact that an insufficiently stimulating environment (underactivation) can also cause inattention in healthy individuals, e.g., in gifted students in schools that are not suitable for gifted students,53, on the other hand, is probably not due to an altered control profile of attention, but rather to an underchallenge that causes boredom.
3.2.1.1.2. Impulsivity (inhibition) can be improved by rewards¶
Impulsivity in ADHD (inhibitory ability) can also be influenced by rewards,54 to outcomes equivalent to controls, whereas the same rewards improved inhibition less in children with brain injury.55 Another study also found identical inhibitory ability in ADHD sufferers and nonafflicted individuals at high rewards.56 Another study found no improvement.57 It would be necessary to examine whether the rewards here may have been too low to arouse personal motivation.
3.2.1.1.3. Reaction times: Reward accelerates reaction times and decreases response variance in ADHD only¶
Test results on reaction times in ADHD are inconsistent. Many tests show decreased, and individual tests show increased, reaction times in ADHD sufferers. ⇒ Reaction time reduction in ADHD?
In one study, under reward, only ADHD sufferers and their unaffected siblings showed accelerated mean reaction times and decreased response variability, but not controls, whereas accuracy improved in all 3 groups.58
3.2.1.2. ADHD symptoms more visible in tests with low demand¶
Activating, exciting tasks can cause test results of ADHD sufferers to match those of controls.59 Thus, test results of ADHD sufferers show inconspicuous(r) results when a high test event rate (fast) is presented, while a low event rate (slow test) shows significant(r) differences.6061
One study hypothesizes that a slower event rate on tests in ADHD sufferers will result in decreased intrinsic motivation due to their peculiarities in motivability.62
The optimal arousal range, in which no under- or overstimulation occurs, is much narrower in ADHD than in non-affected individuals.
Even more important than the optimal arousal range, however, is the fact that ADHD sufferers can direct their attention just as well as non-affected persons if personal motivation is present (example: hyperfocus). Against the background of the stress benefit of altered attentional control in ADHD, this is understandable. ⇒ Stress benefits of distractibility, task switching problems, and attention problems
This limited capacity may exist not only in terms of under- and overload, but also in terms of time, in the sense that the ability to compensate for under- or overload is limited. One teacher described her perception of a child with ADHD-I to us by saying that she could watch him “fill up” in the first lesson and then develop the typical ADHD-I symptoms.
Special features of sleep tests
Another peculiarity was found in sleep tests. Many sleep tests found decreased REM sleep in ADHD sufferers. However, these tests all lasted only one night. In contrast, in sleep tests that included one night of acclimatization, and in which only the second night was evaluated, ADHD sufferers were found to have even more REM sleep than non-ADHD sufferers.2
When the first and second night were evaluated together, the total amount of REM sleep was the same as for non-affected persons. These results could be interpreted to mean that particular excitement (the first night in unfamiliar surroundings) is a stronger stressor for ADHD sufferers than for non-affected persons.
Whether more intense REM sleep is possibly related to the high-sensitivity symptom of more intense, colorful dreams is an open question. In our understanding, high sensitivity underlies all ADHD.
Smoking as self-medication increases dopamine levels - albeit only ever in the short term. It further reduces stress symptoms and irritability. ADHD sufferers smoke about twice as often as non-affected people.
Smoking may therefore complicate the diagnosis of ADHD.64
A study of emotional dysregulation in ADHD-affected smokers found no differences between those who smoked as usual and those who abstained from smoking for 24 hours.65
It is well known that withdrawal from alcohol and other drugs requires a period of 2 to 4 weeks so that the receptors, which are downregulated by the high supply of neurotransmitters (dopamine, etc.), can be upregulated again. Among other things, this is responsible for the withdrawal symptoms. This is also true for nicotine. It is possible that only tests that require nicotine withdrawal of more than 2 to 4 weeks can show a difference.
One study calculated that there were 116,200 different ADHD subtypes - if each symptom combination was considered its own subtype.66
Against this background, the currently (still?) common test procedures, which (using the example of DSM 5) are based on 9 characteristics for hyperactivity/impulsivity and 9 characteristics for inattention, of which at least 6 characteristics must be fulfilled in at least one category, should be questioned. Affected individuals with 5 features in both categories would qualify as “not ADHD” by DSM 5. Not all physicians realize that DSM and ICD are merely guides and are not diagnostic measures - a misunderstanding that Francis Allen, the head of the DSM IV Commission, already strongly warned against.
