After watching for seasonal patterns, I found that Ms. D’s hair-pulling worsened during the winter, although no seasonal change in mood was detected. Phototherapy produced initial success, but Ms. D continued to pull her eyelashes.
Eight weeks later, however, Ms. D’s symptoms escalated. Clomipramine was increased to 150 mg nightly, resulting in blood levels of 99 ng/mL for clomipramine and 204 ng/mL for the metabolite N-desmethylclomipramine—both within the therapeutic range. As she continued pulling, I added buspirone, 10 mg/d.
At this point, would you:
- continue clomipramine and increase the dosage?
- discontinue clomipramine and start another psychotropic?
- or maintain clomipramine at the same dosage and add another psychotropic?
Dr. Lundt’s observations
Drug treatment of trichotillomania has not been studied extensively or long-term, and no consensus exists. Psychoanalysis, cognitive-behavioral therapy (CBT), and hypnotherapy are usually administered with psychotropics.8 Patients often respond to treatment at first, then reach a plateau and resume pulling their hair.9
Numerous psychotropics are used off-label to treat trichotillomania. Several agents have been shown in clinical trials and case reports to reduce hair pulling/eating behaviors (Table), but these findings are limited by small sample size, lack of control groups, and lack of a standard symptom rating scale.
Figure Trichotillomania: Excessive grooming, habit, or vicious circle?
Most clinicians begin with SSRIs because they are generally well tolerated, even at high dosages. Monotherapy often is not adequate for trichotillomania, however. Medication augmentation is common, although little empiric data support this practice.
When clomipramine did not work initally, I explored serotonergic combination strategies.
Table
Medications shown to benefit patients with trichotillomania
| Drug | Evidence | Dosage range (mg/d) | Potential side effects |
|---|---|---|---|
| First-line | |||
| Tricyclic | |||
| Clomipramine | Swedo et al10 | 50 to 300 | Sedation, weight gain, cardiac arrythmias |
| SSRIs | |||
| Fluoxetine | van Minnen et al11 | 20 to 60 | GI symptoms, insomnia |
| Fluvoxamine | Gabriel12 | 50 to 250 | Sexual dysfunction, weight gain |
| Paroxetine | Ravindran et al13 | 20 to 60 | Sexual dysfunction, weight gain |
| Sertraline | Bradford and Gratzer14 | 50 to 200 | Sexual dysfunction, GI symptoms, insomnia |
| Second-line | |||
| Antipsychotics | |||
| Haloperidol | Van Ameringen et al15 | 0.25 to 2 | Sedation, EPS |
| Olanzapine | Gupta and Gupta16 | 2.5 to 10 | Sedation, weight gain |
| Pimozide | Stein and Hollander17 | 25 to 200 | Restlessness, EPS |
| Quetiapine | Khouzam et al8 | 25 to 200 | Sedation |
| Risperidone | Gabriel12 Senturk and Tanriverdi18 | 0.5 to 4.0 | Sedation, hyperprolactinemia |
| Mood stabilizer | |||
| Lithium | Christenson et al19 | 900 to 1,500 | Increased thirst, weight gain, tremor |
| EPS: extrapyramidal symptoms | |||
Further treatment: Relapse, resection
Ms. D was lost to follow-up for 1 year. She returned in 1996, just after undergoing a laparotomy for removal of a trichobezoar large enough to fill two 2-inch-by-6-inch bags. She also had been treated for pneumonia and a pulmonary embolus.
Riddled with shame and embarrassment, Ms. D had stopped pulling for 10 months, during which time she was off medication. Her pulling behaviors re-emerged, however, and clomipramine was restarted and titrated to 250 mg nightly.
One year later, a second trichobezoar was resected. Her clomipramine/N-desmethylclomipramine level reached 1,535 ng/mL, although an ECG reading was normal. Subsequent clomipramine/N-desmethylclomipramine blood levels were within the therapeutic range. Fluvoxamine, 25 mg/d titrated across 6 weeks to 150 mg/d, was added.
Again, Ms. D stopped taking her medications and was lost to follow-up. Her gastroenterologist began managing her care and started sertraline, dosage unknown, to address her depressed mood. A third trichobezoar was removed.
When Ms. D returned to my practice, I resumed CBT and increased sertraline over 1 month from 100 to 300 mg/d. Adding olanzapine, 2.5 mg/d, diminished her anxiety and markedly decreased her hair pulling.
Months later, her hair-pulling/eating behaviors again intensified, resulting in a small-bowel obstruction and a fourth trichobezoar removal. Olanzapine was increased to 5 mg nightly without significant benefit and with sedating effects.
Clomipramine, 125 mg/d, was reintroduced and her symptoms improved dramatically. On a regimen of sertraline, clomipramine and olanzapine, Ms. D remained stable for 2 years.
Last year, however, a fifth trichobezoar measuring 20 x 15 cm was removed. Subsequent trials of methylphenidate, titrated to 72 mg every morning, and tramadol, titrated to 100 mg/d, were unsuccessful.
After 10 years of medication and psychotherapy with three different providers, Ms. D’s hair-pulling/eating behaviors persist. She is taking ziprasidone, 120 mg bid, and naltrexone, 100 mg bid, to help her impulse control, as well as sertraline, 300 mg/d, and clomipramine, 125 mg/d. Another trichobezoar removal—her sixth in 8 years—is scheduled.
What strategies exist for minimizing Ms. D’s hair-pulling behavior and keeping her in therapy?
Dr. Lundt’s observations
Trichotillomania’s waxing and waning course—and its destructive effects on a patient’s self-esteem—pose a clinical challenge. The disorder’s severity can range from cosmetically annoying to life-threatening, as in Ms. D’s case. Patients embarrassed by their behavior often prematurely leave treatment, desperate to cut off all social contact—including medical appointments.
It is crucial to maintain a nonjudgmental, inviting demeanor to alleviate the patient’s fears and facilitate a return to treatment. Support groups, especially online, can help decrease patients’ isolation and provide a reliable information network (see Related resources).