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Impulsivity in ADHD - neurophysiological correlates

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Impulsivity in ADHD - neurophysiological correlates

1. What impulsivity correlates with

Impulsiveness correlates with:

  • Externalizing rather than internalizing mental health problems1
  • Less sleep at weekends2
  • A lower affinity for food after the Mediterranean diet2
  • Use of technical devices for more than 3 hours/day2
  • Birth by caesarean section2
  • Birth weight of more than 2.5 kg2
  • Not breastfed2
  • Sports on more than 3 days / week (low correlation)2
  • Tendency towards risky behavior3
  • Impulsivity and delay aversion seem to correlate with timing skills.4

With the exception of birth circumstances and breastfeeding, we believe that the correlations are more likely to be consequences than causes of impulsivity.

2. Neurophysiological correlates of impulsivity

Impulsivity is associated with activity in a network of orbitofrontal cortex (OFC) → striatum → thalamus.5

2.1. Neurophysiological correlates

Atomoxetine had a stronger effect on action impulsivity than on choice impulsivity in rodents, which was taken as an indication that these are neurophysiologically different constructs.6

2.1.1. Neurophysiological correlates of impulsivity in general

Impulsivity correlates with higher activity in the following brain regions:

  • Ventral amygdala (both sides)78
  • Parahippocampal gyrus7
  • Left dorsal anterior cingulum (Brodmann area 32)7
  • Caudate nucleus (both sides)7

Impulsivity correlates with lower activity in the following brain regions:

  • Dorsal amygdala7
  • Ventral PFC (Brodmann area 47)7
  • Cingulum
    • Anterior910
    • Posterior10
  • Right medial frontal gyrus9
  • Right precentral gyrus9
  • Right frontal pole11

Impulse inhibition correlates neurologically with

  • Increased activity in the orbitomedial PFC (omPFC)
  • Reduced dopaminergic excitation of the omPFC
    • Reduces the ability to inhibit impulsivity.12
  • Increased activity in the right (anterior lateral) obitofrontal cortex (OFC)138 or dorsolateral PFC.14
  • Right middle frontal gyrus and right inferior frontal gyrus:15
    • reduced activation in the right PFC Children with ADHD-I
    • tendency towards increased activation in children with ADHD-C
  • Temporal gyrus and the supplementary motor area:15
    • Activation impaired in children with ADHD-I and ADHD-C

One study found no evidence of abnormalities in neurocognitive processes as represented by the diffusion decision model (DDM) or in go/no-go performance in ADHD. However, responses to failed inhibition in brain regions associated with error monitoring correlated closely with more efficient task performance, externalizing behavior, and ADHD symptoms. This study thus sows doubt as to whether go/no-go task activation truly reflects the neural basis of inhibition and found evidence that error-related contrasts provide better information.16

An FMRI-BOLD study using a Continuous Performance Task with visual and auditory distraction found in children with ADHD:17

  • reduced inhibitory activity in the audiovisual association zones
  • overactivation of the motor areas
  • cerebellar activation that attempted to modulate the responses of the different areas

which in sum led to an executive failure.

2.1.2. Neurophysiological correlates of action impulsivity

Neurophysiologically, inhibition problems are modulated by a circuit consisting of:18

  • pre-supplementary motor area (preSMA)
  • right inferior frontal gyrus (rIFG)
  • Striatum
  • subthalamic nucleus (STN).

Action impulsivity and choice impulsivity are moderated by the genes for:18

  • D4R
  • DAT
  • COMT
  • α2AR

2.1.3. Neurophysiological correlates of elective impulsivity

Choice Impulsivity (Delay Disounting) is modulated by a brain circuit consisting of18

  • ventromedial prefrontal cortex (vmPFC)
    • glutamatergic neurons
  • posterior cingulate cortex (pCC)
    • glutamatergic neurons
  • Nucleus accumbens (NAc)

Action impulsivity and choice impulsivity are moderated by the genes for:18

  • D4R
  • DAT
  • COMT
    • A COMT inhibitor increased the choice of more distant rewards (in healthy subjects). This leads to impairments of the striatum. Since COMT degrades dopamine in the PFC, this suggests a correlation of reduced dopamine levels in the PFC and devaluation of distant rewards 12
  • α2AR

