by David R. Spiegel, MD, and Lindsey Finklea, MD

From Eastern Virginia Medical School, Department of Psychiatry and Behavioral Science, Norfolk, Virginia

Psychiatry (Edgemont) 2009;6(2):38–42

Financial Disclosures: Dr. Spiegel is on the speakers bureau of Janssen Pharmaceuticals. Dr. Finklea reports no conflicts of interest relevant to the content of this article.

Abstract

Pathological skin picking is an impulse control disorder that causes significant anxiety and disfigurement to those afflicted. Standard therapy with a selective serotonin reuptake inhibitor provides variable and often suboptimal responses. We report a case of pathological skin picking treated with paliperidone, a 5-HT2/D2 antagonist.

Key Words: pathological skin picking, impulse control disorders, neurobiology, selective serotonin reuptake inhibitors, serotonin 2/dopamine 2 receptor antagonists

Introduction

Pathological skin picking (PSP) is considered an impulse control disorder (ICD). The disorder can be found in the Diagnostic and Statistical Manual of Mental Disorder, Fourth Edition, Text Revision (DSM-IV-TR) under impulse control disorders not elsewhere cassified, along with explosive disorder, kleptomania, pyromania, pathological gambling, and trichotillomania. The characteristic finding of these disorders is an inability to resist acting on a harmful behavior that relieves a sense of tension or arousal experienced prior to the act. Regret may or may not be experienced afterward.[1]

Demographic studies provide further insight into the “picker.” The patient is usually female, in her teens to late 30s, with marked distress from her compulsion. She preferentially picks on her face (pimples and scabs) but may choose anywhere on her body. The course is chronic and often coexists with one or more comorbid psychiatric conditions, commonly obsessive compulsive disorder (OCD), substance abuse, body dysmorphic disorder, obsessive compulsive personality disorder, or borderline personality disorder. Her family will tend to demonstrate a history of psychiatric disorders.[2,3]

While there are no Food and Drug Administration (FDA)-approved medications for the treatment for ICDs, the therapeutic role of selective serotonin reuptake inhibitors (SSRIs) in ICDs has been tested in various double-blind, placebo-controlled studies for skin picking and other ICDs.[4–7] Other reported pharmacologic treatments have included olanzapine,[8] inositol,[9] lamotrigine,[10] riluzole,[11] naltrexone,[12] clomipramine,[2] and doxepin.[2] Reports of nonpharmacologic treatments include acceptance-enhanced behavior therapy,[13] internet-based support groups,[14] engaging in competitive activities,[15] habit reversal,[16,17] cognitive behavior therapy,[18,19] and contingent glove wearing.[20] We now report on a patient who had a partial response of PSP with fluoxetine (FLU) with subsequent remission of symptoms by the addition of paliperidone (PAL).

Case Report

Our patient was a 35-year-old married woman who reported the sudden onset of PSP of both lower extremities. The patient had a past psychiatric history of major depression and a remote history of sexual abuse and posttraumatic stress disorder. Her major depression was successfully treated with escitalopram. The PSP was unheralded by any psychosocial stressors and had been present for the past two months prior to our evaluation. The patient denied any history of alcohol or illicit drug abuse. She also denied any history of body dysmorphic disorder or OCD.

While she did not report any obsessive symptomology driving the PSP, she did report a sense of “enjoyment” from this behavior despite acknowledging its unsightly consequences and, as a result, avoided going to as many public places as possible. The patient scored a 19 out of a maximal score of 24 on the Skin Picking Scale (SPS).[21]

The SPS is a valid and reliable self-report scale for the assessment of severity in patients who endorse skin picking. Sensitivity and specificity analyses indicate that a total scale score of 7 optimally differentiates severe self-injurious from nonself-injurious skin pickers. Each scale item is rated from 0 (none) to 4 (extreme).

Our patient’s initial score was determined as follows: frequency of urges=3; intensity of urges=3; time spent on picking=4; interference due to skin picking=3; distress=4; and avoidance=2.

The patient was started on (FLU) at an initial dose of 20mg, orally, every morning, titrated to 80mg, orally, every morning, after one month. The patient was evaluated approximately six weeks after initiating FLU therapy. Her score on the SPS was 14; however, she had only been on FLU 80mg per day for a total of 10 days. Nonetheless, with the patient still complaining of significant distress, we initiated PAL 3mg, orally, every morning. Approximately two months after flu was augmented with pal therapy, the patient’s SPS score was an 8. PAL was increased at this time to 6mg/day, and subsequently, two months later, she reported the amelioration of PSP with an SPS score of 2.

The only major side effect the patient reported was symptoms of increased irritability, which the authors felt were due to FLU, as this began prior to starting PAL. The patient agreed to continue FLU 80mg per day, despite the irritability. The patient has been on this medical regimen (FLU 80mg/day and PAL 6mg/day) for approximately nine months and continues to be in remission from PSP.