Against this background, we consider the approach of diagnostics based on a query of a large number of symptoms, which Barkley and we have pursued, to be well worth considering. ⇒ The big ADxS.ORG - ADHD online test
3.2.5. Ratings by parents and teachers differ significantly¶
One study found that teachers’ and parents’ ratings of the effects of drug treatment for ADHD did not correlate. These strong differences demonstrate that different sources should be used when evaluating ADHD.67
For reliable results, tests for ADHD would have to be conducted in different test environments that take into account the degree of underchallenge, appropriate arousal, and overchallenge. Furthermore, smoking behavior would have to be included in the weighting of test results, which has not been done sufficiently so far. Testing on the basis of all possible ADHD symptoms seems to us to be an option worth considering.
4. Objective measurement methods (biomarkers) in ADHD¶
To date, no diagnosis of ADHD has been established by measuring objective biological or neurological scores.
However, measurement procedures have already been researched far enough to validate and support diagnoses. The advantage of measurement procedures is that the result is not distorted by prior knowledge, training or special motivational situations (interest, hyperfocus).
However, it is known that ADHD sufferers “outsource” the functions of disturbed brain areas to other brain areas in order to compensate for the deficit. Similarly, symptoms are reduced by coping, for example by avoiding situations in which the distressing symptom may occur, or by reducing individual symptoms through intensive training. If only symptoms are asked about, the symptom masked by outsourcing to other brain areas or by coping may not be noticed. This is one of the reasons why tests (including our own online tests) alone can never be sufficient to diagnose or rule out ADHD with certainty.
It is hoped that with further refinement of measurement techniques and knowledge of outcome assessment, more objective diagnosis than by questionnaires and tests will become possible in the foreseeable future.
However, the fundamental problem with biomarker measurements is that they can only ever produce a snapshot. The results of this snapshot depend on whether the person concerned is under acute stress at the time of measurement or not. The usual ADHD diagnosis therefore correctly focuses on whether the (stress/ADHD) symptoms exist in the long term, i.e. also outside acute circumstances triggering particular stress.
To date, the relevant literature has not addressed the extent to which biomarkers can reliably distinguish long-term changes from merely acute stress responses.
Attempts have been made to use the theta-beta ratio as a diagnostic tool for ADHD.
Although individual studies on this appeared promising, this diagnostic approach does not seem suitable for diagnosing ADHD so far.
The theta-beta ratio is reported to be significantly altered in ADHD.
Using quantitative encephalographic measurements (QEEG), it was found that ADHD sufferers have too little activation in the range of beta waves (13-30 Hz), which are significant for focused alertness, while theta waves (4-8 Hz), which are associated with daydreaming, slipping away attention, transition to sleep, creativity.
The increased theta-beta ratio was so clear in a study of ADHD sufferers that 98% of ADHD sufferers (of the purely inattentive type, ADHD-I, as well as of the mixed type) could be distinguished from healthy people on the basis of the theta-beta ratio in children. The degree of deviation of the theta-beta ratio correlated with the intensity of ADHD symptoms.68
However, this result could not be replicated in all follow-up studies. Ogirim et al 2012 were able to correctly identify only about 60% of n = 101 subjects, including 63 ADHD sufferers, using the theta-beta ratio, whereas omission errors in a sustained attention task still yielded 85% correct diagnoses.69 Another study found in adults with ADHD that the theta-beta ratio could not diagnose ADHD, whereas absolute and relative EEG power with eyes open differentiated ADHD from controls. The best ADHD predictors were reported to be:70
Increased power in delta, theta and low-alpha over central parietal regions
Increased power in low-beta in frontal regions
Increased power in mid-beta over parietal regions.
A recent meta-review of 17 studies found an overall sample effect size for absolute theta of p = 0.58 and for relative theta of p = 0.92. The beta-theta ratio or the increased theta value would thus be suitable as a diagnostic tool at a certain stage of development and could be further developed as a diagnostic tool.71
The oversized theta-beta ratio reduces in adulthood,7221 so that a diagnosis with this, if any, could probably only be considered for children.
A meta-study found no conclusive relationship between the theta-beta ratio and ADHD. Unfortunately, however, no distinction was made between subtypes.73 However, an increased theta-beta ratio is thought to predict responding to treatment with stimulants or neurofeedback.73
From our discussions with a neurofeedback therapist, interesting findings emerged in this regard:
Not only in ADHD, but also in several other mental disorders, such as depression, compulsions, trauma, or even migraine sufferers, beta increases in the state of relaxation, while it decreases in healthy people when they relax.
This - characteristic - increase in beta levels during relaxation could possibly explain the symptoms of mind spinning and sleep problems.
