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Quetiapine for ADHD


Quetiapine for ADHD

Quetiapine is an atypical antipsychotic.1
It also has an antidepressant effect.2
Quetiapine has addictive potential and is increasingly being abused.3

In lower doses, it is used as a sleeping pill. The relatively short plasma half-life of 2.5 to 5 hours4 is favorable for this.

1. Quetiapine is an antagonist of

  • Serotonin receptor 5-HT2A2
    • Thereby increasing the dopamine level in the PFC
  • Serotonin receptor 5-HT2C via the metabolite norquetiapine2
    • Receptor binding in the PFC of 72 % after 2 hours at 450 mg4
    • Receptor binding of 50 % after 26 hours at 450 mg4
  • Dopamine receptor D2
    • Leads to antipsychotic effect
    • Receptor binding in the striatum of 44 % after 2 hours at 450 mg4
    • Receptor binding after 26 hours as in untreated healthy individuals at 450 mg4
    • The D2 antagonism of quetiapine is therefore weaker than the 5HT antagonism.5
    • Relatively low affinity for dopamine D2 receptors, with an occupancy half-life of 10 hours, which was around twice as long as that of plasma4
  • Σ-Adrenoceptor (especially A2)2
    • Thereby increasing the dopamine level in the PFC
  • Noradrenaline transporter NAT via the metabolite norquetiapine2
    • Resulting in increased noradrenaline levels
  • Histamine receptor H1
  • Glutamate NMDA
    • Quetiapine reduces the mRNA levels for some subunits of the glutamate NMDA receptor NR-1 and NR-2.2
    • Reduction in the density of NMDA receptors in the caudate nucleus (putamen) (but not in the cortex or limbic system), as well as clozapine or haloperidol2

2. Quetiapine is an agonist of

  • Serotonin receptor 5-HT1A (partial)2
    • Thereby increasing the dopamine level in the PFC
  • Glutamate-AMPA
    • Increase in the density of glutamate AMPA receptors in the caudate nucleus (putamen) (but not in the cortex or limbic system), as well as clozapine or haloperidol 2
    • Quetiapine caused a significant increase in the GluR-B and GluR-C subunits of the AMPA receptor in the hippocampus of rats.2
  • Sigma-1 receptors
    • Conveys antidepressant effect6
      • Can be additionally increased by σ1-agonists (+)-pentazocine
      • Can be reduced by σ1 antagonists BD1063

The indirect inhibition of the 5-HT2C receptors causes an inhibition of GABA release in the brain stem, which in turn causes a release of noradrenaline and dopamine in the PFC.2

According to this understanding, GABA is underrepresented in ADHD-I and overrepresented in ADHD-HI. Against this background, quetiapine would hypothetically be more useful in ADHD-HI and less recommended in ADHD-I,

3. Use of quetiapine

Quetiapine is mainly used for schizophrenia and bipolar disorder (manic-depressive).
So far, primary use has tended to be in relation to (massive) comorbidities, not in relation to ADHD itself.

A study on the treatment of ODD by administering quetiapine (= augmentation) in addition to an SSRI did not find any significant improvement in the effect.7

In ADHD, quetiapine is used off-label in low doses for the frequent sleep problems. Due to its short half-life, it can be used for this purpose despite the (albeit relatively weak) D2 antagonism.8 Nevertheless, qetiapine at 450 mg showed a receptor occupancy of 44 % of the dopamine D2 receptors in the striatum within 2 hours, which only fell back to the level of untreated healthy volunteers after 26 hours.4 As a sleeping pill, however, the dosage is much lower at between 12.5 and 100 mg.
In view of the potential for addiction and abuse of quetiapine, it should be used with great caution.3

  1. Edel, Vollmoeller (2006): Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung bei Erwachsenen, Seite 45

  2. Prieto, Micó, Meana, Majadas (2010): Neurobiological bases of quetiapine antidepresant effect in the bipolar disorder. Actas Esp Psiquiatr. 2010 Jan-Feb;38(1):22-32.

  3. Vento AE, Kotzalidis GD, Cacciotti M, Papanti GD, Orsolini L, Rapinesi C, Savoja V, Calabrò G, Del Casale A, Piacentino D, Caloro M, Girardi P, Schifano F (2020): Quetiapine Abuse Fourteen Years Later: Where Are We Now? A Systematic Review. Subst Use Misuse. 2020;55(2):304-313. doi: 10.1080/10826084.2019.1668013. PMID: 31573374.

  4. Gefvert, Bergström, Långström, Lundberg, Lindström, Yates (1998): Time course of central nervous dopamine-D2 and 5-HT2 receptor blockade and plasma drug concentrations after discontinuation of quetiapine (Seroquel) in patients with schizophrenia. Psychopharmacology (Berl). 1998 Jan;135(2):119-26. doi: 10.1007/s002130050492. PMID: 9497016.

  5. Guzman (2019): Mechanism of Action of Quetiapine. Psychopharmacology Institute

  6. Weber, Wünsch (2017): Sigma-Rezeptor – Das unbekannte Target; Pharmazeutische Zeitung, Ausgabe 05/2017, 30.01.2017

  7. Kordon, Wahl, Koch, Zurowski, Anlauf, Vielhaber, Kahl, Broocks, Voderholzer, Hohagen (2008): Quetiapine addition to serotonin reuptake inhibitors in patients with severe obsessive-compulsive disorder: a double-blind, randomized, placebo-controlled study. J Clin Psychopharmacol. 2008 Oct;28(5):550-4. doi: 10.1097/JCP.0b013e318185e735.

  8. Kölle (2021): Schlaf und ADHS, Vortrag auf dem ADHS-Symposium des ADHS Deutschland e.V.

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