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ADHD - different explanatory models in the past and today


ADHD - different explanatory models in the past and today

The explanatory models of ADHD have changed considerably today compared to the earliest descriptions.

Because of the not very specific symptoms, which are all general stress symptoms at the same time, there is not “the one” universal explanation. In addition, although the symptoms are so typical that one can clearly distinguish a group of ADHD sufferers from a group of non-affected individuals based on the frequency of symptoms in each individual, one cannot predict exactly which symptoms an individual sufferer will have. It cannot be predicted whether or not an individual ADHD sufferer is hyperactive or has impulsivity or emotional problems. Not even attention problems are compelling. This complexity often misleads researchers - and even more so lay people. Trying to filter out a solution for each individual from a small group of affected persons leads to serious misunderstandings.

There are many simplistic but few accurate descriptions of ADHD.

1. Symptom-oriented descriptions

The simplest models are based on visible symptoms alone.

1.1. Fidget

This term referred solely to motor hyperactivity. The term was merely a book title. ADHD encompasses much more than hyperactivity and occurs as ADHD-I even without hyperactivity.

1.2. Hans-Guck-in-the-Air; Träumerle

These terms refer to the ADHD-I subtype.

1.3. Attention/hyperactivity syndrome

This term - still abbreviated in the name ADHD-HI - added the attention problems. The two terms lead to the misconception that these two symptoms would comprehensively characterize the problems. The Symptom total list according to manifestations Includes close to 20 symptom groups with more than 50 symptoms.

The reduction to hyperactivity and attention also overlooks the fact that these two symptoms do not occur in all ADHD sufferers.1

The fixation on these terms further caused that it was overlooked for a long time that hyperactivity is often significantly reduced in adulthood. Then, in formerly hyperactive affected persons, Inner Restlessness (probably already existing before, but not recognizable) and an urge for constant activity come to the fore. While hyperactivity and inattention are very easily recognizable for third parties (especially parents and teachers), and have therefore been the sole focus of description for (far too) long, the less visible symptoms from the area of emotional dysregulation and underactivation are far more stressful for the affected persons themselves.

2. Active principle oriented explanatory models

Further descriptions attempted to reduce ADHD to a single “defective” neuro(physio)logical operating principle.

2.1. Disturbance of the ability to concentrate and pay attention

The most obvious description of ADHD, namely that the ability to concentrate and pay attention is neurologically disturbed per se, is not tenable.
The technical ability to concentrate and pay attention is not impaired in ADHD sufferers. ADHD sufferers can very well concentrate - even for long periods of time (keyword: hyperfocus). However, they cannot direct this attention and concentration in the same way as non-affected persons.

But if we look more closely, the ability to control attention and concentration is not “defective” - it merely follows a different model. This model is that an acute serious stress situation would exist, comparable to a situation dangerous for survival. For this situation the attention and concentration abilities including distractibility are optimal.
Stress benefits-The survival-enhancing purpose of stress symptoms.

However, the fully functional attention, concentration and attentional control are so distorted by this model of distress that their suitability for everyday life is limited - there is a “stress without adequate stressor”. The changes in attention, for example, which are functional during severe stress, are permanently applied, which in the result represents a serious dysfunction.
Faulty, then, is neither the ability to concentrate and pay attention, nor the ability to direct attention. What is defective is that they run in stress mode although no adequate stressor is given. What is impaired is the clean activation and or deactivation of the stress regulatory systems.
ADHD as a chronicized stress regulation disorder.

2.2. Irritant filter weakness

In ADHD, among other things, the filter that blocks out unimportant stimuli is regularly too wide open. In particular, there is a weakness in stimulus filtering in situations with low intrinsic interest.2. The cause of ADHD as a stimulus filter weakness is attributed to malfunctions of the striatum3 and the thalamus.
The too wide open stimulus filter leads on the one hand to distraction and thus to inattention and concentration problems and on the other hand, due to the excess of stimuli taken in, to an additional increase in stress load and thus to stress, which can express itself in hyperactivity (ADHD-HI) or in drifting away (Träumerle, ADHD-I) - or in a mixture of these.
Stimulus filter weakness is a part of ADHD, but it can occur without ADHD, so it is not the only causal pathway.

However, in addition to an impaired ability to block out irrelevant stimuli, many ADHD sufferers also report an increased (subjective) sensitivity to stimuli within focused attention. This phenomenon could also be described as the share of high sensitivity in ADHD, whereby Aron’s construct of high sensitivity, which has not yet been validated, includes further elements.

High sensitivity can also exist without ADHD. High sensitivity is not identical with ADHD, even if a certain proximity cannot be overlooked. We know quite a few (partly extremely) highly sensitive people who have very similar reactions to ADHD sufferers in isolated points, but whose (stress) regulation systems are fully functional, i.e. who do not show any subjective overload. In our opinion, it is this overload that makes ADHD out of the stimulus filter weakness (high sensitivity).

2.3. Delay of brain development / brain maturation

At the end of the nineties it was recognized that ADHD develops in childhood, but does not necessarily disappear after puberty, but persists in 50 to 80 % of cases in adulthood, whereby the symptoms change. Hyperactivity decreases strongly, inner restlessness comes to the fore, attention problems and impulsivity problems decrease somewhat, etc.
ADHD in adults

ADHD is associated with a developmental delay (or permanent developmental disorder in the case of ADHD persisting into adulthood) of certain brain functions / brain areas, primarily with regard to the maturation of dopaminergic4 and noradrenergic pathways5. The fact that ADHD attenuates / fades in quite a few affected individuals can be attributed to delayed development of individual brain functions. Some of these brain functions may still postdevelop during adolescence, so that their functionality approaches that of non-affected persons.

However, this post-development of the brain only occurs in some of the affected brain regions, not in others. Furthermore, even in people whose ADHD exposure in childhood has reduced to such an extent in adulthood that there is no longer a disorder, the brain areas relevant here are not completely “postdeveloped”.

It is true that in ADHD, brain development is already delayed in childhood. However, not all brain development delays have to cause ADHD symptoms or correlate with them.
While the first maximum of cortex thickness is reached at the age of 7 to 8 years in non-affected persons, this is the case in ADHD patients only at the age of 10.8 years on average. That this is not necessarily a causal cause of ADHD is conclusive from the fact that the brain developmental delay in giftedness is even slightly stronger (first maximum of cortex thickness on average at 11 years).
Since rats that grow up in “enriched environments” develop a thicker cortex, it would be conceivable that the high sensitivity that correlates with ADHD as well as with giftedness, as the equivalent of an “enriched perception”, leads to a thicker cortex (which at the same time develops later).
In contrast, our hypothesis that the high sensitivity / stimulus filter weakness immanent in ADHD should also be frequently present in giftedness was not confirmed by the data of the ADxS online tests.
See more at Giftedness and ADHD.

If it is true that certain brain regions depend on dopamine for their maturation,6 the fact that in ADHD dopamine levels are reduced in certain brain areas (PFC, striatum) would possibly be suitable to explain a delay in brain maturation. This would then possibly be the consequence and not the cause of ADHD. It is possible that the genetic origins of ADHD lead to a dopamine deficiency, due to which a brain developmental delay occurs. This is consistent with the fact that early childhood stress can also impair the dopamine gene systems, which is also associated with brain developmental delays.78
See more at Early attachment disorder impairs self-organization of the right cerebral hemisphere In the article Brain hemispheres in the chapter Neurological aspects

Overall, ADHD is associated with delayed brain development, but cannot be reduced to this (across the board) or explained monocausally. The developmental delay seems to be rather a reflection of altered neurological processes.

Fascinatingly, in addition to the phenomenon of delayed brain development, gifted individuals and ADHD sufferers are also linked by common specific character traits. Read more at Giftedness and ADHD.

