Dear readers of, please forgive the disruption. needs about $36850 in 2023. In 2022 we received donations from third parties of about $ 13870. Unfortunately, 99.8% of our readers do not donate. If everyone who reads this request makes a small contribution, our fundraising campaign for 2023 would be over after a few days. This donation request is displayed 18,000 times a week, but only 40 people donate. If you find useful, please take a minute and support with your donation. Thank you!

Since 01.06.2021 is supported by the non-profit ADxS e.V..

$7996 of $36850 - as of 2023-05-01
Header Image
Arousal and activation in ADHD - Neurophysiological correlates


Arousal and activation in ADHD - Neurophysiological correlates

1. Arousal control

Arousal is promoted or regulated by different brain regions:12

  • Lateral hypothalamus
    • Orexin
  • Locus coeruleus
    • Norepinephrine
  • Dorsal raphe nuclei
    • Serotonin
  • Nucleus tuberomammillaris in the posterior hypothalamus
    • Histamine
  • Pedunculopontine (PPT) and laterodorsal tegmental (LDT) nuclei
    • Acetylcholine
  • Basal forebrain
    • Acetylcholine

2. The individual optimal excitation level

Attention and concentration needs an optimal arousal level in (all) humans. This general arousal level is called (cortical) arousal3.

** If the amount of stimulus **is too low, attention will not be paid. No interest is aroused.

An optimally strong stimulation Brings the arousallevel into a range that is perceived as pleasant.
Children begin to smile, or, in the case of a very rapid rise in arousal, to laugh.

If the amount of stimuli is too high, Overload begins to affect attention.

The stimulus thresholds are age-dependent. The upper stimulus threshold increases from infancy.

The stimulus thresholds are situation-dependent. Fatigue can lower the upper stimulus threshold, so that stimuli that were previously perceived as pleasant now become unpleasant.4

The stimulus thresholds are personality-dependent.4
To achieve optimal general arousal, people require individually different stimulus inputs.
Some people need absolute silence to learn. Others can only learn with music playing in the background.

  • Introversion / Extraversion:
    • Type and intensity of stimuli
      Introverts respond more intensely to mild stimuli, extroverts to intense stimuli.
      Introverts consequently require less input to achieve optimal cognitive arousal, but are quickly overexcited; extroverts require higher input.
    • Cortical excitation level
      Introverts have higher cortical arousal levels than extroverts.
      The difference in sensitivity to stimuli explains the differences between introverts and extroverts better than the difference in the level of cortical arousal after arousal.
  • Neuroticism
    • People with higher neuroticism achieve higher arousal from emotional stimuli than people with low neuroticism.

Cortical arousal levels are controlled by the ARAS, which is located in the formatio reticularis, a part of the brainstem.

The formatio reticularis

The formatio reticularis consists of 3 parallel columns.

  • Paramedian column
  • Large cell medial column
  • Small cell lateral column

The reticular neurons are sometimes scattered between fiber bundles, sometimes grouped in blurred regions (nuclei), and sometimes in the anatomically definable nuclei:5

  • Raphe seeds (serotonergic)
  • Locus coeruleus (noradrenergic)

The connection of the formatio reticularis (which houses the ARAS) with the locus coeruleus (which produces norepinephrine) may explain why noradergic drugs increase the “green zone” of optimal arousals.

The ARAS activates the brain areas responsible for perceiving and processing stimuli. The ARAS is the stimulus filter that ensures that as many stimuli are processed in the brain that the arousal level is optimal.

Noise versus distortion: the optimal signal level

The effect is comparable to the recording quality of a tape recorder (technology from the end of the last millennium):
If the signal is too low, the playback is quiet and noisy. The signal-to-noise ratio is too low. The more unfortunately and noisier the recording, the more strenuous it becomes to follow the recording.
If the signal is too high, the recording will be overdriven and distorted.

This stimulus filter, which controls the optimal excitation of brain areas, is disturbed in ADHD.


As far as those areas are not optimally controlled which are responsible for the perception of external stimuli, attention is reduced. The ARAS does not activate the brain areas concerned all at the same time, but individually and specifically.
Activation occurs when the required level of interest or importance (internal arousal) is present.
If this control element is disturbed, attention problems result.

In ADHD, the optimal range is smaller (lower arousal threshold is elevated, upper threshold is lowered). At the same time, this optimal range is more difficult to maintain for those affected (see next point).

3. Activation of the consciousness through the ARAS

Activation is mediated by the ascending reticular activating system (ARAS).

The ARAS makes use of the brain regions of the thalamus and basal ganglia.
The thalamus is the stimulus filter that filters the information from the sensory organs before the cortex. This is the seat of the stimulus filter that is too wide open in ADHD. The thalamus is also called the gateway to consciousness. The ARAS is something like the brain pacemaker of consciousness.6 Consciousness is generated by rhythmic excitation of the cortical pyramidal cells by the formatio reticularis (part of the thalamus). The frequency of the ARAS thereby determines how far the thalamus opens the gate to consciousness. The rate of firing of the neurons of the ARAS essentially determines the degree of activation.7 Strong stimuli thereby cause an increase in the frequency of the ARAS, resulting in wide awake consciousness.

