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Citalopram / Escitalopram for ADHD

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Citalopram / Escitalopram for ADHD

Citalopram and escitalopram are selective serotonin reuptake inhibitors (SSRIs).

Escitalopram is the purely active isomer, while citalopram is the racemate of the active and ineffective isomer.1 The effect profile is therefore identical, the side effects should be slightly less with escitalopram. Escitalopram was developed and launched on the market after the patent protection for citalopram had expired.

ATTENTION:
With regard to the entire group of serotonin reuptake inhibitors, in particular citalopram / escitalopram, there are concerns about their use in ADHD.
See also Comments on serotonin reuptake inhibitors (SSRIs) for ADHD In the article Medication for ADHD - overview.

1. Citalopram / Escitalopram in relation to ADHD

  • SSRIs showed no effect on ADHD 2
  • Citalopram / escitalopram appears to increase the activity of the DAT,34 which could potentially be detrimental in ADHD.
    One of the main problems of ADHD is the low level of dopamine in the striatum, which may be largely caused by an excessive number of dopamine transporters that take up the released dopamine presynaptically from the synaptic cleft before it can dock postsynaptically. More active DAT therefore intensify the symptoms of ADHD.
    If there are also sleep problems (as is often the case with ADHD), drugs that increase serotonin levels are also said to be detrimental.5.
  • Escitalopram in higher doses (20 mg) increases the cortisol response to acute stress (TSST).6
    When treating comorbid depression in ADHD, it should be borne in mind that increasing the cortisol response to stress may be beneficial in ADHD-HI sufferers (who often have an excessively flat cortisol response, which is why the HPA axis is not switched off), but may be detrimental from this point of view in ADHD-I sufferers (who very often have an excessive cortisol response). See Comments on serotonin reuptake inhibitors (SSRIs) for ADHD In the article Medication for ADHD - overview.
  • Citalopram reduces the response of the striatum to stimulating or negative stimuli.7
    The effect on the striatum could also be the cause of the emotional blunting and increased indifference caused by SSRIs.8
  • Escitalopram leads to increased anxiety levels at 10 mg and 20 mg on the TSST.6 The HPA axis is directed by the amygdala. Increased anxiety is counterproductive in ADHD and especially in ADHD-I.
  • Citalopram causes a reduction in the activity rate of serotonergic neurons in the dorsal raphe nuclei.9
  • Citalopram increases serotonin, but not dopamine and noradrenaline in the dorsal hippocampus, frontal cortex, nucleus accumbens and striatum.10
  • Citalopram does not reduce the activity of dopaminergic neurons in the ventral tegmentum11
  • Citalopram does not reduce the activity of adrenergic neurons in the nucleus coeruleus9

Most practitioners do not make a clear distinction between the typical ADHD symptom of dysphoria* During inactivity, which is a functional stress symptom (the drop in mood during inactivity is aimed at keeping the affected person active until the stressor is defeated) and “real” depression and therefore treat ADHD sufferers inappropriately as if they had real depression.
*Dysphoria here does not mean a “real” exhaustion depression, which can be the result of ADHD, but a (chronic) drop in mood.
Depression and dysphoria in ADHD.

In practice, it has been shown that treatment with a significantly reduced amount of escitalopram (compared to its use as an antidepressant) can improve dysphoric mood. Here, quantities of 3 to 5 drops a day may already be sufficient.
In our experience, switching treatment from methylphenidate to amphetamine medication (Elvanse), which has a weak serotonergic effect as well as a strong dopaminergic and noradrenergic effect, also has a positive effect on the symptom of dysphoria.

