Dear reader of ADxS.org, please excuse the disruption.

ADxS.org needs around €58,500 in 2024. Unfortunately 99,8 % of our readers do not donate. If everyone reading this appeal made a small contribution, our fundraising campaign for 2024 would be over after a few days. This appeal is displayed 23,000 times a week, but only 75 people donate. If you find ADxS.org useful, please take a minute to support ADxS.org with your donation. Thank you very much!

Since 01.06.2021 ADxS.org is supported by the non-profit ADxS e.V. Donations to ADxS e.V. are tax-deductible in Germany (up to €300, the remittance slip is sufficient as a donation receipt).

If you would prefer to make an active contribution, you can find ideas for Participation or active support here.

$45213 of $63500 - as of 2024-10-31
71%
Header Image
Sensitivity, stress and ADHD

Sitemap

Sensitivity, stress and ADHD

Author: Ulrich Brennecke
Review: Dipl.-Psych. Waldemar Zdero

The brain has several functions:

  • Thinking
  • Perceive
  • Feel
  • Action control

People with ADHD often show increased sensitivity to stimuli and emotions. Increased sensitivity (Sensory Processing Sensitivity, SPS) refers to the functions of perception and feeling: Those who perceive more, who feel more intensely, are more sensitive above a certain level.12

People have varying degrees of sensitivity to stimuli.3 The term high sensitivity, which we used in the past and by which we inaccurately meant heightened sensitivity, is correctly a construct from Aron, which also includes a different form of perceptual processing in addition to heightened sensitivity. 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 that differs from other temperament and personality constructs.45 We use the term heightened sensitivity in the following, also to avoid any unconscious confusion between hypersensitivity and high sensitivity.

Research has shown that people with ADHD are more likely to be hypersensitive to sensory stimuli and may have difficulty distinguishing between relevant and irrelevant stimuli. In ADHD, the ability to make tactile discriminations is impaired. This means that people with ADHD have difficulty distinguishing between different touch stimuli.
There is a connection between increased sensitivity and creativity. People with heightened sensitivity often recover better when they are alone. They also react more strongly to environmental influences and can be traumatized more easily.

Increased sensitivity can be influenced by neurological causes such as an overly open stimulus filter (thalamus) in the brain or altered dopamine levels. Genetic causes can favor increased sensitivity, whereby both certain gene variants and early childhood stress can play a role. Increased sensitivity can cause attention problems, disturbed thought processes and affective and behavioral disorders. The causality of the relationship between increased sensitivity and ADHD, i.e. the question of cause and effect, has not yet been clarified.

1. Causes of increased sensitivity

1.1. Neurological causes

1.1.1. Wide open stimulus filter

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 the part of Aron’s hypothesis on high sensitivity according to which this represents an increased processing of incoming stimuli.
The stimulus filter is controlled by the thalamus. The ARAS (ascending reticular activating system) located in the thalamus activates and deactivates those areas of the brain that are involved in perception and sensory processing. The relevant brain areas are not activated together, but individually. Activation takes place when the required level of interest (inner arousal) is present.
If this control element is disturbed, attention problems arise.
According to this same pattern, attention problems in ADHD are primarily the consequences of motivational 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 filter unit that selects which incoming stimuli are passed on 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.
More on this at Tasks of the basal ganglia: Supporting the thalamus through filtering In the article Basal ganglia in the section The human stress systems - the basics of stress in the chapter Stress.

1.1.1.1.2. Increase in dopamine

Optimal stimulus filtering is achieved at a medium dopamine level.
A slight increase in dopamine, which is typical of mild stress, increases the performance of the PFC. This leads to more intensive processing of incoming stimuli.

1.1.1.2. Noradrenaline and increased sensitivity

An increased noradrenaline level in the brain also increases the sensitivity to stimuli and the 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 the HPA axis and the sympathetic nervous system - primarily in the case of physical stressors such as cold, pain or drug withdrawal.