2.4. Extreme form of a personality trait / dimensional definition

It is hardly discussed anymore whether ADHD could be defined categorically. ADHD is rather to be described dimensionally.9
Categorical means that the presence of certain characteristics or symptoms determines whether ADHD exists. Categorical is: pregnant or not. Dimensional, on the other hand, means that it is not individual specific symptoms that define the presence of ADHD, but the frequency and degree to which they occur. Dimensional is: mildly or severely depressed.

ADHD is sometimes described as an extreme expression of a personality structure (Farmer/Hunter hypothesis).

It is possible that this personality expression is particularly successful,10 because the particular candidate genes of ADHD spread far more rapidly than would be statistically expected.11 This ties in with the opportunity/risk gene model described in How ADHD develops: genes + environment Is presented in detail.

Banaschewski concludes from the fact that ADHD is caused by the interaction of multiple gene variants among each other, possibly under additional environmental influences, that ADHD probably represents the extreme expression of a behavioral dimension.12

Barkley13 has collected 18 symptoms for ADHD in adults. He notes that all of these symptoms can occur in non-ADHD individuals as well. The difference between ADHD and non-ADHD is the frequency of occurrence of the symptoms. While on average only 1 of these 18 symptoms occurs frequently in non-affected individuals, on average 12 of the 18 symptoms occur frequently in adults with ADHD. According to this, ADHD is to be defined dimensionally.

The model of a personality type that manifests itself in an extreme form as a (personality) disorder is basically applicable to all mental disorders. Some people are the opposite of narcissistic - they find any form of exposure and self-expression to be unpleasant.
Others have a solid narcissistic personality component and particularly like to show off what they have created (narcissistic personality as distinct from narcissistic personality disorder).

In all cases, only an extreme form is disturbing for the affected person (and his environment): in the case of narcissism, for example, when the big, great show on the outside has to cover the small helpless being behind it, because the affected person cannot bear his own weak sides, or when, in the other extreme, the hiding of every own greatness reaches the pathological level of echoism14 term and leads to the denial of one’s own justified interests, because it is so unbearable when one’s own needs are not taken into account that this conflict has to be avoided from the beginning.

Another example: Someone can be considered particularly meticulous and careful and thus be very successful in a suitable professional environment (e.g., accounting), or possess these qualities to such an extreme that he himself suffers from them to such an extent that this can be called an obsessive-compulsive disorder.

ADHD is thus to be defined dimensionally in terms of symptoms. However, this does not explain the neurological cause of the disorder, how it manifests itself, and (based on this) how it can be treated.

2.5. Attention model (Posner, Petersen)

In 1990, Petersen and Posner described three neural attentional systems that are disrupted in ADHD.15.
Petersen and Posner revised their account, which has been cited as many as 3500 times, in 2012.16.

The following is based on Drechsler,17 supplemented with information from Review Petersen, Posner (2012)16.

2.5.1. Alertness/alerting/visual orientation

This is noradrenergically controlled.


  • Inattention
  • Alertness impaired
  • Difficulties with sustained attention
  • Do not finish work
  • Aversion to prolonged (monotonous) effort

neural circuits:

  • Locus coreuleus
  • Right frontal
  • Right posterior parietal

2.5.2. Orientation/attention alignment circle


  • Inattention
  • Easily distracted
  • Does not seem to listen
  • Slip of the pen

Neural circuits:

  • Dorsal attention system (top-down)16.
    • Frontal eye fields (FEF)
    • Intraparietal sulcus
    • Superior parietal lobe
  • Ventral attention system (bottom-up)16.
    • Temporoparietal junction (TPJ)
    • Ventral frontal cortex (VFC)
  • Posterior parietal cortex
  • Bilateral parietal cortex
  • Superior colliculus
  • Thalamus
  • Pulvinar15.

2.5.3. Executive control


  • Hyperactive/impulsive
  • Blurts out the answer
  • Interrupts or disturbs others
  • Can wait only with difficulty

Neural circuits:

  • Anterior cingulate (ACC)
    • Left lateral frontal
  • Basal Ganglia
  • Medial prefrontal cortex (mPFC)

2.6. Inhibition disorder (Barkley)

Barkley sees the control of inhibition processes (mechanisms of behavioral inhibition) as being primarily impaired in ADHD. Barkley defines the control of inhibition processes as the ability to self-regulate.18

Barkley divides behavioral inhibition into three components:

  • Suppression of dominant response tendencies
  • Interruption of already started answers
  • Interference control

According to Barkley, the inhibition processes regulate the executive functions. According to him, four areas are disturbed in ADHD:

  • The nonverbal working memory18
    Problems with:
    • Time processing
    • Perception of time
    • Planning with foresight
    • Self-awareness
  • The verbal working memory18
    Problems with:
    • Give yourself instructions
    • Establish internal rules
    • Adhere to rules
  • Motivation, Affect, Arousal18
    Problems with:
    • Deferment of need
    • Need control
    • Perception of the needs and viewpoints of others
    • Goal-oriented action
  • Reconstitution18
    Problems with:
    • Combining knowledge in a new way
    • Conclusions
    • Planning
    • Creative thinking

Barkley does not see a fundamental inability in these areas, but a problem in the control to use the fundamentally available abilities appropriately. It is not the “how” and “what” of behavior that is impaired, but rather the “where” and “when.18

2.7. Altered reward response behavior / altered motivation

Wender postulated as early as 1971 that in ADHD, abnormalities in the brain’s reward center reduce responsiveness to rewards as well as to punishment.19 On this basis, Haenlein and Caul20 developed the hypothesis of an “increased reward threshold” in ADHD, which leads to a certain reward having a lower reward value for ADHD sufferers than for non-affected persons. Stimulants remedy precisely this deficit.
Multiple studies confirm that ADHD sufferers, when given the appropriate rewards, perform as well as non-affected individuals on tests in the following categories

  • Attention
  • Inhibition

which supports the hypothesis of an increased reward threshold.
Likewise, impulsivity and at least partially working memory are affected. For many other ADHD symptoms, it has apparently not been investigated to date whether they still persist in the presence of individual interest elicited by appropriate reward.
See more at Motivation problems In the chapter Symptoms.

2.8. ADHD as an evolutionary consequence

In our view, what speaks against most evolutionary theories is that ADHD has two very contrasting subtypes that hardly promise an evolutionary advantage at the same time. Moreover, the subtypes are not genetically predisposed.

2.8.1. Hunter and Gatherer (Hartmann)

According to Hartmann, ADHD sufferers are the successors of the type of hunters who are less compatible with the living conditions of today’s world than the type of gatherers.

2.8.2. Speed of human development (mismatch theory / anachronism of ADHD)

These hypotheses state that human societies have changed so rapidly that they have outpaced the much slower evolutionary changes required to select for these traits.21

2.8.3. Theory of natural positive selection (Thagaard et al.)

According to this theory, ADHD traits were advantageous under certain circumstances.21 Hartmann’s hunter-gatherer theory is a representative of this direction.
Hyperactivity may have been beneficial in seeking out new opportunities or migrating to a better climate.
Impulsivity associated with reactivity and the ability to fight or flee, as well as inattention as a highly scrutinizing behavior, could likely have been adaptive under these environmental conditions.

