Dear reader of, please excuse the disruption. needs about $63500 in 2024. In 2023 we received donations of about $ 32200. Unfortunately, 99.8% of our readers do not donate. If everyone who reads this request makes a small contribution, our fundraising campaign for 2024 would be over after a few days. This donation request is displayed 23,000 times a week, but only 75 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..

$8975 of $63500 - as of 2024-02-29
Header Image
Arousal and activation in ADHD - neurophysiological correlates


Arousal and activation in ADHD - neurophysiological correlates

1. Arousals control

Arousal is promoted or regulated by different regions of the brain:12

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

2. The individual optimal arousal level

Arousal is a continuum from severe hypoarousal (excessive daytime sleepiness, sedation) to moderate to mild hypoarousal (drowsiness, cognitive dysfunction and inattention) to wakefulness and alertness to mild to moderate hyperarousal (hypervigilance, insomnia, overstimulation, anxiety or panic) to severe hyperarousal (psychosis and hallucinations).3 REVIEW)

Attention and concentration require an optimal arousal level in (all) people. This general arousal level is called (cortical) arousal4.

If the amount of stimuli **** Is too low, attention is lost. No interest is aroused.

A optimally strong stimulation Brings the arousal level into a range that is perceived as pleasant.
Children begin to smile or, if their arousal rises very quickly, to laugh.

If too much stimulation Is provided, overload begins to impair attention.

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

The stimulus thresholds depend on the situation. Fatigue can lower the upper stimulus threshold so that stimuli that were previously perceived as pleasant now become unpleasant.5

The stimulus thresholds are personality-dependent.5
In order to achieve optimal general arousal, people need different stimuli for each individual.
Some people need absolute silence to learn. Others can only learn when music is playing in the background.

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

The cortical arousal level is controlled by the ARAS, which is located in the formatio reticularis, a part of the brain stem.

The reticular formation

The reticular formation consists of 3 parallel columns.

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

The reticular neurons are partly scattered between fiber bundles, partly grouped in vaguely defined regions (nuclei), partly in the anatomically definable nuclei:6

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

The connection between the reticular formation (which houses the ARAS) and the locus coeruleus (which produces noradrenaline) may explain why noradrenergic drugs increase the “green zone” of optimal arousal.

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

Noise versus distortion: the optimum 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 sadder and noisier the recording, the more difficult it is 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 the brain areas, is disturbed in ADHD.


If the areas responsible for the perception of external stimuli are not optimally activated, attention is reduced. The ARAS does not activate the relevant areas of the brain all at the same time, but individually and specifically.
Activation occurs when the required level of interest or importance (inner arousal) is present.
If this control element is disturbed, attention problems arise.

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

3. Activation of consciousness through the ARAS

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

The ARAS uses the brain regions of the thalamus and the basal ganglia.
The thalamus is the stimulus filter that filters the information from the sensory organs before the cortex. This is the location of the stimulus filter that is too wide open in ADHD. The thalamus is also known as the gateway to consciousness. The ARAS is something like the brain pacemaker of consciousness.7 Consciousness is generated through rhythmic excitation of the cortical pyramidal cells by the reticular formation (part of the thalamus). The frequency of the ARAS determines how far the thalamus opens the gateway to consciousness. The rate of firing of the neurons of the ARAS essentially determines the degree of activation.8 Strong stimuli cause an increase in the frequency of the ARAS, which results in a wide-awake consciousness.

By means of activation loops between the thalamus, sensory organs and ARAS, those cortical brain areas are activated into which the strongest sensory stimuli are to be projected - and vice versa.9

The tonic and phasic activation system (ARAS)


The brain is home to 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 the 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 in the reticular formation in the midbrain, among other places. This is an extensive, diffuse neuron network in the brain stem 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 the short-term activation of individual parts of the cortex, is located in the medial thalamus. There, non-specific reticular structures surround the specific nuclei of the sensory organs, which lead from the thalamus to the sensory projection centers of the cerebral cortex. These reticular structures are jointly activated by secondary pathways of all sensory systems (especially the skin and the vestibular system).

These non-specific switching units of the thalamus have a less 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 also shield other cortical fields (stimulus filter function).

The reticular thalamic nuclei lead to the cerebral cortex - but only after a detour of 20 to 40 ms via the striatum (which includes the basal ganglia (basal ganglia, basal nuclei) caudate nucleus and the lenfortis nucleus (putamen and palladium)). The basal ganglia are responsible for the selection and control of motor and non-motor (higher-integrative) actions as well as for the inhibition (suppression) of unwanted activation. The area surrounding the thalamus is therefore connected to the striatum by feedback loops and only then sends signals to the cerebral cortex, where they act on the pyramidal cells via stellate cells.

