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Sensitivity, stress and ADHD

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Sensitivity, stress and ADHD

The brain has several functions:

  • Think
  • Perceive
  • Feel
  • Action control

In relation to ADHD, people often talk about an increased sensitivity to stimuli and emotions. Sensory Processing Sensitivity (SPS) refers to the functions of perceiving and feeling: Those who perceive more, those who feel more intensely, are at a certain level of increased sensitivity. ADHDpedia speaks instead of hypersensitivity in ADHD1, but elsewhere equates hypersensitivity with high sensitivity.2

People have varying degrees of sensitivity to stimuli.3 The term high sensitivity we used earlier, by which we inaccurately meant heightened sensitivity, is correctly a construct of Aron’s, which includes not only heightened sensitivity but also a different form of perceptual processing. Research on this is still in its infancy and awaits greater methodological precision. Nevertheless, there is increasingly good evidence that high sensitivity is a construct distinct from other temperament and personality constructs.45

We use the term heightened sensitivity in the following, also to avoid unconscious confusion between hypersensitivity and high sensitivity.

1. Causes of increased sensitivity

1.1. Neurological causes

1.1.1. Stimulus filter opened wider

Our sensory organs take in far more information than we can consciously process. Most of the information is irrelevant and is therefore filtered out by a stimulus filter in our brain.
An excessively open stimulus filter is often cited as the cause of increased sensitivity.
In this respect, this does not contradict that part of Aron’s hypothesis on high sensitivity according to which it represents an increased processing of incoming stimuli.
The stimulus filter is controlled by the thalamus. The ARAS (Ascending Reticular Activation System) located in the thalamus activates and deactivates those brain areas involved in perception and sensory processing. In this process, the brain areas in question are not activated together, but individually. Activation occurs when the required level of interest (internal arousal) is present.
If this control element is disturbed, attention problems result
According to this same pattern, attention problems in ADHD are primarily consequences of motivation problems

1.1.1.1. Dopamine and increased sensitivity
1.1.1.1.1. Dopamine deficiency in the striatum

The striatum is a control instance of the thalamus. If the function of the striatum is impaired (as in ADHD) due to reduced dopamine levels, this leads to an impairment of the thalamus. The thalamus is the filtering unit that selects which incoming stimuli are relayed to the PFC and which are not. The faulty control of the thalamus by the striatum, which is regularly impaired in ADHD due to dopamine deficiency, could explain the stimulus filtering disorder typical of ADHD.
For more, see Tasks of the basal ganglia: supporting the thalamus by filtering In the article Basal ganglia in the section The stress systems of humans - basics of stress in the chapter Stress.

1.1.1.1.2. Dopamine Rise

Optimal stimulus filtering occurs at an intermediate level of dopamine.
A slight increase in dopamine, typical of mild stress, increases the performance of the PFC. This leads to more intensive processing of incoming stimuli.

1.1.1.2. Norepinephrine and increased sensitivity

Increased norepinephrine in the brain also increases stimulus sensitivity and activation of the PFC.

1.1.1.3. Substance P and increased sensitivity

The stress hormone substance P increases the sensitivity of all sensory systems.6 Substance P is involved in anxiety and pain. Substance P activates - predominantly in physical stressors such as cold, pain or drug withdrawal - the HPA axis and the sympathetic nervous system.

1.1.1.4. CRH and increased sensitivity

The stress hormone CRH, produced by the hypothalamus as part of the HPA axis cascade and in parallel by other parts of the brain (including the PFC), increases alertness, auditory perception, and attention. In addition, it mediates quite a few other stress benefits.7

1.1.1.5. Genetic primordial ashes

A study regarding dopaminergic genes in high sensitivity (iSv Aron) found evidence for the involvement of polymorphisms in:8

  • TH (tyrosine hydroxylase gene)
    • TH catalyzes tyrosine to levodopa (L-DOPA)
  • DβH (dopamine-β-hydroxylase gene)
    • Converts dopamine into norepinephrine
  • DAT (dopamine transporter) gene
  • DRD2 (D2 dopamine receptor gene)
  • NLN
  • NTSR1
  • NTSR2

NLN, NTSR1 and NTSR2 belong to the neurotensin system. These are proteins that are structurally colocalized with the dopamine system and functionally interact with it, especially with DRD2.
The 10 polymorphisms described in the study explained 15% of the high sensitivity. Stress (in combination with lack of parental warmth) explained another 2%.