2.8.4. ADHD as a consequence of increased sexual activity

Positive selection may simply have resulted from the fact that ADHD increased reproductive success, as ADHD sufferers on average have their first sexual intercourse earlier, have more sexual partners, and become parents earlier.21

2.9. ADHD as deviant functional profiles of the brain

By divergent functioning profiles, we mean models that do not view ADHD as the direct result of pathological malfunction of the brain or individual parts of it, but rather view ADHD as the result of a different mode of functioning of the brain that is not itself directly pathological, but rather represents (under different circumstances) healthy functioning. Rather, what is pathological in ADHD according to these models is that the brain is in this other mode of functioning without the conditions or triggers under which the brain should be in this state in a healthy way,

2.9.1. Posteriorization of behavioral control (Dietrich)

Dietrich22 already in 2010 described the cause of ADHD in a shift of the processes of behavior control from the PFC to posterior brain regions. Dietrich describes the posteriorization process as a consequence of uncertainty.

2.9.2. Unusual Management of Information and Functions (Lachenmaier)

Winkler translated this in a 2022 lecture as neurodiverse handling and coordination of perceptions, impulses, emotions, and executive functions.

2.9.3. Variable Attention Stimulus Trait (VAST) (Hallowell, Ratey)

However, Hallowell and Ratey see VAST less as an intrinsically functional profile that is used in inappropriate circumstances, but rather describe VAST in ADHD 2.0 As a trait whose pathological extreme form is ADHD. At the same time, Hallowell and Ratey differentiate between ADHD as biologically induced and VAST as environmentally induced.
In a way, this is reminiscent of Thom Hartmann’s hunter-gatherer hypothesis.

2.9.4. ADHD symptoms as a malfunction of the stress regulation systems (Brennecke)

According to Ulrich Brennecke’s hypothesis, in ADHD the brain is permanently in a specific functional profile that is only healthy and useful in cases of severe (chronic) stress. According to this hypothesis, the problem with ADHD is rather that, first, there is no adequate trigger for the brain to work in this state and, second, that this state is permanent, for which the functional mode is unsuitable and not intended.

The hypothesis explicitly does not say that stress would be the cause of ADHD (even if this, as it has long been undisputed in stress medicine, can certainly contribute to the development of mental disorders in general and ADHD in particular; but ADHD is only hereditary to 75% - and taking into account epigenetics, i.e. over 3 - 4 generations, environmental causes are to be weighted even higher). In any case, it is not meant that one only has to eliminate some stress to get rid of ADHD - that would be esoteric nonsense, which has to be opposed from the beginning. Also according to the stress mode hypothesis ADHD is mainly genetically caused.
Severe stress can certainly cause ADHD symptoms. However, these people then suffer from stress and not from ADHD. The difference is: With stress, the symptoms go with the stressor. ADHD remains. To distinguish ADHD from severe stress, the DSM and ICD require that symptoms last more than 6 months and occur in different areas of life. And likewise, for this reason, the guidelines specify yearly medication omission trials. If it was just stress, and the stressor has passed, medication is no longer needed. However, this is an indication that ADHD medications may also be helpful for severe stress - otherwise this should have been apparent at the time of dosing. As long as this does not lead to unnecessary medication, medication for severe stress with appropriate symptom severity is not objectionable. After all, these are the same symptoms that can be severe enough that ADHD sufferers are recognized to benefit from it. Medication could help reduce the long-term neurotoxic effects of severe stress.

This view could explain why science is so reluctant to recognize the neurophysiological causes of ADHD in the brain. If the brain of ADHD sufferers functions without an adequate stressor basically in the same way as healthy non-affected people (even if there: only in the emergency and exceptional situation of severe (chronic) stress), the functioning of the brain in ADHD is not pathological per se - even if the continuous operation of the brain in the emergency mode, which is actually only intended for severe stress, certainly has long-term consequences.
Thus, when science compares the brain in ADHD with that of unaffected individuals (outside of severe chronic stress), it naturally finds differences. The hypothesis now raises the question to what extent the observed changes really represent ADHD, or whether not only (at least to a good extent) the consequences of the deviating functional mode of the brain are observed. In that case, there would be a risk that the conclusions drawn from the scientific findings for the practice of ADHD treatment might fail. For example, it would be unhealthy to deprive a brain of the ability to function as it does in the stress emergency mode, which has its purpose.
There are hardly any comparisons and studies on the human brain of healthy people on how it functions under severe chronic stress, because this would presuppose deeply unethical test conditions. Stress research must be content with short-term stressors that are not perceived as seriously threatening.

According to Ulrich Brennecke’s hypothesis, ADHD can thus be explained as a (essentially genetically determined) permanent misregulation of the stress systems, primarily the HPA axis (stress axis). The dysregulation of the stress systems is not the cause of ADHD, but the consequence of ADHD. The symptoms of both chronic stress and ADHD are mediated by the same neurotransmitter shifts: a reduction in the action of (primarily) dopamine and norepinephrine in specific brain areas.

Symptoms may be neurophysiologically triggered by acute stress (high phasic DA and NE levels) or downregulation of tonic DA and NE levels by chronic stress, because brain area function requires intermediate neurotransmitter levels, and excessively high or low neurotransmitter levels cause very similar disturbance patterns.
Stress symptoms are not a disorder per se, but first of all a healthy and useful reaction to cope with threatening situations.
Stress utility-the survival-enhancing purpose of stress symptoms.

As far as it is reported that ADHD sufferers lose all (or at least many) symptoms when they spend several weeks in a remote mountain hut (without internet, cell phone, computer), whereby unfortunately all symptoms are immediately back when the sufferers participate in normal life, this would be explained conclusively according to the hypothesis that in ADHD the stress systems are already activated under normal everyday stress as they are in non-affected persons only under threatening severe stress.

Certain genes or early childhood prolonged stress, among other things, shift the relationship between mineralocorticoid receptors and glucocorticoid receptors (be it receptor expression or sensitivity), disrupting the threshold at which the HPA axis and other stress systems kick in and shut down. Changes in the release response of neurotransmitters and stress hormones also contribute to this. These are caused, for example, by a prolonged excessive release of certain stress neurotransmitters, hormones and peptides, leading to downregulation of the corresponding receptors and/or transporters.

ADHD is characterized by dopamine and norepinephrine deficiency in PFC and striatum. Dopamine deficiency correlates with an increase in dopamine transporter number,23 as is also typical in ADHD. While acute stress increases DA and NE in the PFC, chronic stress can cause a decrease in DA and NE levels depending on the stressor and age of onset.

In ADHD-HI, according to Ulrich Brennecke’s hypothesis, a flattened endocrine stress response leads to a deficient shutdown of the HPA axis due to the associated flattened cortisol stress response, which would normally be shut down again by cortisol at the end of the stress response. This causes a steady state of stress that manifests in the ADHD-HI-typical (and ADHD-I-untypical) state of inability to recover.

In ADHD-I, according to the hypothesis, the excessive endocrine stress response could lead to frequent overactivation (mild norepinephrine increase) and then shutdown of the PFC (strong norepinephrine increase; consequence: thinking blocks, decision-making difficulties). The distinct cortisol stress response results in a clean shutdown of the HPA axis, which drives norepinephrine and dopamine levels back down and removes the blockade of the PFC again.
Presumably because of the frequent alternation between overactivation and deactivation of the PFC, there is not such a pervasive deficiency of dopamine as in ADHD and therefore not such a pronounced elevation of DAT. The excessive cortisol stress response leads to frequent alternation of activation and deactivation of the stress systems (e.g., HPA axis).

The hypothesis further relies on the fact that almost all typical ADHD symptoms have functional benefits in severe life-threatening circumstances. For example, in severe chronic stress, it makes sense that extrinsic stimuli appear less interesting and motivation shifts toward covering personal interests, as this helps in survival in the case of a (life)threatening stressor.

See more at ADHD as a chronicized stress regulation disorder.

3. Cause-oriented explanatory models

Other explanations attempted to describe the causes of ADHD.

3.1. Nutritional consequences / food intolerances

ADHD is not categorically caused by food or additives.