2. Degradation of escitalopram

Source: Schmotz12

Escitalopram is significantly influenced by

  • Cytochrome P450 (CYP) isoenzyme CYP3A4
  • Cytochrome P450 (CYP) isoenzyme 2C19
  • Cytochrome P450 (CYP) isoenzyme 2D6

to demethyl-escitalopram. This still has 10% of the efficacy of escitalopram and is subsequently metabolized to a didemethyl metabolite.
In patients with liver damage, escitalopram degradation is reduced and plasma levels are increased.
Escitalopram and its demethyl metabolite hardly inhibit the hepatic enzyme system (CYP1A2, -2C9, -2C19, -2E1 and -3A) and 2D6 only weakly.
There are hardly any relevant drug interactions with inhibitors of CYP3A4, CYP2C19
or CYP2D6 (von Moltke, Greenblatt et al. 2001; Rao 2007).
Citalopram and escitalopram are primarily excreted via the kidneys, with only a small amount excreted via the faeces.

The elimination half-life of escitalopram is approx. 30 hours.


  1. http://www.pharmazeutische-zeitung.de/index.php?id=pharm7_29_2004

  2. Dodson WW (2005): Pharmacotherapy of adult ADHD. J Clin Psychol. 2005 May;61(5):589-606. doi: 10.1002/jclp.20122. PMID: 15723384. REVIEW

  3. http://www.adhs.org/therapie/

  4. Krause, Krause (2014): ADHS im Erwachsenenalter: Symptome – Differenzialdiagnose – Therapie, Seiten 276, 129

  5. Krause, Krause (2014): ADHS im Erwachsenenalter: Symptome – Differenzialdiagnose – Therapie, Seite 289

  6. Garcia-Leal, Del-Ben, Leal, Graeff, Guimarães (2010): Escitalopram prolonged fear induced by simulated public speaking and released hypothalamic-pituitary-adrenal axis activation. J. Psychopharmacol. 24, 683–694.; http://dx.doi.org/10.1177/0269881108101782

  7. McCabe, Mishor, Cowen, Harmer (2009): Diminished neural processing of aversive and rewarding stimuli during selective serotonin reuptake inhibitor treatment. Biol Psychiatry. 2010 Mar 1;67(5):439-45. doi: 10.1016/j.biopsych.2009.11.001.

  8. Sternat, Katzman (2016): Neurobiology of hedonic tone: the relationship between treatment-resistant depression, attention-deficit hyperactivity disorder, and substance abuse. Neuropsychiatr Dis Treat. 2016 Aug 25;12:2149-64. doi: 10.2147/NDT.S111818. eCollection 2016.

  9. Millan, Gobert, Rivet, Adhumeau-Auclair, Cussac, Newman-Tancredi, Dekeyne, Nicolas, Lejeune (2000): Mirtazapine enhances frontocortical dopaminergic and corticolimbic adrenergic, but not serotonergic, transmission by blockade of α2-adrenergic and serotonin2C receptors: a comparison with citalopram; DOI: 10.1046/j.1460-9568.2000.00982.x

  10. Millan, Gobert, Rivet, Adhumeau-Auclair, Cussac, Newman-Tancredi, Dekeyne, Nicolas, Lejeune (2000): Mirtazapine enhances frontocortical dopaminergic and corticolimbic adrenergic, but not serotonergic, transmission by blockade of α2-adrenergic and serotonin2C receptors: a comparison with citalopram; First published: March 2000 DOI: 10.1046/j.1460-9568.2000.00982.x

  11. Millan, Gobert, Rivet, Adhumeau-Auclair, Cussac, Newman-Tancredi, Dekeyne, Nicolas, Lejeune (2000): Mirtazapine enhances frontocortical dopaminergic and corticolimbic adrenergic, but not serotonergic, transmission by blockade of α2-adrenergic and serotonin2C receptors: a comparison with citalopram; March 2000 DOI: 10.1046/j.1460-9568.2000.00982.x

  12. Schmotz (2013): Kombinationstherapie mit Escitalopram und Quetiapin versus Monotherapie mit Escitalopram: Eine vergleichende Studie zur pharmakologischen antidepressiven Therapie unter besonderer Betrachtung der Wirkung auf die Hypothalamus-Hypophysen-Nebennierenrinden-Achse. Dissertation. S. 78

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