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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 efficacy profile is therefore identical, and side effects should be somewhat less with escitalopram. Escitalopram was developed and launched after patent protection for citalopram expired.

ATTENTION:
Regarding the entire group of serotonin reuptake inhibitors, especially citalopram / escitalopram, there are concerns about their use in ADHD.
See Notes on serotonin reuptake inhibitors (SSRIs) in ADHD In the article Medications for ADHD - Overview.

1. Citalopram / Escitalopram in relation to ADHD

  • Citalopram / Escitalopram appears to enhance DAT activity,23 which could potentially be detrimental in ADHD.
    One of the main problems of ADHD is the low level of dopamine in the striatum, which is possibly caused by an excessive number of dopamine transporters, which 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 sleep problems also exist (as is often the case with ADHD), medications that increase serotonin levels are also thought to be detrimental.4.
  • Escitalopram at higher doses (20 mg) increases the cortisol response to acute stress (TSST).5
    When treating comorbid depression in ADHD, it should be kept in mind that increasing the cortisol response to stress may be beneficial in ADHD-HI sufferers (who often have a cortisol response that is too flat, which is why the HPA axis is not shut down) but may be detrimental from this standpoint in ADHD-I sufferers (who very often have an exaggerated cortisol response). See Notes on serotonin reuptake inhibitors (SSRIs) in ADHD In the article Medications in ADHD - Overview.
  • Citalopram decreases the response of the striatum to excitatory or negative stimuli.6
    The effect on the striatum could at the same time be the cause of the emotional blunting and increased indifference caused by SSRI.7
  • Escitalopram results in increased anxiety levels at 10 mg and 20 mg on the TSST.5 The HPA axis is directed by the amygdala. Increased anxiety is counterproductive in ADHD and especially in ADHD-I.
  • Citalopram causes a decrease in the activity rate of serotonergic neurons in the dorsal raphe nuclei.8
  • Citalopram increases serotonin but not dopamine and norepinephrine in the dorsal hippocampus, frontal cortex, nucleus accumbens, and striatum.9
  • Citalopram does not reduce the activity of dopaminergic neurons in the ventral tegmentum10
  • Citalopram does not cause a reduction in the activity of adrenergic neurons in the nucleus coeruleus8

Most practitioners do not make a clear distinction between the typical ADHD symptom of dysphoria* With inactivity, which is a functional stress symptom (the mood drop with inactivity aims to keep the sufferer active until the stressor is defeated) and “real” depression and therefore improperly treat ADHD sufferers as if they had real depression.
*Dysphoria here does not mean a “real” exhaustion depression, which can be a consequence 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, amounts of 3 to 5 drops a day can already be sufficient.
In our experience, a positive effect on the symptom of dysphoria is also achieved by switching treatment from methylphenidate to amphetamine medication (Elvanse), which has a weak serotonergic effect in addition to the strong dopaminergic and noradrenergic effects.

2. Degradation of escitalopram

Source: Schmotz11

Escitalopram is significantly influenced by

  • CytochromeP450 (CYP) isoenzyme CYP3A4
  • CytochromeP450 (CYP) isoenzyme 2C19
  • CytochromeP450 (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 decreased and plasma levels increased.
Escitalopram and its demethyl metabolite barely 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, like escitalopram, is excreted primarily by the kidney, with only minor excretion by the faeces.

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


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

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

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

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

  5. 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

  6. 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.

  7. 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.

  8. 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

  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; First published: March 2000 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; March 2000 DOI: 10.1046/j.1460-9568.2000.00982.x

  11. 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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