Food intolerances, however, can increase the intensity of ADHD as stressors, or in affected persons who have such a weak ADHD that it is not disturbing without additional stressors (keyword: dimensional disorder), they can intensify this ADHD, which is not yet present in itself, into the pathological range.
This is not a pattern unique to ADHD: eliminating food intolerances can also reduce or eliminate symptom intensity in other mental disorders.
However, the effect size of eliminating an existing food intolerance is, at about 0.25, quite considerably lower than that of medication (up to 1.1).

See the article Nutrition and diet in ADHD.

3.2. Dopamine as a cause of ADHD

3.2.1. Dopamine level too low

Neurologically, ADHD can be accurately described as a neurotransmitter disorder in specific areas of the brain, primarily dopamine deficiency in the striatum (reward/reinforcement system).

Those affected by the encephalitis epidemic of 1914 to 1917 showed typical symptoms of ADHD as it progressed. Children developed hyperactive motor skills, adults Parkinson’s symptoms. Encephalitis destroys the cells in the substantia nigra that produce dopamine. This cause could be reproduced in animal experiments as the trigger of the symptoms. The symptoms are therefore consequences of a dopamine deficiency.24
Since a dopamine deficiency can have various causes, a proper differential diagnosis is necessary. For example, an encephalitis must always be excluded from an ADHD diagnosis.

Similarly, in Parkinson’s patients, the cells of the substantia nigra are damaged, causing the concentration of dopamine to drop by up to 90 percent. This causes motor impairments such as rigor, tremor and akinesia. Depression is many times more common in Parkinson’s patients, which is also said to be due to the dopaminergic deficiency.25

But if you take a closer look, things get complicated again.
Dopamine deficiency is admittedly the clearest cause, which subsequently explains many symptoms.
But first, other neutrotransmitters are also imbalanced, especially norepinephrine, although less pronounced than dopamine, and probably marginally also serotonin. In addition, acetylcholine, GABA and other neurotransmitters are involved to a lesser extent. It is unclear whether the imbalances of the other neurotransmitters have their own cause or whether they are a consequence of the dopamine deficiency. Dopamine, in addition to its own neurotransmitter functions, also has the role of a prodrug (precursor) of (nor-)epinephrine.
If a neurotransmitter is not present in the brain in the optimal quantity, signal transmission in the brain is disturbed. This applies to “too little” just as much as to “too much”.
The symptoms are then further dependent on which neurotransmitters are too much or too little present (or act more strongly or less strongly, e.g. because receptors are (un)sensitive) and in which brain area this occurs.

Each neurotransmitter has specific brain regions in which it plays a particular role.
Similarly, the individual brain regions have different functions and are interconnected.
With these two dimensions (which neurotransmitter, which brain region), individual symptoms of ADHD can be assigned to specific brain regions.
This is important because each ADHD sufferer has their own mix of symptoms and symptom intensity. Understanding which symptom is triggered by which neurotransmitter in which brain region opens up opportunities for improvement in treatment.

Dopamine deficiency causes the symptoms - but is it also the cause?

The main symptoms of ADHD are quite predominantly caused by a dopamine deficiency in the PFC and striatum. To put it so simply, effects of a reduction of dopamine receptors at the postsynapse are included in this picture.

Increasing dopamine levels in the dlPFC remedies the problems of working memory and thus executive functions; increasing dopamine in the striatum remedies the ADHD symptoms of more interest-directed attention, including to irrelevant stimuli, motivation, and hyperactivity and impulsivity.

Nevertheless, there is strong evidence that the dopamine deficiency is not the actual cause, but merely a consequence of a problem that exists elsewhere.

The fact is that ADHD sufferers do not lack the ability to concentrate. The phenomenon of hyperfocus, which can be vividly described by almost every ADHD sufferer, proves that the basic ability to concentrate, to pay sustained attention and not to be distracted is present. The real problem lies in the lack of controllability of motivation for the affected person.

Since ADHD symptoms are largely eliminated in the hyperfocus state, we hypothesize that in the hyperfocus state there is no longer a lack of dopamine in the striatum.

Studies on the existence of the individual symptoms in hyperfocus are not known on this side. The impressively unanimous statements of affected persons available to us indicate that at least the dimensions of concentration, attention, distractibility, frustration tolerance and mood would quite clearly not fulfill any diagnostic criteria in the state of hyperfocus. This phenomenon further leads, for example, to the fact that some sufferers are not detected in ADHD tests - and this is because they are very interested in the tests. This strong personal interest creates a state of hyperfocus in which the test results do not reflect the attention deficits that exist in normal life.

We therefore consider it conceivable that a higher-level instance or some other mechanism exists that raises the (phasic) dopamine level in the striatum in the case of intrinsic interest and drops the dopamine level in the case of disinterest (imposed interest, extrinsic interest). According to our hypothesis, the control of this instance is impaired in ADHD sufferers. In contrast, in the context of a (threatening) stress response, the change in control makes sense and is beneficial for survival.
Stress utility-the survival-promoting purpose of stress symptoms

3.2.2. Tonic and phasic dopamine

There are several models of how dopamine affects ADHD.26
Together, they assume reduced dopamine levels in various dopaminergic circuits, leading to deficits in reinforcement and extinction of behaviors. The dynamic development theory

Dynamic developmental theory27 is based on the hypothesis that altered dopaminergic function plays a central role by not adequately modulating non-transaminergic (primarily glutamate and GABA) signaling. In this context, three dopaminergic networks are impaired. The mesolimbic dopamine pathway

A disturbance in this system causes altered behavior reinforcement and deficient behavior extinction.
This leads to

  • Delay aversion
  • Hyperactivity in novel situations
  • Impulsivity
  • Lack of sustained attention
  • Increased behavioral variability
  • Failure to “inhibit” reactions (“disinhibition”) The mesocortical dopamine pathway

A problem in this system causes

  • Attention Deficits
    • Inadequate orientation reactions
    • Impaired saccadic eye movements (rapid involuntary gaze jumps)
    • Poorer attentional responses to a target
  • Poor behavior planning
    • Poor executive functions The nigrostriatal dopamine pathway

Functional impairments in this system cause

  • Disturbed modulation of motor functions
  • Lack of non-declarative habit learning and memory.

These three impairments together lead to

  • An obvious developmental delay
  • Clumsiness
  • Neurological “soft signs” and
  • A “failure to inhibit responses” when rapid responses are required.

According to the dynamic developmental theory, hypofunctional dopamine networks significantly determine individual predispositions. According to this theory, behavioral problems and symptoms of ADHD result from an interaction of (genetic) disposition and environmental influences. The respective ADHD symptoms of the affected person change over the lifetime. Altered or inadequate learning and motor functions make optimal parenting styles and coping styles particularly important. Medications can normalize the underlying dopamine dysfunction to some degree and reduce the increased demands (needs) of these children. The theory describes how individual predispositions interact with these conditions to produce behavioral, emotional, and cognitive effects that can become relatively stable patterns of behavior. Decreased tonic dopamine release increases phasic dopamine release

This theory suggests that reduced tonic release of dopamine as a feedback mechanism leads to reduced stimulation of presynaptic autoreceptors and thus increased phasic dopamine release.2829

Extracellular dopamine is the result of a tonic or phasic release of dopamine. In addition to the tonic release of dopamine (in rather small amounts) via varicosities directly into the extracellular space, a (phasic) dopamine burst releases a large amount of dopamine into the synaptic cleft, from where it diffuses into the extracellular space.30

Phasic dopamine increases affect and distractibility.31
A similar mechanism exists in the interaction of dopamine levels between the PFC and the striatum. Stress increases dopamine levels in the PFC. Moderate increases improve the performance of the PFC; severe increases weaken it and shut down the PFC. Increased dopamine levels in the mPFC cause decreased dopamine levels in the striatum. For more, see The neurological explanation of drive and motivation problems.

