Version May 2024
INTRODUCTION — Skin picking disorder (SPD) is characterized by deliberate and repetitive manipulation of the skin, causing tissue damage. Excoriation disorder, psychogenic excoriation, neurodermatitis, neurotic excoriation, acne excoriée, and dermatillomania (dermatotillomania) are in the spectrum of SPD and may be considered synonyms.
This topic will discuss the clinical manifestations, diagnosis, and treatment of SPD and related conditions. Obsessive-compulsive disorder and body dysmorphic disorder are discussed separately.
●(See "Obsessive-compulsive disorder in adults: Epidemiology, clinical features, and diagnosis".)
●(See "Body dysmorphic disorder: Clinical features".)
●(See "Body dysmorphic disorder: Assessment, diagnosis, and differential diagnosis".)
DEFINITION AND CLASSIFICATION — SPD is defined as the repetitive picking, scratching, rubbing, digging, or squeezing of skin, resulting in visible tissue damage and impairment in social functioning [1]. In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), SPD is included as a separate diagnosis in the group of the obsessive-compulsive and related disorders, along with trichotillomania and body dysmorphic disorder [2].
EPIDEMIOLOGY
●Prevalence – The exact prevalence of SPD in the general population is unknown. In a survey of over 10,000 participants aged 18 to 69 years representative of the United States population, the prevalence of SPD was 2 percent [3]. SPD accounts for approximately 2 percent of all visits to the dermatology clinic [4,5]. In a telephone survey, 1.6 percent of a random sample of 2511 adults residing in the United States reported skin picking with noticeable skin damage [6]. These individuals also reported distress and psychosocial impact associated with skin picking. In another United States population-based study, 5.4 percent of 354 participants reported SPD and associated impairment in daily functioning [7]. In a web-based, anonymous survey including over 7600 participants, the prevalence of SPD was 3.4 percent (95% CI 3.0-3.8 percent) [8].
In three samples of college students, the rates of severe, self-injurious skin picking ranged from 3.8 to 4.6 percent [9-11]. SPD was associated with high lifetime rates of affective disorders, anxiety disorders, eating disorders, substance abuse, and impulse control disorders and was usually triggered by cutaneous stimuli or specific emotional situations. In a large sample of over 4000 college students, nearly 60 percent of participants reported engaging occasionally in body-focused repetitive behaviors (BFRBs), including skin picking, hair pulling, and nail biting, while 12 percent met the criteria for pathologic BFRB [12].
●Sex predominance – SPD is most common in females, with a female-to-male ratio of approximately 8:1 [6-8,13-15].
●Age of onset – The age of onset of SPD spans between 15 and 45 years, with a peak noted in the early twenties [10]. In a study of 700 patients with SPD, latent profile analysis identified a large group (93 percent) with onset in adolescence at a mean age of 14 years and a small group (7 percent) with onset in middle adulthood (mean age 43 years) [16]. The duration of illness ranges from 5 to 21 years [9,10]. Childhood onset may progress into adulthood in up to 47 percent of cases [10]. Individuals with childhood-onset disease share similar characteristics with those with late-onset disease [1]. However, childhood onset is associated with longer disease duration and less motivation for treatment [17].
PATHOGENESIS — The pathogenesis of SPD is unknown. Research is focused on identifying the neural circuitry involved in the pathophysiology of SPD and other obsessive-compulsive disorders by using neuroimaging techniques. A functional magnetic resonance imaging (fMRI) study found abnormal activation of brain areas involved in habit formation, action monitoring, and inhibition [18]. Another study using diffuser tensor imaging found that SPD was associated with bilateral disorganization or damage of white matter tracts in the anterior cingulate cortex [19]. Another fMRI study found that SPD patients had decreased gray matter volumes in left cerebellar lobules V (motor) and VI (affective-cognitive) compared with controls. This may indicate a structural pathogenesis in SPD. When performing picking activities, affected patients had more activation of the left crus I and enhanced coupling with the left ventrolateral prefrontal cortex. This may suggest that SPD is a maladaptive response to an emotional trigger [20]. fMRI with visual symptom provocation found higher activity levels in the insula and amygdala, which correlated with emotional distress (ie, disgust and self-loathing) [21]. Furthermore, there appears to be differences in the insular cortex and parietal and occipital regions associated with motor impulsivity in SPD [22].
COMORBID CONDITIONS — Multiple psychiatric comorbidities are associated with SPD. These include major psychiatric disorders as well as related disorders, such as trichotillomania and onychophagia. In several studies, the following conditions were associated with SPD, with higher prevalences reported among patients attending psychiatric outpatient facilities [8,13,23-26]:
●Depression
●Bipolar disorder
●Obsessive-compulsive disorder
●Alcohol abuse/dependence
●Substance abuse/dependence
●Body dysmorphic disorder
●Trichotillomania
●Onychophagia
●Kleptomania
●Bulimia nervosa
Skin picking is a characteristic common feature of Prader-Willi syndrome, a complex neurodevelopmental disorder caused by an abnormality on the long arm of chromosome 15 (q11-q13) and characterized by obesity, excessive interest in food, skin picking, and obsessive and compulsive behaviors. (See "Prader-Willi syndrome: Management".)
Self-mutilation and skin picking can also be seen in patients with Lesch-Nyhan syndrome, autistic spectrum disorders, schizophrenia, intellectual disability and developmental delay, Smith-Magenis syndrome, Tourette syndrome, and chronic tic disorders. (See "Hyperkinetic movement disorders in children", section on 'Lesch-Nyhan syndrome' and "Microdeletion syndromes (chromosomes 12 to 22)", section on '17p11.2 deletion syndrome (Smith-Magenis syndrome)' and "Tourette syndrome: Pathogenesis, clinical features, and diagnosis".)