Discussion

It has been proposed that OCD, currently acknowledged as an anxiety disorder in the DSM-IV-TR, be reassigned as an obsessive compulsive spectrum disorder (OCSD)[24,25] and that ICDs also be considered under the OCSD model.[23,26] In support of this notion is that both conditions have related neurobiology, epidemiology, neuroimaging, familial tendency, and benefits gained from psychotherapeutic and pharmacologic approaches.[2,3,22–24] Phenomenological similarities may include the lack of ability to control the will, some degree of resistance, the repetitive pattern of the behavior, and the fact that both can coexist in the same person. Statistically significant differences between the groups include the ability or inability to delay an impulse, quick response or action planning, feelings of pleasure or guilt during or after an act, ritualization, and whether the patient believes he or she has losses or benefits if prevented from acting.[27]

The therapeutic role of SSRIs in OCD, ICD, and OCSD would seem to strengthen the relation between these three entities. However, a study by Simeon found improvement in skin picking on therapeutic dosages of SSRIs without concurrent improvement in obsessive compulsive symptoms in the same patient.[28] Also in a case report by Denys, two patients with OCD were provoked to engage in skin-picking behavior following treatment with an SSRI.[29] Although many successes have been reported with SSRIs, its failures, incomplete resolution of symptoms, and worsened behaviors have prompted continued need for other pharmacological options.29,30 The use of SSRIs in combination with dopamine antagonists for refractory OCD support the use of a multidrug approach to treating the behavior.[31]

Although researchers have yet to reliably identify the circuitry and neurotransmitters involved in ICDs, response to pharmacology, brain imaging, and animal models have provided theoretic value. Insight into PSP and other ICDs can also be gleaned by evaluating what is already known about impulse control dysregulation as it pertains to OCD. Functional imaging studies have shown metabolic and hemodynamic differences in the thalamus, caudate, and the orbitofrontal cortex of patients with OCD compared to their healthy counterparts.[32] Within these brain areas, monoamines, specifically dopamine and serotonin, are thought to signal in a hyperexcitatory, reverberating pathway known as the corticostriatothalamic circuit.[33] At the ventral lateral caudate nucleus portion of this pathway, serotonin receptors are found in increased concentrations. Studies also support the importance of dopamine, particularly in the region of the caudate nucleus as it is purported to control behavioral programs, including stereotypal and repetitive behaviors.[34]

A possible mechanism underlying impulsive behavior is that different subloops of the topographically organized cortico-basal ganglia network are specialized for reward prediction at different time scales and that they are differentially activated by the ascending serotonergic system. The anatomy of the cortico-basal ganglia loops contains four major segregated yet integrated circuits, i.e., limbic, cognitive, motor, and oculomotor.[35] The areas within the limbic loop, namely the lateral orbitofrontal cortex (OFC) and ventral striatum, are involved in immediate reward prediction. On the other hand, areas within the cognitive and motor loops, including the dorsal lateral prefrontal cortex (DLPFC) and dorsal striatum, are involved in future reward prediction.[36]

It has been proposed that impulsive choices are under the control of both the dorsal and ventral striatum,[35] which are differentially modulated by the central serotonergic system. Tanaka et al[37] further report that under a hyposerotonergic state, the ventral part of the striatum is preferentially activated, which results in choosing behavior of immediate reward, i.e. consistent with impulsivity. Additionally, the dorsal part of the striatum is preferentially activated when future rewards are taken into consideration, i.e., less impulsive behavior. Therefore, from a neurobiological perspective, increasing serotonergic transmission, such as administration of SSRIs, results in less impulsivity.[37]

While our patient did have attenuation of her symptoms on flu, she was still in enough distress that we felt augmentation with pal was warranted. We propose a potential neurobiological explanation as to why pal may have offered a more robust response in our patient. First, multiple studies have demonstrated reciprocal interactions between serotonin and dopamine systems of the brain.[38] Thus, if our premise of a hyposerotonergic state underlies impulsivity, then we posit that a hyperdopaminergic state would be the consequence of hyposerotonergia. Dopamine antagonism, which does occur with treatment of the 5HT-2/D2 antagonist pal, could be efficacious in this context. Beyond this indirect evidence, Robbins reports that infusion of dopamine agonists results in impulsive responses. He further reports that depletion of dopamine in the ventral striatum reduces impulsive responding produced by dopamine agonists. Again, this potentially could occur with pal treatment.[39]

Conclusion

Using both the OCD model and the ICD studies, it is clear that pharmacotherapy directed at both serotonin and dopamine is potentially needed to maximize response in the PSP patient. Our patient initially showed a minimal response on monotherapy with an SSRI. PAL, a metabolite of risperidone, is FDA-approved for the treatment of schizophrenia. It is antagonistic to centrally located dopamine (D2) and serotonin (5HT2A) receptors. After four months on a combination of pal and FLU, our patient showed nearly complete resolution of symptoms. To our knowledge this is the first reported use of pal for PSP. We propose that hyperdopaminergia at the caudate nucleus is treated by the D2 receptor antagonism of pal, thereby resulting in a decreased in the stereotypal PSP. Further functional imaging studies may help to further elucidate the pathophysiology and potential treatments of PSP.

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