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

3.3. The neuronal oscillator in the striatum

The sensory organs send signals to the thalamus. This activates the reticular formation, which sends the signal to the striatum (basal ganglia). From there, the signal - slowed down variably in time by intermediate neurons - 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 oscillation by the ARAS, which differs depending on the state of the brain. During sleep, the frequency is much lower than during alertness, while the amplitude is higher during alertness than during sleep.11 External stimuli influence these brain waves. Strong stimuli activate more strongly. For example, strong activation of the reticular formation can wake the cortex from sleep. Brain waves are slower during sleep or anaesthesia, which increases the distance to the “firing threshold” for the pyramidal cells to such an extent that only very strong “wake-up stimuli” lead to the activation of perception.

The brain waves serve to synchronize the pyramidal cells of the cortex. Pyramidal cells should be excited by the signals from the sensory organs and connect with other pyramidal cells that are excited at the same time to form complexes in order to exchange information. As pyramidal cells are in contact with all nervous systems through a large number of connections, an uncoordinated exchange of signals would trigger a large amount of information noise, which would prevent differentiated perception or action. This is the case with epileptic seizures, for example, 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 the brain waves according to the incoming sensory stimuli in order to enable the 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 same frequency as the brain waves.

The frequency-dependent pulse sequence causes the membrane potential of all pyramidal cells to rise and fall synchronously. This prevents an unlimited spread of the action potentials of the pyramidal cells. After each drop in the potential, which corresponds to a deletion process, a new signal can be exchanged and synchronized.

These considerations reveal the meaning of the EEG waves: the thalamic reticular formation raises and lowers the membrane potential of the cortical pyramidal cells in a variable rhythm. 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 “ignition threshold”, the specific sensory stimuli arriving from the sensory organs can be excited together and trigger specific nerve networks which, due to the self-similar interpenetration of all sensory organs, create a whole from many sub-complexes; a holistically connected structure that is newly formed approximately ten times per second.
In addition to the connections described above, there are other signaling pathways from the cortex to the thalamus. These explain why the brain is active even without input signals from the sensory organs, in that the cortex re(produces) ideas, thoughts and hallucinations.

3.4. Malfunctions of the ARAS

If the brain pacemaker is incorrectly controlled, 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, during an epileptic seizure.
If the rhythmic excitation of the pyramidal cells is too weak, their “ignition threshold” is barely reached. This leads to movement problems such as 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 ladder-like contacts with the stellate cells, which are excited by the impulse sequence of the formatio reticularis. These ladder-like contacts with the stellate cells only develop after birth and primarily in the first years of life. They are necessary for the maturation of the cerebrum in connection with learning processes.

This brings us full circle to ADHD. ADHD is caused by genetic constellations or stress in the first years of life, which activate a specific genetic disposition.
How ADHD develops
Stress hormones, in particular cortisol, can impair the formation of contacts between the pyramidal cells and the stellate cells. Stress, which occurs 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, noradrenaline and (probably) serotonin. Activation can also be induced by antagonists of sedative neurotransmitters, e.g. acetylcholine.12

The ARAS has around 30 nuclei, which can be assigned to the projection target areas in the cortex depending on the neurotransmitter.13 While efferents that project directly into cortical regions can be noradrenergic, serotonergic, glutamatergic, dopaminergic or cholinergic, projections that initially send into nuclei of the basal forebrain are serotonergic, noradrenergic and dopaminergic. Projections that initially send to the intralaminar nuclei of the thalamus are glutamatergic and projections that initially send to the reticular nucleus of the thalamus are controlled via acetylcholine.13

In the dlPFC, attention is aroused by noradrenergic projections and inhibited by dopaminergic projections.13

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. Each ARAS nucleus has its own neurotransmitter-specific fiber pathway to the cortex.14

4. Further activation mechanisms

The ARAS is not the only element of the brain that mediates activation processes.
Activation is also 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.
Noradrenaline increases vigilance as well as the readiness to act and outward orientation of consciousness
Dopamine activates voluntary movements and reinforces behavior (learning reinforcement, increases the frequency of behavior).

4.1. Activation through the speed of a dopamine level change

Encoding dopamine level changes

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

4.2. Activation through the site of a dopamine level change

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

More on this 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.

  3. [Ross JA, Van Bockstaele EJ (2021): The Locus Coeruleus- Norepinephrine System in Stress and Arousal: Unraveling Historical, Current, and Future Perspectives. Front Psychiatry. 2021 Jan 27;11:601519. doi: 10.3389/fpsyt.2020.601519. PMID: 33584368; PMCID: PMC7873441.](


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


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

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

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


  11. 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

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

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

  14. 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 01.03.2024 zuletzt aktualisiert.