In SHR, in vivo electrophysiological recordings revealed neural coding of discounting behavior in the prefrontal and orbitofrontal cortex when rewards were present:19

  • OFC neurons
    • were activated regardless of the value of the reward
    • showed significantly higher neuronal discharge rates
    • the reward-predicting OFC neurons
      • coded the value of the rewards in control animals
      • were strongly activated at SHR after receiving a small direct amplifier
  • mPFC neurons
    • for large rewards: similarly active as for controls
    • for smaller rewards: higher discharge rates than for controls
    • no reaction to the value of the rewards

Delay discounting in ADHD correlated with:11

  • significant increase in the concentration of oxygenated hemoglobin (oxy-Hb) bilaterally in the frontal pole and in the dlPFC
  • Activity of the left PFC

2.2. Overexpression of the ATXN7 gene

Hyperactivity and impulsivity are also caused by overexpression of the Atxn7 gene in the PFC and striatum.20 In this case, atomoxetine was able to eliminate the hyperactivity and impulsivity.

2.3. Amygdala

The connectivity of the brain networks is increased locally around the amygdala and decreased to the anterior cingulate and posterior cingulate in the cortex. The predominance of connections around the amygdala over cortical connections results in an increased impulsive response to stimuli with reduced cortical inhibition.10

Delay aversion (impatience) correlates with a reduced amygdala.21

2.4. Ventral striatum

A study on monkeys came to the conclusion that low doses of MPH reduce impulsivity, while higher doses have a sedative effect. The impulsivity-inhibiting effect occurred in the ventral striatum in particular.22
This follows on from empirical experience that people with ADHD, especially children, can sometimes appear apathetic when taking MPH. In our opinion, following this study, this indicates an overdose.

2.5. Increased connectivity between ventral tegmentum and middle cingulum

One study found a correlation between subjectively perceived impulsivity and significantly increased functional connectivity between the ventral tegmentum and the middle cingulate during L-dopa administration.23

2.6. Reduced myo-inositol levels in the vlPFC, but not in the striatum

In rats with high impulsivity, a significant reduction in myo-inositol concentration was reported in the infralimbic PFC, but not in the striatum, compared to rats with low impulsivity. In the infralimbic PFC, significant reductions in transcript levels of key proteins involved in the synthesis and recycling of inositol (IMPase1) were also evident. Deactivation of IMPase1 in the infralimbic PFC increased impulsivity.24
Myo-inositol (cyclohexane-cis-1,2,3,5-trans-4,6-hexol) is the most common isomer of inositol (inositol = cyclohexanehexol, a hexavalent cyclic alcohol). It is an intracellular “second messenger”. Oral administration improves insulin resistance as well as fat and glucose metabolism and lowers androgen levels.25

2.7. Increased lateralization of the posterior thalamic radiation

A significantly higher lateralization of the posterior thalamic radiation (PTR) was found in children with ADHD. The lateralization of the PTR correlated with inhibition in healthy controls, but not in children with ADHD.26

2.8. Nucleus accumbens

In rodents, lesions of the nucleus accumbens or the basolateral amygdala lead to impulsive decisions, but not lesions of the ACC or the mPFC. Lesions of the OFC reduce impulsivity. Impulsive decisions could thus be the result of abnormal processing of reward size or a reduced effect of delayed reinforcement.
Rodents with a lesion of the nucleus accumbens perceive the size of rewards normally, but show a selective deficit in learning instrumental responses with delayed reinforcement. This may indicate that the nucleus accumbens is a reinforcement learning system that mediates the effects of delayed rewards.27

2.9. Iron content in the putamen

Elevated iron levels in the putamen correlated - not only in ADHD - with worsened inhibition28

2.10. No indication of parietal involvement

One study found no evidence of expected parietal modulation with an increased need for inhibition. However, this lack of modulation was mediated by individual ADHD symptom severity. A correlation between intraparietal sulcus (IPS) activity and events to be inhibited was evident in less severe ADHD symptoms. However, this correlation disappeared for more severe ADHD symptoms. Similarly, functional connectivity between the IPS and the right inferior frontal gyrus correlated with conditions of high inhibitory demand, while this correlation decreased with increasing symptom severity.29