1.1.1.4. CRH and increased sensitivity

The stress hormone CRH, which is produced by the hypothalamus as part of the cascade of the HPA axis and in parallel by other parts of the brain (including the PFC), increases alertness, auditory perception and attention. It also has a number of other stress benefits.7

1.1.1.5. Genetic causes

A study on dopaminergic genes in high sensitivity (i.e. 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 noradrenaline
  • 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 interact functionally with it, in particular with DRD2.
The 10 polymorphisms described in the study explained 15 % of the high sensitivity. Stress (in conjunction with a lack of parental warmth) explained a further 2 %.

Another study describes a connection between increased sensitivity and the serotonin transporter gene variant 5HTTLPR-short/short.9

1.1.2. Stimulus filter opening and perception

If the stimulus filter is opened further, more information is absorbed. This is of course exhausting - the stimulus filter exists for a reason.
The open stimulus filter model explains that increased sensitivity triggers more intensive perception.

In our opinion, this can only explain the more intense feeling to a limited extent.

People with ADHD who suffer from 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 degree 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 there are various gene dispositions that experience their epigenetic expression in the event of (primarily early childhood) massive stress and, depending on which gene disposition is affected, manifest different mental disorders as a consequence. For more information, see How ADHD develops: genes or genes + environment.

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

As a - possibly daring - hypothesis, we consider it possible that there is a connection between these gene dispositions and increased sensitivity in that these gene dispositions reduce the stress impact required to trigger the psychological and neurophysiological injuries that, in more resilient people without the increased sensitivity, are only achieved with very severe stress experiences such as sexual abuse or physical or psychological abuse. The result would be that even minor stresses (e.g. insecure attachment to parents, lack of warmth, lack of understanding, unreliable rules) could be sufficient to cause a dysregulation of the stress system (ADHD) in the first step (first hit), which, if further stresses occur in the second step (second hit), could lead to the development of mental disorders such as depression, anxiety disorders or others. There are also indications of the effect of the second hit with regard to the severity of symptoms of ASD.12

A possible argument against the assumption of ADHD as a first hit for other disorders is that a study did not find any increased specificity of symptoms of a disorder with increasing disorder severity.13

5-HTTLPR is not the only gene variant that increases sensitivity. For example, the DRD4-7R gene variant involved in ADHD can cause people with ADHD to be particularly sensitive to environmental stimuli.14

We have to make a distinction here:

  • Do certain gene dispositions alone cause increased sensitivity? On this -> 1.2.1.
    or
  • Does increased sensitivity only develop as a result of stress in the case of a genetic disposition?
    1.2.2
  • Or is it perhaps just intensifying?

1.2.1. Increased sensitivity even without early childhood stress exposure

The gene variants mentioned are, as at How ADHD develops: genes or genes + environment Not only risk genes, but also opportunity genes.
Not only do children with these gene variants react more vulnerably to early childhood stress, manifesting barely reversible mental disorders even when exposed to stressors that could not hurt children without these gene variants, but these children also respond much better to encouragement and support than children without these gene variants.

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

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

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

  • Hypervigilance (increased alertness), e.g. in trauma / PTSD/PTSD15
  • Wider open stimulus filter, e.g. for ADHD

The wider open stimulus filter is often described as increased sensitivity in people with ADHD.
This could suggest that increased sensitivity is a consequence of early childhood stress, but does not prove it. If a corresponding gene disposition is necessary or frequent in order to develop a mental Disorder as a result of early childhood stress, the symptoms could also have been present before the stress injury. It is obvious that symptoms are not accepted as an element of a disorder, but as a character trait, as long as no other disruptive behavior occurs.

1.2.3. Parallel causes possible

It is also conceivable that the genetic disposition itself already involves a high level 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 the already inherent characteristics and traits, an (injury-related) overly open stimulus filter could also represent an intensification of the already existing increased sensitivity, which is caused by the overreactivity of the stress regulation systems and by a general state of arousal overdriven to hyperarousal.

2. Increased sensitivity / sensory overload and ADHD

So far, the causality between increased sensitivity and ADHD has not been clarified. It is possible that there is no clear chicken-and-egg constellation, but rather a reciprocal mutual influence.

