Pathologic skin picking (PSP) is characterized by repetitive and compulsive picking of skin which causes tissue damage. Although there have been no population-wide epidemiological studies of PSP, it has an estimated prevalence rates of 2.0%–5.4% in the general population (1–2). Individuals with PSP report that picking behavior causes scarring and infections, impairment in daily functioning, and significant distress stemming from their inability to control the behavior (3–6).
Treatment research for PSP is sparse. There has been only one randomized controlled study of psychotherapy for PSP (habit reversal compared to wait list) (7), and only two placebo-controlled, double-blind pharmacotherapy studies published to date (8–9). In the first pharmacotherapy study, 20 subjects were randomized to either fluoxetine or placebo for 10 weeks (n=10 per treatment arm). Fluoxetine demonstrated significant reduction in PSP symptoms on only one of three measures used to rate improvement (a self-report visual analog scale assessing change in skin-picking behavior with a Cohen’s d effect size of 1.31) (8). The lack of significant active treatment benefits across other outcome measures may have been due to actual non-significance from the medication or possible due to type II error and limited statistical power. The other study consisted of 45 subjects treated with citalopram 20mg/day for 4 weeks (n=23 in citalopram group; n=22 in placebo group). In that study, citalopram failed to produce a greater benefit than placebo on the primary outcome measure although a secondary measure of quality of life found some additional improvement for medication (9).
Because data on the treatment response of PSP to pharmacotherapy are limited, the primary aim of the proposed study was to evaluate the efficacy and safety of lamotrigine in PSP. The rationale for the use of lamotrigine was twofold: first, glutamatergic dysfunction has been implicated in the pathophysiology of obsessive compulsive disorder (OCD) (10–11), a disorder with some phenomenological and possible neurobiological links to PSP (for example, both PSP and OCD have similar ages of onset, individuals with both disorders spend excessive amount of time engaged in behaviors that are intended to reduce tension or anxiety, rates of co-occurring OCD are elevated in PSP samples and vice versa, and PSP is more common in first-degree relatives on OCD patients compared to controls (12–13)); and second, clinical reports supported possible efficacy of glutamatergic modulators in the treatment of both impulse control and obsessive compulsive disorders (14–16). Lamotrigine is thought to act via inactivation of voltage-sensitive Na+ and possibly Ca2+ channels, leading to suppression of abnormally increased neuronal firing and thus inhibiting excessive release of glutamate (17–18).
Because lamotrigine may target medial prefrontal glutamatergic drive to the nucleus accumbens (19), it may correct the underlying pathophysiology and symptoms of PSP. In fact, an earlier open-label study of lamotrigine in 24 subjects with PSP found that 67% had significant improvement in picking symptoms after 12 weeks of treatment (20). Therefore, our hypothesis was that lamotrigine would be more effective than placebo in treating individuals with PSP. The secondary aim of this study was to evaluate whether treatment responders and non-responders differed in terms of baseline cognitive flexibility and inhibitory control. Because cognitive flexibility appears dependent upon prefrontal cortical integrity (21), and because lamotrigine should modulate prefrontal glutamate functioning, we hypothesized that PSP subjects with impaired cognitive flexibility at baseline would respond preferentially to treatment in this study.