2.11. No unique genes in GWAS

A genome-wide association study (GWAS) found no unique genes that coded for impulsivity based on stop signal task, i.e. go reaction time (GoRT), go reaction time variability (GoRT SD) and stop signal reaction time (SSRT).30
Nevertheless, GoRT SD and SSRT showed a significant and similar SNP heritability of 8.2 %, indicating a genetic influence. However, the heritability seems to originate from a high number of genes. In Europeans, polygenic risk for ADHD was significantly associated with GoRT SD and polygenic risk for schizophrenia was associated with GoRT, while in East Asians, polygenic risk for schizophrenia was associated with SSRT.

3. Impulsivity and neurotransmitters / hormones

3.1. Dopamine

Impulsivity (as well as distractibility and depression) is characterized by1

  • A reduced tonic (long-lasting) dopamine level
    and
  • A reduced phasic (short-term) dopamine response to stimuli in the mesolimbic system.

The ADHD symptom of lack of inhibition of executive functions is caused dopaminergically by the basal ganglia (striatum, putamen), while the lack of inhibition of emotion regulation is caused noradenergically by the hippocampus.31 Therefore, the former is more amenable to dopaminergic treatment. Emotion regulation and affect control, on the other hand, are more amenable to noradrenergic treatment.

3.2. Serotonin

Other sources describe that impulsivity is induced by a lack of serotonin.3233 A low affinity of the serotonin transporter in platelets correlated with high impulsivity, while an increased SERT affinity correlated moderately with increased aggressiveness and externalizing behaviour. SERT expression had no influence. Serotonin availability in the synaptic cleft seems to depend more on the affinity than the number of SERTs. 34

Serotonin inhibits aggression, so a lack of serotonin (in conjunction with high testosterone and low cortisol levels) promotes aggression. More on this under ⇒ Aggression as a consequence of high testosterone with a simultaneously weakened cortisol response.

A high serotonin level in the PFC reduces aggression and impulsivity.3536373839
Zuckermann’s theory that impulsivity goes hand in hand with increased dopamine levels does not seem to be confirmed. Rather, Cloninger’s theory that impulsivity is promoted by low serotonin and low dopamine levels seems to be confirmed.40 Against the background of the inverted-U theory4142 , according to which low and high neurotransmitter levels in one area of the brain can cause very similar problems, these two possibilities should not be mutually exclusive,

One study found identical serotonin concentrations in platelets in children with and without ADHD, and no relation to attention problems or hyperactivity, but a positive correlation to impulsive behavior.43

We have observed that low doses (2 to 5 mg/day) of SSRIs (e.g. escitalopram) improve impulsivity very quickly in ADHD-HI. There appears to be an immediate effect of serotonin, as the effect does not occur after several weeks, as it occurs as a consequence of downregulation of the 5-HT receptors when higher doses of SSRIs are administered as antidepressants (escitalopram: 10 to 20 mg / day). In this case, downregulation of the receptors should be avoided as far as possible, which is why the lowest dosage that is still helpful should be used.

3.3. Adenosine, cannabinoids

SHR rats, representing a model of ADHD-HI, responded to a cannabinoid CB1 receptor agonist with increased impulsivity (increased preference for short-term reward). This response was suppressed by a single dose of caffeine (a non-specific adenosine receptor antagonist), but was enhanced by chronic caffeine administration.44
In contrast, a cannabinoid antagonist reduced impulsivity and increased the preference for later, but larger rewards.44

3.4. Corticoids

The response inhibition improved by mild stress in healthy subjects in a stop-signal task is worsened by a mineralocorticoid antagonist.45
This indicates the involvement of mineralocorticoid receptors or the balance between mineralocorticoid receptors and glucocorticoid receptors during inhibition.

4. Lack of sleep impairs inhibition

ADHD correlates with sleep deprivation. An increase in sleep duration significantly improved inhibition in children with ADHD.46


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