3.2.3. Dopamine transfer deficit model (DTD; Tripp and Wickens, 2008)

The dopamine transfer deficit (DTD) model of Tripp and Wickens32 postulates that ADHD symptoms are caused by temporal fluctuations in dopamine release, which in turn result from environmental stimuli. The model implies that dopaminergic neuronal responses to positive reinforcement are transferred to preceding neutral signals in neurotypical individuals, whereas this transfer is absent in ADHD. Therefore, ADHD sufferers dopamine signaling to the anticipatory cue of reinforcement. The lack of anticipatory dopamine signaling of the cue causes faster behavioral extinction when reinforcement is delayed or interrupted. This would explain some core symptoms of ADHD, including devaluation of delayed rewards.33

3.2.4. ADHD as a developmental disorder of dopaminergic brain pathways

The brain consists of different areas that developed at different times during mammalian evolution. Within these brain areas, in turn, local areas can be delineated, which can be well defined on the basis of metabolism, modes of communication, neurotransmitter basing, specific functions and meanings, and their communication links with other brain areas. These 52 areas were already described in 1909 by Brodmann (Brodmann Areas).

In children suffering from ADHD, individual brain areas are delayed in development. This developmental delay is triggered by the roots mentioned above. However, not every developmental delay is equally relevant to the disorder. The disturbance of the development of the dopaminergic pathways originating from the nucleus accumbens (which can be triggered by early childhood stress) is a clear ADHD problem, whereas the (considerable) delay in the development of the first maximum cortex thickness in ADHD corresponds quite exactly to the developmental delay in giftedness, which is rather not to be considered a mental disorder.

Something similar happens - in a weaker form - during puberty. Puberty is the time when the brain develops particularly quickly. The typical puberty symptoms also result from the fact that individual brain areas do not develop as quickly as others during puberty, and an imbalance arises between the mutually regulating and controlling brain areas. By the end of puberty, the brain areas that mature late have “caught up” with development - the puberty symptoms disappear.

The areas affected in ADHD communicate primarily by means of the neurotransmitters dopamine and norepinephrine (and to a lesser extent by means of serotonin). It is known that the development of the dopaminergic pathways of the brain can be delayed by external stress.4 The maturation of dopaminergic pathways

The central dopaminergic circuit in the brain is the nucleus accumbens in the striatum. It mediates between emotional and motor stimuli.

The following presentation is largely based on the work of Lesting.34

During the first years of life, when the monoamine neurotransmitter system is developing and maturing, it is particularly vulnerable to pharmacological and environmentally induced perturbations.3536373839

The nucleus accumbens is the control center between the limbic system and motor control.40 Many mental disorders are caused by defects of the nucleus accumbens.41

Dopamine and serotonin are the central neurotransmitters that control the functions of the nucleus accumbens.424344

The nucleus accumbens is addressed by the limbic system, the PFC, the amygdala, and the hippocampus. A disturbance of these signal inputs leads to distraction problems because irrelevant perceptions can no longer be blanked out (inhibited).4546

If the maturation of the dopaminergic pathways originating from the nucleus accumbens is disrupted during their development, the resulting damage leads to permanent problems in the processing of sensorimotor stimuli into adulthood.47

In this context, the timing of the disruption is crucial. If the disruption occurs in the pre- and postnatal time window of maturation of the affected brain region, this leads to much more intense damage.4849

During the maturation phase, dopamine and serotonin act not only as neurotransmitters but also as morphogenic substances that directly influence the structuring of nerve networks.5051 Post-maturation of the brain?

The human brain is not mature at birth, not at childhood, and not at sexual maturity.
The full maturation of the PFC lasts at least until the 23rd - 25th year of life.52

That the PFC is involved in quite a few ADHD symptoms explains why ADHD changes over a lifetime and may eventually disappear in adults or show a markedly altered symptom pattern.
In ADHD, the development of the PFC is disturbed,53 so that it matures completely with a delay (symptoms disappear in adulthood) or not completely (symptoms decrease in adulthood). By adulthood, the brain of some affected individuals can (partially) catch up with the developmental delay.

In adolescence (youth), about 80% of affected individuals still have the symptoms. In the remaining 20%, the affected brain areas may have matured sufficiently.
In adulthood, about 50% of those affected as children still have ADHD symptoms, but in a different form.

Due to the (partial) post-development of the affected brain areas, the symptoms weaken and change. Whereas an ADHD-HI child (with hyperactivity) cannot remain seated quietly and must be constantly on the move (lack of inhibition of the impulse of activity), this changes in adulthood to the point that an inner restlessness still remains, which no longer necessarily becomes physically noticeable. What remains is the impulse to always have to do something. Meditation, mindfulness, keeping still without being able to do something is very difficult for these people (even perceived as torture). If they manage to do it anyway, it is highly effective therapy, as this breaks the symptom of inability to recover, which otherwise perpetuates the vicious cycle of stress symptoms.

In principle, epigenetic change in genes by means of methylation is possible at any age. Even short-term sport causes methylation in the muscles. However, experiences in childhood cause longer lasting methylations than experiences in old age.54

3.3. Dysfunction in the anterior cingulate cortex

Dysfunction in the anterior cingulate cortex can lead to anxiety, emotional instability, and hyperactivation in ADHD.55

4. More complex neurological models

4.1. Cognitive-energetic model according to Sergeant (2000)

The cognitive-energetic model assumes a lack of overall cortical activation due to dysfunction of the brainstem ascending reticular system.5657 It focuses on arousal, activation, and effort readiness.58

  • Activation: “general alertness”; tonic-physiological readiness to respond
  • Arousal: phasic readiness to react in anticipation of relevant stimuli
  • Willingness to make an effort
  • Consequences: Effects on primary levels of processing and behavior, e.g., decoding, central processing, response and reaction organization

Studies show that children with ADHD-HI perform worse at slow event rates, while their results on exciting, challenging tasks were comparable to those of non-affected individuals.59 The cause is thought to be insufficient activation of the arousal.

For ADHD sufferers, it is therefore particularly important (especially in school and other learning situations) to be actively addressed and motivated. Tasks should be divided into small parts. Praise/improvement must be given directly and immediately (reinforcement that does not coincide directly with the action is ineffective).

4.2. 2 Or 3 - causes model according to Sonuga-Barke (Dual-Pathway / Triple-Pathway)

2 or 3 development paths606162

  • cognitive path
    Impairment of the mesocortical system
    dorsal striatum and dorsolateral (posterior lateral) prefrontal cortex
    Consequence: executive functions impaired, including lack of inhibition, cognitive dysregulation, behavioral dysregulation
  • motivational path
    Impairment of the mesolimbic system
    ventral striatum (here mainly nucleus accumbens)
    frontal regions (incl. anterior (frontal) cingulate and orbitofrontal cortex)
    Consequence: reward problems, especially delay aversion and aversion to reward deferral.

According to Sonuga-Barke, three separate regulatory circuits are independently responsible for different disorders and symptoms of ADHD:

  1. the mesocortical control circuit
    for disorders of inhibition and inhibition,
  2. the mesolimbic control circuit
    for disturbances of the reward system and
  3. the cerebellum (cerebellum)
    for disturbances of the time processing.

According to this model, the ADHD-typical delay aversion and inhibition problems (which should subsequently rather lead to hyperactivity) are each due to their own, independent neurological mechanisms of action.636465

Delay aversion is thought to correlate with what is known as the chance-risk gene variant DRD4-7R, which is implicated in high sensitivity as well as many disorders, including ADHD.66

Sonuga-Barke later extended his first model (dual-pathway) to a triple-pathway model because in ADHD, in addition to inhibition problems and delay aversion, time processing problems are also caused by separate neurological mechanisms of action in each case.