Another study describes an association of increased sensitivity and the serotonin transporter gene variant 5HTTLPR-short/short.9

1.1.2. Stimulus filter opening and perception

A stimulus filter that is opened wider now causes more information to be absorbed. This is of course exhausting - the stimulus filter exists for a reason.
The open stimulus filter model explains that increased sensitivity triggers more intense perception.

In our opinion, the more intense feeling can only be explained to a limited extent.

In sufferers of sensory over-responsivity (SOR), defined as a negative reaction to or avoidance of sensory stimuli, are

  • Primary sensory cortex areas
    • Auditory cortices
    • Visual cortices
  • Amygdala
  • Hippocampus and
  • Orbital-frontal cortex

overactivated. The overactivation correlates with the level of SOR.10

A change in P50 amplitude, P50 gating, N100, or P200 does not appear to be a feature of increased auditory sensitivity.11

1.2. Genetic causes

It is known that different gene dispositions exist, which experience their epigenetic expression during (primarily early childhood) massive stress and subsequently manifest different mental disorders, depending on which gene disposition is affected. For more details, see How ADHD develops: Genes or genes + environment.

About 20% of people are endowed with the 5-HTTLPR gene variant of the serotonin transporter gene, which favors the manifestation of ADHD and depression in those affected under early childhood stress.

We assume a connection between these gene dispositions and increased sensitivity in the sense that these gene dispositions reduce the stress impact required to trigger the psychological and neurophysiological injuries that are only reached in more resilient people without increased sensitivity with very strong stress experiences such as sexual abuse or physical or psychological abuse. The result would be that already small stresses (e.g. insecure attachment to parents, lack of warmth, uncomprehending treatment, not reliable rules) could be sufficient to cause a dysregulation of the stress system (ADHD) in the first step (first hit), which in case of further added stresses in the second step (second hit) could develop psychological disorders such as depression, anxiety disorders or others.

A possible argument against the assumption of ADHD as a first hit for other disorders is that one study did not find an increased specificity of symptoms of one disorder with increasing disorder severity.12

5-HTTLPR is not the only gene variant that increases sensitivity. For example, the DRD4-7R gene variant involved in ADHD can cause a particularly high sensitivity of affected individuals to environmental stimuli.13

Here we have to distinguish:

  • Do certain gene dispositions alone cause an increased sensitivity? For this -> 1.2.1.
    or
  • Does heightened sensitivity develop only as a result of stress exposure in genetic predisposition?
    For this purpose 1.2.2
  • Or is it perhaps just amplifying?

1.2.1. Increased sensitivity even without early childhood stress exposure

The gene variants addressed are, as How ADHD develops: genes or genes + environment Not only risk genes, but also opportunity genes.
Not only do children with these gene variants respond more vulnerably to early childhood stress, manifesting barely reversible psychological disorders even in the face of stressful exposures that might not injure children without these gene variants, but these children also respond much better to encouragement and support than children without these gene variants.

This suggests that there is a higher sensitivity and susceptibility that is not only triggered by the epigenetic gene manifestation (which is, after all, only caused by early childhood stress), but is also already present independently of it, i.e. before an early childhood stress load.

1.2.2. Increased sensitivity as a result of stress in early childhood

If a corresponding gene disposition is activated by an early childhood stress load, this often leads to a permanent damage of the stress regulation systems. Overactivated stress regulation systems can cause (among several others) symptoms that can be (mis)understood as increased sensitivity:

  • Hypervigilance (increased attention), e.g. in trauma / PTSD/PTSD14
  • Wider opened stimulus filter e.g. with ADHD

The more widely opened stimulus filter is often described as increased sensitivity in ADHD sufferers.
This could suggest that increased sensitivity is a consequence of early childhood stress exposure, but does not prove it. If a corresponding gene disposition is necessary or frequent for the development of a mental disorder due to early childhood stress, the symptoms could also have been present before the stress injury. It is obvious that symptoms are not accepted as a disturbing element, but as a character trait, as long as no disturbing behavior occurs otherwise.

1.2.3. Parallel causes possible

It is further conceivable that genetic disposition in itself already contains a high degree of sensitivity, which is further intensified by early childhood stress.