By means of activation loops between thalamus, sensory organs and ARAS, those cortical brain areas are activated to which the strongest sensory stimuli are to be projected - and vice versa.8

The tonic and the phasic activation system (ARAS)


The brain houses two activation systems:

3.1. The tonic activation system in the hypothalamus

The tonic activation system (tonic: long phases, like swells in relation to waves), regulates tonic activation and attenuation of cortical activity through the hypothalamus by means of the neurotransmitters (nor-)adrenaline and serotonin. It controls, for example, the day-night rhythm.
The tonic activation system is located, among other places, in the formatio reticularis in the midbrain. This is an extensive, diffuse neuron network in the brainstem that extends from the medulla oblongata (medulla oblongata) to the diencephalon and into the medial forebrain bundle and includes the raphe nuclei and the locus coeruleus.

3.2. The phasic activation system in the thalamus

The phasic activation system, which controls brief activations of individual cortical parts, is located in the medial thalamus. There, nonspecific reticular structures surround the specific nuclei of the sensory organs that lead from the thalamus to the sensory projection centers of the cerebral cortex. These reticular structures are activated collectively by accessory pathways of all sensory systems (especially skin and vestibular).

These non-specific switching units of the thalamus have a lower general effect on the corresponding cerebral hemisphere than the formatio reticularis of the midbrain. They have a much more selective effect on individual cortical fields and can at the same time shield other cortical fields (stimulus filter function).

The reticular thalamic nuclei lead to the cerebral cortex - but only after detours of 20 to 40 ms via the striatum (which includes the basal ganglia (trunk ganglia, basal nuclei) caudate nucleus and the lenfortis nucleus (putamen and palladium)). The basal ganglia are responsible for selecting and controlling motor and non-motor (higher-integrative) actions, as well as inhibiting (suppressing) unwanted activation. Thus, the environment of the thalamus is connected to the striatum by feedback loops and only then transmits to the cerebral cortex (cortex), where they act on the pyramidal cells via stellate cells.

As a result, this feedback loop acts like a neural oscillator.

3.3. The neuronal oscillator in the striatum

The sensory organs send signals to the thalamus. The thalamus activates the reticular formation, which sends the signal to the striatum (basal ganglia). From there, the signal returns to the thalamus after 20 to 40 ms and is only then transmitted to the cerebral cortex.

The cerebral cortex is set into electrical oscillations by the ARAS, which differ depending on the brain state. During sleep, the frequency is much lower than during attention, while the amplitude is higher during attention than during sleep.10 External stimuli influence these brain waves. Strong stimuli activate more strongly. Thus, the formatio reticularis can wake the cortex from sleep by strong activation. During sleep or anesthesia, brain waves are slower, which increases the distance to the “firing threshold” for the pyramidal cells such that only very strong “wake-up” stimuli lead to activation of perception.

Brain waves are used to synchronize the pyramidal cells of the cortex. Pyramidal cells are supposed to be excited by the signals from the sensory organs and connect to simultaneously excited other pyramidal cells to form complexes to exchange information. Because pyramidal cells are in contact with all nervous systems through a great many connections, an uncoordinated exchange of signals would cause a great deal of information noise, which would prevent differentiated perception or action. This is the case, for example, in epileptic seizures, when the brain pacemaker excites the cells so strongly that they communicate in an uncoordinated manner.

The delay circuit within the thalamus serves as an oscillator that influences the frequency of brain waves according to incoming sensory stimuli to allow cells to exchange information in a coordinated manner. As a result, signals from the sensory organs are sent from the thalamus to the cortex at the frequency of the brain waves.

The frequency-dependent pulse sequence causes a synchronous rise and fall of the membrane potential of all pyramidal cells. This prevents a limitless propagation of the action potentials of the pyramidal cells. After each drop of the potential, which corresponds to a deletion process, a new signal can be exchanged and adjusted.

With these considerations the sense of the EEG waves becomes recognizable: The thalamic formatio reticularis raises and lowers in variable rhythm the membrane potential of the cortical pyramidal cells. These are additionally stimulated by the strength of the input stimuli from the sensory organs. Whenever the membrane potential of the pyramidal cells reaches the “firing threshold”, the specific sensory stimuli arriving from the sensory organs can be excited together and evoke specific nerve networks which, due to the self-similar interpenetration of all sensory organs, give rise to a whole from many partial complexes; a holistically connected structure which is newly formed approximately ten times per second.
In addition to the connections described, there are other signaling pathways from the cortex to the thalamus. These explain why the brain is active even without input signals from the perceptual organs, in that the cortex re(produces ideas, thoughts, and hallucinations.)

3.4. Malfunctions of the ARAS

When the brain pacemaker is malfunctioning, typical psychological and physical problems arise.
If the pyramidal cells are excited too frequently, their “firing threshold” is exceeded even without specific nerve cell input triggered by sensory stimuli. This is the case, for example, in an epileptic seizure.
If the rhythmic excitation of the pyramidal cells is too weak, their “firing threshold” is hardly reached. This leads to movement problems such as in Parkinson’s disease. Too weak rhythmic excitation is underactivation.