The model is based on studies according to which ADHD sufferers with symptoms from one of the 3 domains do not necessarily have to show symptoms from one of the other domains as well, whereas non-ADHD affected twins of the (ADHD affected) subjects were also conspicuous in each of the exact domains from which the symptoms of the sufferers arose.67

4.3. 3 Endophenotypes according to Castellanos and Tannock


  • Problems in the reward system
  • Problems with temporal processing
  • Working memory disorders

In ADHD, according to this account, there is dysfunction of the prefrontal-striato-thalamic system due to smaller brain volumes in the cerebellum (hemispheric) area and changes in right prefrontal brain regions, the caudate nucleus, the pallidum, and a subset of the cerebellar vermis.6970

4.4. 4-Category model according to Hunt


  • Selective attention disorder
    Cause: dopaminergic dysfunction in
    • Nucleus accumbens
    • Cortical integration regions
  • Excessive arousal
    • Impact:
      • Aggressiveness
      • Impulsivity
      • Attention Deficit Disorder
    • Cause: noradrenergic hyperactivity in
      • Locus coeruleus
      • Reticular activation system
  • Behavioral disinhibition or impulsivity/hyperactivity
    Cause: serotonergic-dopaminergic dysfunction in
    • PFC
    • Subcortical regions
  • Problems in the reward system
    • Disturbed affect regulation
    • Anhedonia

4.5. Reduced inhibition / overactivity of the default mode network (DMN)


  • The default mode network (DMN) is a network that spans multiple brain areas73
    • Ventrolateral and ventromedial PFC
    • Posterior cingulate cortex (PCC)
    • Cuneus
    • Inferior parietal lobe74
  • A reduced negative correlation between DMN and task-active networks was observed in ADHD.757677
    It has been suggested that inattention in ADHD results from inadequate suppression of the DMN (daydreaming).78
  • A meta-analysis of 55 task-based fMRI studies on ADHD suggested, as the most consistent finding, that in ADHD there is excessive activity in the DMN and decreased activity in the task-positive frontoparietal and ventral attentional networks during cognitive tasks.79
  • Decreased activity in the DMN causes slower and more variable responses80 indicating increased neural noise.
  • Methylphenidate enhances the inhibition of DMN.81

4.5. Rolandic wave spikes and epileptiform EEG abnormalities

Rolandic wave spikes (sharp waves) were found in 1.7% of all ADHD sufferers.82 Rolandic wave spikes in ADHD are also reported by Duane.83

Epileptiform EEG abnormalities were found in 5.4% of all ADHD sufferers without epilepsy findings and correlated significantly with female gender and ADHD-I subtype.82

  1. Steinhausen, Rothenberger, Döpfner (2010): Handbuch AD(H)S, Kohlhammer, Seite 106, 107

  2. Rossi (2012): ADHS, Seite 17

  3. Winkler (2014) ADHS Rolle des Striatum bei sensomotorischen Reizen

  4. Müller, Candrian, Kropotov (2011): ADHS – Neurodiagnostik in der Praxis, Springer, Seite 84

  5. Müller, Candrian, Kropotov (2011): ADHS – Neurodiagnostik in der Praxis, Springer, Seite 86

  6. Kuo, Liu (2019): Synaptic Wiring of Corticostriatal Circuits in Basal Ganglia: Insights into the Pathogenesis of Neuropsychiatric Disorders. eNeuro. 2019 Jun 5;6(3). pii: ENEURO.0076-19.2019. doi: 10.1523/ENEURO.0076-19.2019.

  7. Brandau (2004): Das ADHS-Puzzle; Systemisch-evolutionäre Aspekte, Unfallrisiko und klinische Perspektiven. Seite 40

  8. Schore (2000): The self-organisation of the right brain and the neurobiology of emotional development. S. 155 – 185, 167 In: Lewis, Granic (Herausgeber): Emotion, development, and self-organisation.

  9. Greven, Buitelaar, Salum (2018): From positive psychology to psychopathology: the continuum of attention-deficit hyperactivity disorder. J Child Psychol Psychiatry. 2018 Mar;59(3):203-212. doi: 10.1111/jcpp.12786.

  10. Renner, Gerlach, Romanos, Herrmann, Reif, Fallgatter, Lesch (2008): Neurobiologie des Aufmerksamkeitsdefizit-/Hyperaktivitätssyndroms; Nervenarzt 2008, DOI 10.1007/s00115-008-2513-3

  11. Krause, Krause (2014): ADHS im Erwachsenenalter, Schattauer, Einführung im Kapitel Genetik

  12. Banaschewski in Steinhausen, Rothenberger, Döpfner (2010) Handbuch AD(H)S, Kohlhammer, Seite 121

  13. Barkley, Benton (2017): Das große Handbuch für Erwachsene mit ADHS, Seite 47

  14. Malkin (2015): Rethinking Narcissism – Der Narzissten-Test

  15. Posner, Petersen (1990): The attention system of the human brain. Annu Rev Neurosci. 1990;13:25–42.

  16. Petersen, Posner (2012): The Attention System of the Human Brain: 20 Years After; Annu Rev Neurosci. 2012 Jul 21; 35: 73–89. doi: 10.1146/annurev-neuro-062111-150525; PMCID: PMC3413263; NIHMSID: NIHMS394960

  17. Drechsler in Steinhausen, Rothenberger, Döpfner (2010) Handbuch AD(H)S, Kohlhammer, Seite 94

  18. Drechsler in Steinhausen, Rothenberger, Döpfner (2010) Handbuch AD(H)S, Kohlhammer, Seite 92, 93

  19. berichtet von Douglas, Parry (1994): Effects of reward and nonreward on frustration and attention in attention deficit disorder. J Abnorm Child Psychol. 1994 Jun;22(3):281-302. doi: 10.1007/BF02168075. PMID: 8064034.

  20. Haenlein, Caul (1987): Attention deficit disorder with hyperactivity: a specific hypothesis of reward dysfunction. J Am Acad Child Adolesc Psychiatry. 1987 May;26(3):356-62. doi: 10.1097/00004583-198705000-00014. PMID: 3597291.

  21. Balogh, Pulay, Réthelyi (2022): Genetics in the ADHD Clinic: How Can Genetic Testing Support the Current Clinical Practice? Front Psychol. 2022 Mar 8;13:751041. doi: 10.3389/fpsyg.2022.751041. PMID: 35350735; PMCID: PMC8957927.

  22. Dietrich (2010): Aufmerksamkeitsdefizit-Syndrom, ADHS – Die Einsamkeit in unserer Mitte.

  23. Brake, Sullivan, Gratton (2000): Perinatal Distress Leads to Lateralized Medial Prefrontal Cortical Dopamine Hypofunction in Adult Rats; Journal of Neuroscience 15 July 2000, 20 (14) 5538-5543

  24. Hässler, Irmisch: Biochemische Störungen bei Kindern mit AD(H)S in Steinhausen (Hrsg.) (2000): Hyperkinetische Störungen bei Kindern, Jugendlichen und Erwachsenen, 2. Aufl., Kohlhammer, Seite 87

  25. Scheidtmann (2010): Bedeutung der Neuropharmakologie für die Neuroreha – Wirkung von Medikamenten auf Motivation und Lernen; neuroreha 2010; 2(2): 80-85; DOI: 10.1055/s-0030-1254343

  26. Roessner, Rothenberger in: Steinhausen, Rothenberger, Döpfner (2010) Handbuch AD(H)S, Kohlhammer, Seite 80

  27. Johansen, Sagvolden, Aase, Russell (2005). The dynamic developmental theory of attention-deficit/hyperactivity disorder (ADHD): Present status and future perspectives. Behavioral and Brain Sciences. 28. 451 – 454. 10.1017/S0140525X05430071

  28. Grace (2001): Psychostimulant actions on dopamine and limbic system function: Relevance to the pathophysiology and treatment of ADHD. In Solanto, Arnsten, Castellanos (Herausgeber): Stimulant drugs and ADHD: Basic and clinical neuroscience (pp. 134-157). New York: Oxford University Press.