We conclude from this that the theta-beta ratio in the laboratory setting can at best enable an unambiguous diagnosis as a delineation of a group of ADHD sufferers in comparison to a group of (proven) healthy individuals. However, it is probably not suitable as a diagnostic tool in real life - for persons who do not know whether they suffer from ADHD or another disorder, or whether they are healthy - because deviations in the theta and beta range occur in a large number of mental disorders and the alternative to the presence of ADHD, unlike in the test environment, is not necessarily “healthy”, but includes the possibility of several other mental disorders or tendencies.
ADHD-HI and ADHD-I have characteristically different theta/beta profiles.
In ADHD-HI and ADHD-C (with hyperactivity), theta is typically too low and beta is typically too high
In ADHD-I sufferers (without hyperactivity, dreamers) theta is typically too high and beta typically too low. Here, the theta-beta ratio should be rather too low - contrary to what is postulated in the studies cited above.
In both groups, theta/beta training (relaxation training) proves to be helpful - in ADHD-HI, theta is trained up and beta is trained down at the same time, while in ADHD-I the exact opposite happens: theta is reduced and beta is increased (concentration training). Therapeutically effective in both cases is not only the objective change of the values, but the learned influenceability of the values, even if this changes the values in the direction of average values.
Joint experiments with a neurofeedback therapist revealed a significant influence of medication and food (sugar) on QEEG values.
Methylphenidate causes greater agitation within the QEEG values within a few minutes. This is unsurprising because methylphenidate is a stimulant. As expected, methylphenidate impeded the theta increase and beta decrease in ADHD-HI targeted by neurofeedback. This is not surprising because MPH is a stimulant. It justifies why MPH should be taken in such a way that the effect has worn off by bedtime.
Sugar (2 candy bars within 5 minutes at 90 kg body weight) caused significant changes in QEEG in an ADHD-HI subject.
Within 10 minutes, Beta1 increased significantly.
The threshold values during theta up / beta down training had to be reduced considerably. The 85% of target values reached before sugar intake had dropped to 50%. This means that the ability to relax had decreased drastically.
After 20 minutes, all values (theta, alpha, beta1, beta 2, hi-beta) were significantly reduced. Relatively speaking, however, Beta 1 was now well above SMR. (Beta1 should be below SMR, which is why SMR training (targeting it) is the first step of neurofeedback treatment for ADHD).
After 30 minutes, Beta1 had caught up somewhat with SMR. Hi-Beta was now significantly higher.
This is a single test with a single subject and therefore cannot be generalized. The subject knew about the expected reaction. The aggravation of his ADHD symptoms after sugar consumption had been mirrored to the subject by quite a few people and coincided with his own observation.
We understand that the observation fits the description of the effect of oligoantigenic diet for a person who is sensitive to sugar. More on oligoantigenic diet and other food influences on ADHD at ⇒ Diet and Nutrition in ADHD
On the occasion of a conversation about this result, we were told by another ADHD-HI sufferer that he reproducibly noticed a considerable increase in his ADHD symptoms, here especially procrastination, after sugar consumption (chocolate).
Furthermore, there is the problem that different EEG measurement software products seem to use different calculation methods to determine the beta-theta ratio and therefore produce significantly different results with the same data.74 Therefore, the International Collaborative ADHD Neurofeedback (ICAN) randomized clinical trial used a fixed theta beta ration cutoff of ≥ 4.5 to be measured with the Thought Technology Monastra-Lubar Assessment Suite, 1.5 SD above the norms collected with this system.
One study concluded that the theta-beta ratio of the EEG is a reflection of cognitive processing activity in both unaffected and ADHD-C affected individuals and can be measured by P 300 latency in the acoustic oddball test. In contrast, absolute alpha power did not correlate with P 300 latency or amplitude in ADHD-C affected subjects.75
4.1.2. Changed slope / offset of the 1/f noise in the EEG¶
“1/f noise” in the EEG are arrhythmic signals in the cortex, which are neural noise typical for ADHD. Increased individual reaction time variance is a sign of increased neural noise. MPH improves this.76
In 3 to 7-year-old children with ADHD, a steeper slope and a larger offset were found with respect to the “1/f noise” in the EEG. These data correlated with altered theta/beta ratios. Both values were normalized by medication. In addition, a larger alpha power was found.77
Another objectified diagnostic method is the measurement of evoked potentials. Here, characteristic EEG amplitude curves triggered by stimuli or actions are measured in various brain regions typically affected in ADHD. A typical average amplitude curve is determined from a large number of test runs. These EEG courses can be compared with data from non-affected persons and data from affected persons with other disorders, which are collected in so-called QEEG databases.
