Trichotillomania Medication

Updated: Aug 05, 2019
  • Author: Dirk M Elston, MD; Chief Editor: William D James, MD  more...
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Medication Summary

Currently, no pharmacotherapy for trichotillomania is consistently effective. Current recommendations suggest that N-acetylcysteine (NAC) should be considered in all cases of trichotillomania given the moderate demonstrated efficacy and favorable adverse effect profile. [44] Selective serotonin reuptake inhibitors (SSRIs) have demonstrated a degree of effectiveness in some patients with trichotillomania and can be considered in patients with significant psychiatric comorbidities or in those in whom behavioral therapy and NAC are ineffective. [44] In children, SSRIs may be more advantageous as a medication choice than tricyclic antidepressants (TCAs) because of their milder adverse effects.



Acetylcysteine (Mucomyst, N-acetylcysteine)

N-acetylcysteine (NAC) is an antioxidant that also modulates glutamate neurotransmission, which has been linked to reward-seeking behavior. The adverse effect profile is favorable and generally includes gastrointestinal effects (nausea, vomiting, diarrhea, constipation) and altered taste perception.


Antidepressants, SSRIs

Class Summary

SSRIs are antidepressant agents that are chemically unrelated to TCAs, tetracyclic antidepressants (TeCAs), or other available antidepressants. They inhibits central nervous system (CNS) neuronal uptake of serotonin and may also have a weak effect on norepinephrine and dopamine neuronal reuptake.

SSRIs are greatly preferred to the other classes of antidepressants in this setting. Because their adverse effect profile is less prominent, compliance is improved. SSRIs do not have the cardiac arrhythmia risk associated with TCAs. Arrhythmia risk is especially pertinent in overdose, and suicide risk must always be considered in the treatment of a child or adolescent with mood disorder.

Fluoxetine (Prozac)

Fluoxetine selectively inhibits presynaptic serotonin reuptake, with minimal or no effect on reuptake of norepinephrine or dopamine. It is approved in children aged 8-18 years for major depressive disorder and in children aged 7-17 years for obsessive-compulsive disorder (OCD).

Sertraline (Zoloft)

Sertraline selectively inhibits presynaptic serotonin reuptake. It is approved for OCD in children aged 6-17 years.

Fluvoxamine (Luvox CR)

Fluvoxamine is a potent selective inhibitor of neuronal serotonin reuptake. It does not bind significantly to alpha-adrenergic, histamine, or cholinergic receptors and thus has fewer adverse effects than TCAs do. It is approved for OCD in children aged 8 years or older.

Citalopram (Celexa)

Citalopram enhances serotonin activity through selective reuptake inhibition at the neuronal membrane. It is the least activating of the SSRIs and is particularly useful in autism spectrum disorders. The incidence of adverse effects (especially sexual) is less than with other SSRIs.

Escitalopram (Lexapro)

Escitalopram is the S-enantiomer of citalopram. It may have a faster onset of depression relief (1-2 wk) compared with other antidepressants.


Antidepressants, TCAs

Class Summary

TCAs are structurally related to phenothiazine antipsychotic agents. They exhibit the following 3 major pharmacologic actions, in varying degrees: amine pump inhibition, sedation, and anticholinergic action (peripheral and central). They also inhibit reuptake of norepinephrine or serotonin at the presynaptic neuron.

Clomipramine (Anafranil)

Clomipramine inhibits reuptake of norepinephrine or serotonin at the presynaptic neuron. It is approved for OCD in children aged 10-17 years.

Imipramine (Tofranil)

Imipramine inhibits the reuptake of norepinephrine or serotonin (5-hydroxytryptamine [5-HT]) at the presynaptic neuron. Use parenteral administration for starting therapy only in patients unable or unwilling to use oral medication.

Nortriptyline (Pamelor)

Nortriptyline works by inhibiting the reuptake of serotonin and/or norepinephrine by the presynaptic neuronal membrane, thus increasing the synaptic concentration of these neurotransmitters in the CNS. Pharmacodynamic effects such as the desensitization of adenyl cyclase and down-regulation of beta-adrenergic receptors and serotonin receptors also appear to play a role in its mechanisms of action.

Desipramine (Norpramin)

Desipramine may increase the synaptic concentration of norepinephrine in the CNS by inhibiting reuptake by the presynaptic neuronal membrane. It may have effects in the desensitization of adenyl cyclase, down-regulation of beta-adrenergic receptors, and down-regulation of serotonin receptors. Extreme caution should be used when desipramine is prescribed to patients with a family history of sudden death, conduction abnormalities, or cardiac dysrhythmias. In addition, in certain patients, seizures may precede dysrhythmias and death.


Amitriptyline inhibits the reuptake of serotonin and/or norepinephrine at the presynaptic neuronal membrane, thus increasing the concentration of these neurotransmitters in the CNS.