  29. Solanto (2002): Dopamine Dysfunction in AD/HD: Integrating clinical and basic neuroscience research. Behavioural brain research. 130. 65-71. 10.1016/S0166-4328(01)00431-4.

  30. Müller (2007): Dopamin und kognitive Handlungssteuerung: Flexibilität und Stabilität in einem Set-Shifting Paradigma; Dissertation, Seite 30 unter Verweis auf Giertler (2003): Die Rolle des Nucleus accumbens bei der Akquisition und Expression von instrumentellem Verhalten der Ratte. Universität Stuttgart: Dissertation

  31. Müller (2007): Dopamin und kognitive Handlungssteuerung: Flexibilität und Stabilität in einem Set-Shifting Paradigma; Dissertation, Seite 11

  32. Tripp G, Wickens JR. Research review: dopamine transfer deficit: a neurobiological theory of altered reinforcement mechanisms in ADHD. J Child Psychol Psychiatry. 2008 Jul;49(7):691-704. doi: 10.1111/j.1469-7610.2007.01851.x. Epub 2008 Jul 1. PMID: 18081766., REVIEW

  33. Taylor, Carrasco, Carrasco, Basu (2022): Tobacco and ADHD: A Role of MAO-Inhibition in Nicotine Dependence and Alleviation of ADHD Symptoms. Front Neurosci. 2022 Apr 12;16:845646. doi: 10.3389/fnins.2022.845646. PMID: 35495050; PMCID: PMC9039335.

  34. Lesting (2005): Adaptive Reifung von Dopamin und Serotonin im Nucleus accumbens, der integrativen Schnittebene zwischen Emotion und Bewegung: Isolationsaufzucht und Methamphetamin-Intoxikation als Induktoren einer gestörten Reifung bei Meriones unguiculatus, Dissertation

  35. Alquicer, Silva-Gomez, Peralta, Flores (2004): Neonatal ventral hippocampus lesion alters the dopamine content in the limbic regions in postpubertal rats. Int. J. Dev. Neurosci. Vol. 22(2): 103-111.

  36. Bennay, Gernert, Schwabe, Enkel, Koch (2004): Neonatal medial prefrontal cortex lesion enhances the sensitivity of the mesoaccumbal dopamine system. Eur. J. Neurosci. Vol. 19(12): 3277-3290.

  37. Brake, Flores, Francis, Meaney, Srivastava, Gratton (2000): Enhanced nucleus accumbens dopamine and plasma corticosterone stress responses in adult rats with neonatal excitotoxic lesions to the medial prefrontal cortex. Neuroscience Vol. 96(4): 687-695.

  38. Brake, Zhang, Diorio, Meaney, Gratton (2004): Influence of early postnatal rearing conditions on mesocorticolimbic dopamine and behavioural responses to psychostimulants and stressors in adult rats. Eur. J. Neurosci. Vol. 19(7): 1863-1874.

  39. Miura, Qiao, Ohta (2002): Attenuating effects of the isolated rearing condition on increased brain serotonin and dopamine turnover elicited by novelty stress. Brain Res. Vol. 926(1-2): 10-17.

  40. Mogenson, Jones, Yim (1980): From motivation to action: functional interface between the limbic system and the motor system. Prog. Neurobiol. Vol. 14(2-3): 69-97.

  41. Lesting (2005): Adaptive Reifung von Dopamin und Serotonin im Nucleus accumbens, der integrativen Schnittebene zwischen Emotion und Bewegung: Isolationsaufzucht und Methamphetamin-Intoxikation als Induktoren einer gestörten Reifung bei Meriones unguiculatus. Dissertation

  42. Banjaw, Fendt, Schmidt (2005): Clozapine attenuates the locomotor sensitisation and the prepulse inhibition deficit induced by a repeated oral administration of Catha edulis extract and cathinone in rats. Behav. Brain Res. Vol. 160(2): 365-373.

  43. Swerdlow, Geyer (1998): Using an animal model of deficient sensorimotor gating to study the pathophysiology and new treatments of schizophrenia. Schizophr. Bull. Vol. 24(2): 285-301.

  44. Weiner, Feldon (1997): The switching model of latent inhibition: an update of neural substrates. Behav. Brain Res. Vol. 88(1): 11-25.

  45. Weiner (2003): The “two-headed” latent inhibition model of schizophrenia: modeling positive and negative symptoms and their treatment. Psychopharmacology (Berl) Vol. 169(3-4): 257-297.

  46. Weiner, Feldon (1997): The switching model of latent inhibition: an update of neural substrates. Behav. Brain Res. Vol. 88(1): 11-25.

  47. Heidbreder, Weiss, Domeney, Pryce, Homberg, Hedou, Feldon, Moran, Nelson (2000): Behavioral, neurochemical and endocrinological characterization of the early social isolation syndrome, Neuroscience 100 (2000) 749-768.

  48. Lehmann, Teuchert-Noodt (2005): Trauma und Hirnentwicklung. In: Resch, Schulte-Markwort (Hrsg.): Kursbuch für integrative Kinder- und Jugendpsychotherapie. Schwerpunkt: Dissoziation und Trauma, pp 4-20. Basel: Beltz Verlag.

  49. Teuchert-Noodt, Lehmann (2003) in: Herpertz-Dahlmann, Resch, SchulteMarkwort, Warnke (Hrsg.): Entwicklungspsychiatrie – Biopsychologische Grundlagen und die Entwicklung psychischer Störungen. Schattauer

  50. Lauder (1988): Neurotransmitters as morphogens. [Review] [159 refs]. Prog. Brain Res. Vol. 73: 365-387.

  51. Mattson (1988): Neurotransmitters in the regulation of neuronal cytoarchitecture. [Review] [199 refs]. Brain Research Vol. 472(2): 179-212.

  52. van Eden, Uylings (1985): Postnatal volumetric development of the prefrontal cortex in the rat. In: J.Comp Neurol. 241, S. 268-274; zitiert nach Zehle (2007): Einfluss früher postnataler Stresserfahrung auf die Entwicklung des limbischen Systems bei Octodon degus: Verhaltenspharmakologische und neuroanatomische Untersuchungen zur Beteiligung des dopaminergen Systems, Seite 7

  53. Zehle (2007): Einfluss früher postnataler Stresserfahrung auf die Entwicklung des limbischen Systems bei Octodon degus: Verhaltenspharmakologische und neuroanatomische Untersuchungen zur Beteiligung des dopaminergen Systems, Seite 5 ff mit weiteren Nachweisen

  54. Berndt (2013): Resilienz, S. 149 ff

  55. Albrecht, Brandeis, Uebel, Heinrich, Mueller, Hasselhorn, Steinhausen, Rothenberger, Banaschewski (2008): Action monitoring in boys with attention-deficit/hyperactivity disorder, their nonaffected siblings, and normal control subjects: evidence for an endophenotype. Biological Psychiatry, 64, 615-625.

