Desipramine for ADHD
Desipramine is a metabolite of imipramine
Trade names: Pertofran, Petylyl
Desipramine is no longer available in Switzerland.1
1. Mechanism of action of desipramine:
- Norepinephrine reuptake inhibitor
- Serotonin reuptake inhibitor
- Dopamine reuptake inhibitor
- Alpha-Adrenerg
- Acts as a FIASMA (functional inhibitor of acid sphingomyelinase)
- Antinociceptive: suppresses the perception of pain by acting on the nociceptors
Acts as an alpha-2 adrenoreceptor agonist, thereby facilitating dopamine metabolism in the mesolimbic system (reward center).2
Serotonin and dopamine transporter binding is stronger than with imipramine, nortriptyline, protriptyline, amitriptyline, or doxepin.3
According to other opinions, the noradrenergic effect predominates.4
2. Desipramine for ADHD
A Cochrane metastudy on the effects of tricyclic antidepressants in ADHD found good ratings for desipramine in teacher ratings and physician ratings compared with placebo.5 The same was found in comparison to clonidine in comorbid Tourette’s in parent ratings.
Desipramine is recommended for comorbid tics.6
Cortisol decreases ACTH formation and thus inhibits the HPA axis through which cortisol secretion was initiated (negative feedback loop). Desipramine reverses this negative feedback into a positive one, Resipin reverses the reversal in Cushing’s disease.7
We do not consider inhibition of HPA axis shutdown to be beneficial in ADHD.
3. Desipramine side effects
Treatment discontinuations for desipramine were similar to those for placebo.5
- Weight loss
- May prolong QT time
- Micturition disorders (disorders during urination)
- Inner restlessness
- Feeling thirsty
- Sedative (weak)
- States of confusion (occasionally)
- Intestinal paralysis / intestinal obstruction (occasional)
- Urinary retention (occasional)
http://www.pharmawiki.ch/wiki/index.php?wiki=Desipramin, Stand 2016 ↥
Nurse, Russell, Taljaard (1985): Effect of chronic desipramine treatment on adrenoceptor modulation of [3H]dopamine release from rat nucleus accumbens slices.Brain Res. 1985 May 20;334(2):235-42 ↥
Zhou, Zhen, Karpowich, Goetz, Law, Reith, Wang (2007): LeuT-desipramine structure suggests how antidepressants inhibit human neurotransmitter transporters; Science. 2007 Sep 7; 317(5843): 1390–1393. doi: 10.1126/science.1147614; PMCID: PMC3711652; NIHMSID: NIHMS452952 ↥
Häßler (2009): substanzgebundene Alternativen in der Therapie von ADHS, Seite 174, in: Häßler (Hrsg) das ADHS Kaleidoskop – State of the Art und bisher nicht beachtete Aspekte von hoher Relevanz; medizinisch wissenschaftliche Verlagsgesellschaft ↥
Otasowie, Castells, Ehimare, Smith (2014): Tricyclic antidepressants for attention deficit hyperactivity disorder (ADHD) in children and adolescents. Cochrane Database Syst Rev. 2014 Sep 19;(9):CD006997. doi: 10.1002/14651858.CD006997.pub2. PMID: 25238582., METASTUDY ↥ ↥
Häßler (2009): substanzgebundene Alternativen in der Therapie von ADHS, Seite 175, in: Häßler (Hrsg) das ADHS Kaleidoskop – State of the Art und bisher nicht beachtete Aspekte von hoher Relevanz; medizinisch wissenschaftliche Verlagsgesellschaft ↥
Fehm, Voigt, Pfeiffer: Die Bedeutung des Zentralnervensystems in der Ätiologie des Morbus Cushing, in: Deutsche Gesellschaft der inneren Medizin, 86. Kongress: Gehalten zu Wiesbaden vom 13. bis 17. April 1980; Seite 62 ↥