The diagnostic accuracy of the measurement of evoked potentials is growing rapidly. While Strehl et al cite studies from 2005 with a (not yet satisfactory) diagnostic accuracy of 70 to 80 %, Müller et al 201178 already claim 89 % diagnostic accuracy: from a group of 212 adults with 106 ADHD sufferers, 89 % of the sufferers were correctly diagnosed using a 19-channel system through automatic evaluation of EVP. Models with machine learning achieve 94 %79
However, these results were obtained in laboratory situations in which only ADHD was to be distinguished from non-affected persons. In real-life diagnostics, ADHD has to be distinguished from a multitude of other disorders. It remains to be seen when this will be possible in practice using such models.
By comparison, trained diagnosticians and experienced clinicians achieved 88% diagnostic agreement80
One study found no significant differences in evoked potentials between twins with and without ADHD on a continuous performance task.81
A meta-analysis of 52 studies involving 3,370 subjects on early (P100, N100, P200, N200, ERNNe) and late (P300, Pe, CNV) evoked potentials found that in ADHD82
Shorter Go-P100 latencies
Smaller Cue-P300 amplitudes
Longer Go-P300 latencies
Smaller NoGo P300 amplitudes
Longer NoGo P300 latencies
Smaller CNV amplitudes
Smaller Pe amplitudes.
with considerable heterogeneity of results and moderate effect sizes (d<0.6) at the same time.
Another study concluded that evoked potentials show very different correlations to symptoms depending on the age of the subjects (childhood or adolescence).83
The diagnosis by means of evoked potentials is unfortunately time-consuming (4 hours of tests, which are subsequently evaluated) and consequently not cheap. At the Brain and Trauma Foundation Graubünden Switzerland in Chur, a diagnosis cost around 1250 francs (as of 2015).
The measurement of 14 resting state EEG parameters was able to identify participating ADHD sufferers with an accuracy of around 85% in a process optimized by machine learning.84 Since in the wild it is not only possible to diagnose against healthy individuals but also against other disorders, it is questionable whether the result will be accurate enough in practice to allow a meaningful application.
One study found that a phase space reconstruction of the EEG can very well differentiate ADHD from non-affected individuals. 86 However, for diagnostic application, a method must also be able to differentiate well from other disorders.
One study reported elevated resting gamma levels in adults with ADHD in the range of 30 to 39 Hz (gamma1), but not in the range 39 - 48 Hz (gamma2). Resting gamma1 power increased with age and was significantly lower in ADHD than in controls in early adulthood.87
4.1.8. EPSPatNet86: 8-point EEG measurement on 85 wavelets¶
A study of 85 EEG wavelet factors was able to correctly classify 87% of ADHD subjects using machine learning.88 It remains to be seen what the recognition rate will be in an open group of subjects.
To date, no usable genetic tests exist for the diagnosis of ADHD.
Meanwhile, first voices advocate (2020) to integrate certain genetic tests (here: array-CGH) into the standards of ADHD diagnostics.89
There are several difficulties for genetic diagnosis in ADHD:
ADHD is usually not caused by single gene variants, but by an interaction of a high number (several hundred to thousands) of gene variants (⇒ Gene candidates in ADHD)
The (epigenetic) expression of genes (e.g., due to early childhood or chronic severe stress) may additionally alter gene action independent of gene variant.
It can be assumed that different combinations of the genes and forms of expression considered coincide in different affected persons, but not all genes that contribute, for example, to the fact that the dopamine balance is disturbed.
There is not yet a complete set of candidate genes, which is why there is not yet a genetic test for ADHD. We have collected over one hundred and fifty candidate genes. ⇒ Gene candidates in ADHD.
Genetic tests are still too expensive to be able to test the required number of genes.
It is possible that in the coming years genetic tests will be affordable enough to be used diagnostically - and subsequently to tailor individual-specific treatment.
One study examined miRNAs from extracellular vesicles in serum. A longitudinal analysis examining changes in miRNA expression over time between four groups with different diagnostic histories (persistent diagnosis, first onset, remitted, and typical development/control) found no statistically significant results. In the cross-sectional analysis, upregulation of miR-328-3p was found in only 1 of 2 ADHD groups. These miRNAs may regulate the expression of genes associated with these traits in genome-wide association studies90
Basal cortisol levels are reduced in ADHD compared to non-affected individuals because of long-term ongoing stress. In the case of short-term stress, the basal cortisol level initially rises.
This difference would, in purely theoretical terms, be usable to distinguish acute stress response (elevated cortisol levels) from collapsed HPA axis regulation (decreased levels)-if not for the fact that individual variation between individuals within a group would be greater than the increase or decrease in cortisol levels to levels in a healthy state.