Hypersensitivity and irritability are described as typical ADHD symptoms.161718

Lane reports that children with ADHD generally 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 seen in people with ADHD with marked hyperactivity/impulsivity), while an internalizing stress phenotype as seen in persons with ADHD-I is more likely to correlate with an increased cortisol stress response. Combined, this would mean that increased SOR would primarily affect the ADHD-I subtype.
However, the data from our ADHD symptom test with over 6,400 participants (as of 12/2021) show a slightly higher correlation between increased sensitivity and the externalizing subtype (correlation of 0.37 to persons with ADHD with hyperactivity/impulsivity and 0.31 to persons without these symptoms). The questions of the symptom test are:

  • Are you sensitive to light?
  • How sensitive are you to noise?
  • How intensely do you perceive positive and negative feelings?
  • How uncomfortable are rough fabrics for you?
  • Do you sometimes find the moods of others unpleasantly intense?
  • How jumpy are you?
  • Are you the first to turn up the heating or open the window because it’s too hot or too cold?

Abnormalities in sensory processing are frequently described in ADHD (Sensory Processing Disorder, SPD, for an abnormal way of processing stimuli; Sensory Modulation Dysfunction, SMD, for an abnormal intensity of perception of stimuli),19 although no differences were observed between the subtypes.20 One study reports a correlation of SMD with reduced activity of the parasympathetic nervous system.21

Increased sensitivity/stimulus overload appears to lead to various Consequences, some of which are typical of ADHD, while others are not. A meta-study found the following effects of sensory overload:22

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

The only obvious categories are

  • Attention and concentration disorders:
  • Stress reactions:
  • Affect and behavioral abnormalities, ineffective coping,

in other words, those for whom sensory overload triggers symptoms of ADHD.

In the category

  • Perceptual disorders

is only the fourth point,

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

at least partially affected. The following are atypical for ADHD

  • Illusions
  • Hallucinations
  • Body schema changes

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

Nevertheless, this result ties in with 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 symptoms triggered by the opened stimulus filter are also ADHD symptoms. 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 a wider stimulus filter

There seems to be a connection between creativity and increased sensitivity, which can be attributed to a more open stimulus filter.
Eysenck suspects that in creative people (possibly similar to schizophrenics), previously learned, stored memory content is weighted less, so that new perceptions are weighted higher, which expands the association horizon.23 Carson (Harvard) confirmed this. He found that creative people are more easily distracted and attributes this to a weaker latent inhibition, which means that the stimulus filter is wider open. According to this, creative people are more sensitive to sensory stimuli and therefore more distractible. Carson sees a connection between a “shared vulnerability” of creativity and psychopathology, according to which highly creative individuals on the one hand and psychotic and psychosis-prone individuals on the other share a “cognitive disinhibition” as a common resource and/or burden.24

In our opinion, a more intensive feeling is only partially explained by a more open 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 in solitude.
    The latter is the typical recovery pattern for more sensitive / introverted people.

If there is “too much” external stimuli, withdrawal from social contact is an obvious stimulus reduction mechanism. This is consistent with the fact that, according to the data from the ADxS.org symptom test (as of June 2020, n = 1.889) correlates slightly higher with ADHD-I (0.37) than with ADHD-HI subtypes (0.27), while social withdrawal (0.21) and social phobia (0.30) are typical behavioral patterns of the ADHD-I subtype (correlation 0.30) and are almost unknown in the ADHD-HI subtypes 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 stress 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 intensely to environmental influences than extroverts.25 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.26

7. Measurement of increased sensitivity

The “SENSE” - Sensory and Behavioral Modulation Questionnaire for adults is a test to measure increased sensitivity, which also provides stable results in adults.18


  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. Waizbard-Bartov E, Ferrer E, Heath B, Andrews DS, Rogers S, Kerns CM, Wu Nordahl C, Solomon M, Amaral DG (2023): Changes in the severity of autism symptom domains are related to mental health challenges during middle childhood. Autism. 2023 Sep 10:13623613231195108. doi: 10.1177/13623613231195108. PMID: 37691349.

  13. 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

  14. 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

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

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

  17. 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.

  18. Engel-Yeger B (2024): The development and validation of the “SENSE” - Sensory and Behavioral Modulation Questionnaire for adults. Res Dev Disabil. 2024 Mar 11;147:104715. doi: 10.1016/j.ridd.2024.104715. PMID: 38471295.

  19. 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.

  20. 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. PMID: 21324640.

  21. 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.

  22. 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

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

  24. 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

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

  26. 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.