3.5. Causes of malfunctions of the ARAS

The ability to raise and lower the membrane potential of the pyramidal cells is mediated by the rope ladder-like contacts with stellate cells, which are excited by the impulse train of the formatio reticularis. These cord-like contacts with stellate cells arise only after birth and primarily during the first years of life. They are necessary for the maturation of the cerebrum in connection with learning processes.

Here we come full circle to ADHD. ADHD arises from genetic constellations or from stress in the first years of life, which activate a specific genetic disposition.
How ADHD develops
Stress hormones, especially cortisol, can impair the formation of the contacts of the pyramidal cells to the stellate cells. Stress occurring in the first years of life particularly prevents the formation of these contacts.

Too weak rhythmic excitation is underactivation.

Activation of the ARAS is mediated by various neurotransmitters, including histamine, glutamate, dopamine, norepinephrine, and (probably) serotonin. Further, antagonists of sedating neurotransmitters, e.g. acetylcholine, can induce activation.11

The ARAS has about 30 nuclei that can be assigned to projection target areas in the cortex depending on the neurotransmitter.12 While efferents that project directly to cortical regions can be noradrenergic, serotonergic, glutamatergic, dopaminergic, or cholinergic, projections that first send to nuclei of the basal forebrain are serotonergic, noradrenergic, and dopaminergic controlled. Projections that send first to the intralaminar nuclei of the thalamus are glutamatergic controlled, and the projection that sends first to the nucleus reticularis of the thalamus is controlled via acetylcholine.12

In the dlPFC, attention is excited by noradrenergic projections and inhibited by dopaminergic projections.12

The ARAS communicates with other parts of the brain via fiber bundles, within which different neurotransmitters have their own specialized fiber pathways. The fiber bundle pathways of the ARAS in humans differ from those in animals. Here, each ARAS nucleus has its own neurotransmitter-specific fiber pathway to the cortex.13

4. Other activation mechanisms

The ARAS is not the only element of the brain that mediates activation processes.
Activation is at the same time mediated by neuromodulators, which, however, usually act more specifically.
Acetylcholine activates the entire cortex and stimulates learning processes.
However, content is mediated via glutamate and GABA.
Norepinephrine increases vigilance as well as readiness for action and external orientation of consciousness
Dopamine activates voluntary movements and reinforces behavior (learning reinforcement, increases frequency of behavior).

4.1. Activation due to speed of a dopamine level change

Encode dopamine level changes

  • In the 10-minute range: strength of motivation and behavioral activation
  • In seconds: the value of a future reward
  • In the subsecond range: the search for the reward

4.2. Activation by site of a dopamine level change

Depending on the brain area, changes in dopamine levels encode different behaviors.

See more at Control ranges of dopamine In the chapter Neurological Aspects, ⇒ Neurotransmitters in ADHDDopamine.

  1. Carter, de Lecea, Adamantidis (2013): Functional wiring of hypocretin and LC-NE neurons: implications for arousal. Front Behav Neurosci. 2013 May 20;7:43. doi: 10.3389/fnbeh.2013.00043. PMID: 23730276; PMCID: PMC3657625.

  2. Jones (2003): BE. Arousal systems. Front Biosci. 2003 May 1;8:s438-51. doi: 10.2741/1074. PMID: 12700104.


  4. Glöggler (2005): Entwicklung von Emotionsregulationsstrategien im Kleinkindalter: Zusammenhänge zum frühkindlichen Temperament und Merkmalen der primären Bezugsperson, Dissertation, Seite 6


  6. Haase (2008): Differentialdiagnose der akuten Bewusstseinsstörung. Vortrag 26.01.2008

  7. Köhler: Aktivierung. In Dorsch: Lexikon der Psychologie

  8. Haase (2008): Differentialdiagnose der akuten Bewusstseinsstörung. Vortrag 26.01.2008


  10. Brown, Basheer, McKenna, Strecker, McCarley (2013): CONTROL OF SLEEP AND WAKEFULNESS; Physiol Rev. 2012 Jul; 92(3): 1087–1187. doi: 10.1152/physrev.00032.2011: PMCID: PMC3621793; NIHMSID: NIHMS453513

  11. Köhler: Aktivierung. In Dorsch: Lexikon der Psychologie

  12. Gekle (Hrgsg.) (2010): Physiologie, Seite 796; Georg Thieme Verlag

  13. Edlow, Takahashi, Wu, Benner, Dai, Bu, Grant, Greer, Greenberg, Kinney, Folkerth (2012): Neuroanatomic connectivity of the human ascending arousal system critical to consciousness and its disorders. J Neuropathol Exp Neurol. 2012 Jun;71(6):531-46. doi: 10.1097/NEN.0b013e3182588293.

Diese Seite wurde am 20.05.2023 zuletzt aktualisiert.