According to this hypothesis, however, an individual upward or downward change in cortisol levels could be detected if they were recorded regularly (annually) from the earliest age (in children: on the occasion of standard examinations).
However, without historical values of basal cortisol levels, such measurement is useless.
In addition, a measurement of the morning cortisol awakening response (CAR) could provide information about the state of the HPA axis. The CAR is a persistent increase in cortisol levels occurring 20 to 40 minutes after waking.
A comparative graphical representation of the cortisol profiles of healthy, acutely stressed, chronically stressed, in partial burnout and in full burnout people can be found in Bieger.91
However, even here there is the difficulty that without individual comparative data an evaluation of the 24-hour picture of cortisol levels is hardly diagnostically usable.
A measurement of cortisol in hair (reflecting long-term levels) showed that low cortisol levels in preschool children predicted the expression of ADHD.92
This could possibly be a result of a long-term stress response. The third stress development phase (resistance phase) typically shows a collapse of basal cortisol levels. The fourth phase (exhaustion phase) is then characterized by a breakdown of neurotransmitter systems. See more at ⇒ Resistance phase In the section ⇒ The stress response chain / stress phases of the article ⇒ The stress systems of humans - basics of stress.
However, changes in basal cortisol levels are not specific to ADHD and therefore have little utility for ADHD diagnosis.
4.3.1.2. Measurement of phasic cortisol response to psychological stressors¶
Based on the phasic cortisol response, the cortisol tolerant subtype of ADHD can be identified.
ADHD-I is typically associated with an exaggerated cortisol response compared to unaffected individuals, ADHD-HI with a flattened cortisol response compared to unaffected individuals.
The differences are relevant to treatment. In ADHD-I sufferers, SSRIs should be used judiciously. In ADHD-HI, possibly low-dose SSRIs (2 to 4 mg, i.e., 1/5 to 1/10 of the measure used in depression) could improve impulsivity, thereby allowing lower dosing with stimulants.
The Trier Stress Test (TSST) is typically used as the psychological stressor.
This is unlikely to be suitable for repeated (even annual) examination in view of the expected habituation.
By means of a dexamethasone/ACTH/CRH test, it can be determined whether there is a permanent dysregulation at individual levels of the HPA axis.
If ADHD is characterized by a permanent dysregulation of the stress regulation systems, first and foremost the HPA axis, it should be possible to prove the individual dysregulation by appropriate testing of the HPA axis reactions (level changes of the stress hormones CRH, ACTH, cortisol to acute stressors). At the very least, corresponding tests should yield informative clues for the individual differentiation of membership in subtypes.
Dexamethasone is a glucocorticoid that selectively binds to glucocorticoid receptors and should thereby trigger downregulation of the HPA axis (after the stress response has occurred). If this downregulation fails to occur, this is a strong indication of a disturbance in the deactivation of the HPA axis.
One study was able to create an impressively clear distinction between non-affected, ADHD, ASD, and affected comorbidities by analyzing zinc, lead, copper, cobalt, and vanadium from teeth.93
A study of 50 untreated ADHD sufferers compared with their unaffected twins and 50 control subjects found higher axonal diffusivity in the ADHD sufferers’94
Perpendicular fasciculus
Superior longitudinal fasciculus I
Tractus corticospinalis lateralis
Corpus callosum
The values correlated significantly (except in the perpendicular fasciculus) with ADHD symptoms such as inattention and working memory problems and were intermediate between those of ADHD-affected and unaffected twins. Axial diffusivity is a marker of axonal undamage.
One study concluded that there may be a close relationship between ADHD and nose width, ear length, and upper face depth, which may be related to genetic signaling processes and a close relationship between brain and face formation processes in the embryonic period.96
Optimized machine learning was able to discriminate very well between ADHD and controls and between persistent and remitting ADHD in young adults using MRI neuroimaging images. Relevant features of ADHD compared to controls were identified as:97
Nodal efficiency in the right inferior frontal gyrus
Functional connectivity between brain regions right medial frontal and inferior parietal
Volume of the right amygdala
Remission of inattention and hyperactivity/impulsivity correlated with
Higher nodal efficiency right medial frontal
Lower functional connectivity between brain areas right medial frontal and inferior parietal
Differential diagnosis should be performed in parallel with ADHD diagnosis to ensure that symptoms do not result from other dominant organic causes. ⇒ Differential diagnostics in ADHD
In mental differential diagnosis, particular care should be taken not to confuse the ADHD symptom of dysphoria with inactivity with depression. In our estimation, this is likely to be one of the most frequent misdiagnoses in ADHD and contributes to frequent mistreatment. ⇒ Depression and dysphoria in ADHD