Just as we understand ADHD-HI as a typical stress reaction of extroverted characters and ADHD-I as a stress reaction of introverted characters, i.e., as an amplification and exaggeration of their own characteristics and traits that are laid out anyway, an overly wide-open stimulus filter (due to injury) could also represent an intensification of the already existing heightened sensitivity that results from the overreactivity of the stress regulatory systems and from a general state of arousal that has been overdriven to hyperarousal.

2. Increased sensitivity / sensory overload and ADHD

So far, the causality between increased sensitivity and ADHD is unclear. Possibly there is no clear chicken-and-egg constellation, but a reciprocal mutual influence.

Hypersensitivity and openness to stimuli is described as a typical ADHD symptom.1516

Lane reports research that children with ADHD basically showed increased sensitivity (here as Sensory Over-Responsivity, SOR) unless they also had a flattened cortisol stress response. Our own research strongly suggests that a flattened cortisol stress response is associated with an externalizing stress phenotype (as exists in ADHD sufferers with marked hyperactivity/impulsivity), whereas an internalizing stress phenotype as in ADHD-I sufferers is more likely to correlate with an elevated cortisol stress response. This combined would mean that elevated SOR would primarily affect the ADHD-I subtype.
Meanwhile, the data from our ADHD symptom test with over 6,400 participants (as of 12/2021) tends to show a slightly higher correlation between increased sensitivity and the externalizing subtype (correlation of 0.37 to sufferers with hyperactivity/impulsivity and 0.31 to sufferers without these symptoms). The questions of the symptom test on this are:

  • Are you photosensitive?
  • How sensitive are you to noise?
  • How intensively do you perceive positive and negative feelings?
  • How uncomfortable are rough fabrics for you?
  • Do you sometimes feel moods of others unpleasantly intense?
  • How jumpy are you?
  • Are you the first to turn up the heat or open the window because you’re too hot or too cold?

Sensory processing abnormalities are frequently described in ADHD (Sensory Processing Disorder, SPD, for an aberrant mode of processing stimuli; Sensory Modulation Dysfunction, SMD, for an aberrant perceptual intensity of stimuli),17 with no differences observed between subtypes.18 One study reported a correlation of SMD with decreased parasympathetic nervous system activity.19

Increased sensitivity/stimulus overload appears to lead to various consequences, some of which are ADHD-typical, while others are not. One meta-study found the following effects of stimulus overload:20

  • Attention and concentration disorders
    • High distractibility
    • Lack of attention focus
    • Poor concentration
  • Perceptual disorders
    • Illusions
    • Hallucinations
    • Body schema changes
    • Change in the perception of time/disruption of the experience of time
  • Stress responses
    • Physical: increase in heart rate, blood pressure, respiratory rate, physical restlessness
    • Psychological: psychological exhaustion, low psychological well-being
  • Disturbed thought processes
    • Formal thought disorders: e.g. incoherence or disjointedness, flight of ideas, decrease in problem-solving ability
    • Content-related thought disorders: especially the formation of delusions
  • Affective and behavioral disorders, ineffective coping
    • Mood swings in the areas of aggression, anxiety and sadness
    • Increased and partly persistent excitability
    • Avoidance behavior (e.g., avoiding crowds, etc.)
    • Withdrawal behavior (e.g., retreating to room at a party)
    • Statements about not being able to separate or shield oneself

Apparently, only the categories

  • Attention and concentration disorders:
  • Stress responses:
  • Affective and behavioral problems, ineffective coping,

i.e. those for whom stimulus overload triggers symptoms of ADHD.

In the category

  • Perceptual disorders

is only the fourth point,

  • Change in the perception of time/disruption of the experience of time

at least partially affected. Untypical for ADHD are

  • Illusions
  • Hallucinations
  • Body schema changes

On the other hand, the symptoms of rejection sensitivity and dysfunctional perfectionism, which may originate from ADHD, could be considered as perceptual disorders in a broader sense.

Nevertheless, this result connects to our perception that while almost all ADHD symptoms are stress symptoms, not all stress symptoms are also ADHD symptoms. While stress causes an opening of the stimulus filter in the thalamus, not all stress symptoms triggered by the opened stimulus filter (if one wants to call the mentioned categories that) are ADHD symptoms at the same time. This confirms the view that ADHD mediates its symptoms in the same way as chronic over-responsive stress systems, but not every effect of over-responsive stress systems is also ADHD.