  56. Sergeant (2005): Modeling attention-deficit/ hyperactivity disorder: a critical appraisal of the cognitive-energetic model. Biological Psychiatry, 57, 1248-1255

  57. Conzelmann, Gerdes, Mucha, Weyers, Lesch, Bähne, Fallgatter, Renner, Warnke, Romanos, Pauli (2014): Autonomic hypoactivity in boys with attention-deficit/hyperactivity disorder and the influence of methylphenidate. World Journal of Biological Psychiatry, 15, 56-65., n = 102

  58. Havenstein (2014): Arbeitsgedächtnisleistung und emotionale Interferenzkontrolle bei Erwachsenen mit Aufmerksamkeitsdefizit-/Hyperativitätsstörung (ADHS); Dissertation

  59. Havenstein (2014): Arbeitsgedächtnisleistung und emotionale Interferenzkontrolle bei Erwachsenen mit Aufmerksamkeitsdefizit-/Hyperativitätsstörung (ADHS); Dissertation unter Verweis auf Sergeant und van der Meere, 1988 sowie van der Meere und Sergeant, 1988

  60. Sonuga-Barke (2002): Psychological heterogeneity in AD/HD—a dual pathway model of behaviour and cognition; Behavioural Brain Research, Volume 130, Issues 1–2, 10 March 2002, Pages 29-36;

  61. Sonuga-Barke (2005): Causal Models of Attention-Deficit/Hyperactivity Disorder: From Common Simple Deficits to Multiple Developmental Pathways; Biological Psychiatry; Volume 57, Issue 11, 1 June 2005, Pages 1231-1238;

  62. Sonuga-Barke, Bitsakou, Thompson (2010): Beyond the Dual Pathway Model: Evidence for the Dissociation of Timing, Inhibitory, and Delay-Related Impairments in Attention-Deficit/Hyperactivity Disorder; Journal of the American Academy of Child & Adolescent Psychiatry, Volume 49, Issue 4, April 2010, Pages 295-296;

  63. Solanto, Abikoff, Sonuga-Barke, Schachar, Logan, Wigal, Hechtman, Hinshaw, Turkel (2001): The ecological validity of delay aversion and response inhibition as measures of impulsivity in AD/HD: a supplement to the NIMH multimodal treatment study of AD/HD; J Abnorm Child Psychol. 2001 Jun;29(3):215-28., zitiert nach Krause, Krause (2014): ADHS im Erwachsenenalter, Schattauer, Seite 24

  64. Sonuga-Barke, Wiersema, van der Meere, Roeyers (2009): Context dependent dynamic models of attention deficit/hyperactivity disorder: differentiating common and unique elements of the state regulation deficit and delay aversion models. Neuropsychol Rev.2009;online first.

  65. Dalen, Sonuga-Barke, Hall, Remington (2004): Inhibitory Deficits, Delay Aversion and Preschool AD/HD: Implications the Dual Pathway Model; NEURAL PLASTICITY VOLUME 11, NO. 1-2, 2004

  66. Jiang, Chew, Ebstein (2013) The role of D4 receptor gene exon III polymorphisms in shaping human altruism and prosocial behavior; Front. Hum. Neurosci., 14 May 2013 | mit Verweis auf Sweitzer, Halder, Flory, Craig, Gianaros, Ferrell, Manuck (2012): Polymorphic variation in the dopamine D4 receptor predicts delay discounting as a function of childhood socioeconomic status: evidence for differential susceptibility; Soc Cogn Affect Neurosci (2013) 8(5): 499-508.doi: 10.1093/scan/nss020

  67. Sonuga-Barke, Bitsakou, Thompson (2010): Beyond the dual pathway model: Evidence for the dissociation of timing, inhibitory and delay-related impairments in Attention Deficit/Hyperactivity Disorder.

  68. Castellanos, Tannock (2002): Neurosience of attention-deficit/hyperactivity disorder: the search for endophenotypes. Nature Reviews Neuroscience, 3, 617-628

  69. Castellanos (2002): Anatomic magnetic resonance imaging studies of attention-deficit/hyperactivity disorder. Dialogues Clinical Neuroscience, 4, 444-448.

  70. Kieling, Goncalves, Tannock, Castellanos (2008): Neurobiology of attention deficit hyperactivity disorder. Child Adolescent Psychiatric Clinics North America, 17, 285-307., zitiert nach Kropotov, Pachalska, Müller (2014): New neurotechnologies for the diagnosis and modulation of brain dysfunctions, health psychology report · volume 2(2), 2014

  71. Hunt (1997): ATTENTION DEFICIT HYPERACTIVITY DISORDER IN ADULTHOOD; Nosology, Neurobiology, and Clinical Patterns of ADHD in Adults:Psychiatric Annals; August 1997 – Volume 27 · Issue 8: 572-581; DOI: 10.3928/0048-5713-19970801-10, zitiert nach Edel Vollmöller, Aufmerksamkeitsdefizit-/Aktivitätsstörung bei Erwachsenen, Seite 114

  72. Silberstein, Pipingas, Farrow, Levy, Stough (2016): Dopaminergic modulation of default mode network brain functional connectivity in attention deficit hyperactivity disorder; Brain Behav. 2016 Dec; 6(12): e00582; doi: 10.1002/brb3.582; PMCID: PMC5167011

  73. Buckner, Andrews-Hanna, Schacter (2008): The brain’s default network: anatomy, function, and relevance to disease; Ann N Y Acad Sci. 2008 Mar;1124:1-38. doi: 10.1196/annals.1440.011

  74. Buckner, Andrews-Hanna, Schacter (2008): The brain’s default network: anatomy, function, and relevance to disease. Ann N Y Acad Sci. 2008 Mar;1124:1-38. doi: 10.1196/annals.1440.011.

  75. Castellanos, Margulies, Kelly, Uddin, Ghaffari, Kirsch, Shaw, Shehzad, Di Martino, Biswal, Sonuga-Barke, Rotrosen, Adler, Milham (2008): Cingulate-precuneus interactions: a new locus of dysfunction in adult attention-deficit/hyperactivity disorder.Biol Psychiatry. 2008 Feb 1;63(3):332-7.

  76. Christakou, Murphy, Chantiluke, Cubillo, Smith, Giampietro, Rubia (2013). Disorder‐specific functional abnormalities during sustained attention in youth with attention deficit hyperactivity disorder (ADHD) and with autism. Molecular psychiatry, 18, 236–244

  77. Liston, Cohen, Teslovich, Levenson, Casey (2011): Atypical prefrontal connectivity in attention‐deficit/hyperactivity disorder: Pathway to disease or pathological end point? Biological Psychiatry, 69, 1168–1177

  78. Sonuga‐Barke E. J., & Castellanos F. X. (2007). Spontaneous attentional fluctuations in impaired states and pathological conditions: A neurobiological hypothesis. Neuroscience & Biobehavioral Reviews, 31, 977–986

  79. Cortese, Kelly, Chabernaud, Proal, Di Martino, Milham, Castellanos (2012): Toward systems neuroscience of ADHD: A meta‐analysis of 55 fMRI studies. Perspectives, 169,1038–1055

  80. Buckner, Andrews‐Hanna, Schacter (2008): The brain’s default network: Anatomy, function and relevance to disease. Annals of the New York Academy of Sciences, 1124, 1–38

  81. Silberstein, Pipingas, Farrow, Levy, Stough (2016): Dopaminergic modulation of default mode network brain functional connectivity in attention deficit hyperactivity disorder; Brain Behav. 2016 Dec; 6(12): e00582; doi: 10.1002/brb3.582; PMCID: PMC5167011 mwNw.

  82. Socanski, Herigstad, Thomsen, Dag, Larsen (2010): Epileptiform abnormalities in children diagnosed with attention deficit/hyperactivity disorder. Epilepsy & Behavior, 19, 483-486. n = 517

  83. Duane (2004): Increased frequency of rolandic spikes in ADHD children. Epilepsia, 45, 564-565.