3. Creativity, increased sensitivity and wider open stimulus filter

There seems to be a correlation between creativity and heightened sensitivity due to a more wide-open stimulus filter.
Eysenck assumes that in creative people (possibly similar to schizophrenics) already learned, stored memory content is weighted lower, so that new perceptions are weighted higher, which expands the horizon of association.21 Carson (Harvard) confirmed this. He found that creative people are more easily distracted and attributed this to weaker latent inhibition, which opens the stimulus filter wider. According to this, creative people are more sensitive to sensory stimuli and therefore more distractible. Carson sees a connection between a “common vulnerability” of creativity and psychopathology, according to which highly creative individuals on the one hand and psychotic and psychosis-prone persons on the other hand share a “cognitive disinhibition” as a common resource and/or burden.22

In our opinion, a more intensive sensing is only conditionally explained by a more widely opened stimulus filter.

4. Increased sensitivity and recovery

There are two typical patterns of how people recover:

  • Some draw strength from social contacts
  • The others rather be in the alone.
    The latter is the typical(r) recovery pattern in heightened sensitives / introverts.

When there is “too much” external stimuli, withdrawal from social contacts as a stimulus reduction mechanism is obvious. This is consistent with the fact that increased sensitivity, according to data from the ADxS.org symptom test (as of June 2020, n = 1.889) correlates slightly higher in ADHD-I (0.37) than with ADHD-HI subtypes (0.27), whereas social withdrawal (0.21) and social phobia (0.30) are typical behaviors of the ADHD-I subtype (correlation 0.30) and are almost unknown in the ADHD-HI subtype social withdrawal (-0.06) or social phobia (-0.05).

5. Increased sensitivity and reaction to environmental influences

The more sensitive a person is, the lower the required impact of a threatening stressful situation to neurologically implement a traumatizing manifestation of stress regulation dysfunction.

It is well known that different personality types react differently to environmental influences. Introverts react more intensively to environmental influences than extroverts.23 The concept of high sensitivity according to Aron is closely linked to introversion.

6. Differentiated stimulus perception reduced in ADHD

In ADHD, tactile discrimination, i.e., the ability to distinguish between different touch stimuli, appears to be reduced.24


  1. ADHSpedia: ADHS-Persönlichkeit; Abruf 21.02.21

  2. ADHSpedia: Hochsensibilität, Abruf 05.04.2021

  3. Lionetti, Aron, Aron, Burns, Jagiellowicz, Pluess (2018): Dandelions, tulips and orchids: evidence for the existence of low-sensitive, medium-sensitive and high-sensitive individuals. Transl Psychiatry 8, 24 (2018). https://doi.org/10.1038/s41398-017-0090-6

  4. Greven, Lionetti, Booth, Aron, Fox, Schendan, Pluess, Bruining, Acevedo, Bijttebier, Homberg (2019): Sensory Processing Sensitivity in the context of Environmental Sensitivity: A critical review and development of research agenda. Neurosci Biobehav Rev. 2019 Mar;98:287-305. doi: 10.1016/j.neubiorev.2019.01.009. PMID: 30639671. REVIEW

  5. Lionetti, Pastore, Moscardino, Nocentini, Pluess, Pluess (2019): Sensory Processing Sensitivity and its association with personality traits and affect: A meta-analysis. Journal of Research in PersonalityVolume 81, August 2019, Pages 138-152

  6. Otsuka, Yashioka (1993): Neurotransmitter functions of mammalian tachykinins; Physiol Rev. 1993 Apr; 73(2):229-308; zitiert nach Rensing, Koch, Rippe, Rippe (2006): Mensch im Stress; Psyche, Körper Moleküle; Elsevier (jetzt Springer), Seite 97

  7. Rensing, Koch, Rippe, Rippe (2006): Der Mensch im Stress; Psyche, Körper, Moleküle; Elsevier Spektrum (heute: Springer), Seite 151

  8. Chen, Chen, Moyzis, Stern, He, Li, Li, Zhu, Dong (2011): Contributions of dopamine-related genes and environmental factors to highly sensitive personality: a multi-step neuronal system-level approach. PLoS One. 2011;6(7):e21636. doi: 10.1371/journal.pone.0021636. PMID: 21765900; PMCID: PMC3135587.

  9. Licht, Mortensen, Knudsen (2011): Association between sensory processing sensitivity and the 5-HTTLPR Short/Short genotype. Biol. Psychiatry 69, 152S–153S (Supplement for Society of Biological Psychiatry Convention and Annual Meeting, abstract, 510

  10. Green, Rudie, Colich, Wood, Shirinyan, Hernandez, Tottenham, Dapretto, Bookheimer (2013): Overreactive Brain Responses to Sensory Stimuli in Youth With Autism Spectrum Disorders, Journal of the American Academy of Child & Adolescent Psychiatry, Volume 52, Issue 11, 1158 – 1172; DOI: https://doi.org/10.1016/j.jaac.2013.08.004

  11. Lemvigh, Jepsen, Fagerlund, Pagsberg, Glenthøj, Rydkjær, Oranje (2019): Auditory sensory gating in young adolescents with early-onset psychosis: a comparison with attention deficit/hyperactivity disorder. Neuropsychopharmacology. 2019 Oct 24. doi: 10.1038/s41386-019-0555-9.

  12. Groen, Wichers, Wigman, Hartman (2019): Specificity of psychopathology across levels of severity: a transdiagnostic network analysis. Sci Rep. 2019 Dec 4;9(1):18298. doi: 10.1038/s41598-019-54801-y. n = 1.933

  13. 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 | http://dx.doi.org/10.3389/fnhum.2013.00195 mit Verweis auf Sasaki, Kim, Mojaverian, Kelley, Park Janušonis (2011): Religion priming differentially increases prosocial behavior among variants of the dopamine D4 receptor (DRD4) gene; Soc Cogn Affect Neurosci (2013) 8(2): 209-215.doi: 10.1093/scan/nsr089First published online: December 23, 2011

  14. http://www.traumatherapie.org/docs/index.html#Kernsymptomatik

  15. Ryffel-Rawak (2007): ADHS bei Erwachsenen Betroffene berichten aus ihrem Leben; Hinweise für Fachleute, S. 144

  16. Lane, Reynolds, Thacker (2010): Sensory Over-Responsivity and ADHD: Differentiating Using Electrodermal Responses, Cortisol, and Anxiety. Front Integr Neurosci. 2010 Mar 29;4:8. doi: 10.3389/fnint.2010.00008. PMID: 20556242; PMCID: PMC2885866.

  17. Mangeot, Miller, McIntosh, McGrath-Clarke, Simon, Hagerman, Goldson (2001): Sensory modulation dysfunction in children with attention-deficit-hyperactivity disorder. Dev Med Child Neurol. 2001 Jun;43(6):399-406. doi: 10.1017/s0012162201000743. PMID: 11409829.

  18. Engel-Yeger, Ziv-On (2011): The relationship between sensory processing difficulties and leisure activity preference of children with different types of ADHD. Res Dev Disabil. 2011 May-Jun;32(3):1154-62. doi: 10.1016/j.ridd.2011.01.008. Epub 2011 Feb 15. PMID: 21324640.

  19. Schaaf, Benevides, Blanche, Brett-Green, Burke, Cohn, Koomar, Lane, Miller, May-Benson, Parham, Reynolds, Schoen (2010): Parasympathetic functions in children with sensory processing disorder. Front Integr Neurosci. 2010 Mar 9;4:4. doi: 10.3389/fnint.2010.00004. PMID: 20300470; PMCID: PMC2839854.

  20. Scheydt, Needham (2017): Mögliche Kennzeichen der Reizüberflutung / Possible Signs of Sensory Overload; Psychiat Prax 2017; 44(03): 128-133; DOI: 10.1055/s-0042-118988

  21. Eysenck: Genius: The Natural History of Creativity. Kap. Neurophysiology of Creativity, Seite 260 ff., Cambridge University Press, 1995, zitiert aus Wikipedia: Genie

  22. Carson (2014): Cognitive Disinhibition, Creativity, and Psychopathology – In: Dean Keith Simonton (editor): The Wiley Handbook of Genius. John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9781118367377.ch11

  23. Lexikon der Biologie: Genotyp-Umwelt-Interaktion. Spektrum.de Abruf 12.10.2019.

  24. Romero-Ayuso, Maciver, Richmond, Jorquera-Cabrera, Garra-Palud, Zabala-Baños, Toledano-González, Triviño-Juárez (2020): Tactile Discrimination, Praxis and Cognitive Impulsivity in ADHD Children: A Cross-Sectional Study. Int J Environ Res Public Health. 2020 Mar 14;17(6):1897. doi: 10.3390/ijerph17061897. PMID: 32183331; PMCID: PMC7143737.