CLINICAL MANIFESTATIONS — SPD appears as excoriated, polymorphic lesions of varying size, with wide variation in extent and severity. All stages of evolution may be represented on a background of postinflammatory hypo- or hyperpigmentation [27-29]. Recently induced lesions appear as angular excoriations with a serosanguineous crust; older lesions may be crusted or appear as hypertrophic nodules or atrophic scars. The appearance also depends on the specific method of SPD. Instrumentation may be employed by the use of fingers or fingernails, teeth, scissors, tweezers, or pins, producing deeper lesions that extend into the dermis [10]. Complications of SPD include ulceration, infection, scarring, and disfigurement. Severe medical complications have also been reported [14].
Frequently targeted sites are the face (in particular the nose, forehead, cheeks, and chin), the scalp, cuticles, extensor aspects of the extremities, shoulders, back, perianal region, and the scrotal area [10]. Lesions are usually symmetrically distributed within reach of the hands (picture 1A-G).
Patients with SPD will usually acknowledge an urge to pick and gouge at their skin. Although there may be an initial reluctance to disclose self-damage, patients are generally willing to discuss the need to pick as a response to itch to relieve tension.
Patients may begin with the urge to manipulate a trivial skin lesion, such as an arthropod bite, acne lesion, scab, inflammatory lesion, wart, mole, or keratin plug [10,29-31]. Others may manipulate perfectly normal skin or pick the skin as a response to a cutaneous sensation of pruritus, burning, or pain [32].
An SPD episode typically lasts 6 to 10 minutes; however, it is not uncommon for patients to dedicate hours to the process on a daily basis [10,23]. Activity peaks in the evening between the hours of 8:00 PM and 12:00 AM [9,10]. Situations correlated with SPD activity include looking in a mirror, speaking on the telephone, lying in bed, reading, watching television, waiting, and bathing [10].
Patients may give various explanations for their SPD. They may report anxiety or emotional distress until they are able to pick their skin, which relieves these feelings [10,33]. There are also a proportion of patients who report an attempt to improve the appearance of their skin, those that report that it is simply a common habit, and others who find the actions pleasurable [10].
PATIENT EVALUATION AND DIAGNOSIS
Clinical interview — Medical, psychiatric, and skin picking-related history should be elicited from patients with SPD [34]. Taking ample time to interview the patient is useful to assess the individual's current clinical manifestations, the associated impairment and distress, and any underlying psychiatric disorder(s) [34].
Some patients may spontaneously report a concomitant psychiatric illness at presentation. Others may be reluctant to reveal their diagnosis or do not have a previous diagnosis. In these cases, psychiatric referral should be strongly considered, although many patients will not readily accept referral.
Physical examination — Physical examination should include a thorough dermatologic evaluation to assess the severity of excoriation, the presence of complications (scarring, infections), or coexistent primary skin disorders associated with chronic pruritus, including atopic dermatitis, psoriasis, scabies, prurigo nodularis, or bullous pemphigoid. (See 'Differential diagnosis' below and 'Primary skin disorders' below.)
If a medical or organic cause is suspected to be the underlying etiology of chronic pruritus and skin picking, appropriate work-up should be instituted to rule out organ dysfunction, nutritional deficiencies, or malignancies. (See "Pruritus: Etiology and patient evaluation".)
Diagnostic criteria — The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic criteria for SPD are as follows [2]:
●Recurrent skin picking resulting in skin lesions.
●Repeated attempts to decrease or stop skin picking.
●The skin picking causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
●The skin picking is not attributable to the physiologic effect of a substance (eg, cocaine) or another medical condition (eg, scabies).
●The skin picking is not better explained by symptoms of another mental disorder (eg, delusions or tactile hallucinations in a psychotic disorder, attempts to improve a perceived defect or flaw in appearance in body dysmorphic disorder, stereotypes in stereotypic movement disorder, or intention to harm oneself in nonsuicidal self-injury).
Severity assessment tools — Disease severity and behavioral styles can be assessed by using several validated instruments, including:
●Skin Picking Severity Scale (SPS) [35,36]
●Skin Picking Severity Scale-Revised (SPS-R) [36]
●Milwaukee Inventory for the Dimensions of Adult Skin Picking (MIDAS) [37]
DIFFERENTIAL DIAGNOSIS — SPD should be differentiated from excoriations seen in patients with primary pruritic skin disorders or in patients with systemic conditions associated with chronic pruritus. (See "Pruritus: Etiology and patient evaluation".)
Other psychocutaneous syndromes associated with self-injurious behavior, including dermatitis artefacta, delusional infestation (also called delusional parasitosis), and body dysmorphic disorder, should be differentiated from primary SPD. (See "Delusional infestation: Epidemiology, clinical presentation, assessment, and diagnosis" and "Body dysmorphic disorder: Clinical features".)
Primary skin disorders — Patients with pruritic skin diseases may present with psychiatric disorders, most often depression or anxiety disorders, which are secondary to the skin disease. Preoccupation with poor quality of life, decreased self-esteem and self-confidence, experience of rejection, and feelings of shame or guilt may be present in patients with chronic skin conditions [9,38]. The skin disease may affect interpersonal relationships and interactions and lead to social avoidance [9,38]. In addition, the itch-scratch cycle in these patients can be triggered or exacerbated by stressors, such as psychologic stress or environmental changes [39].
Primary pruritic dermatoses include:
●Atopic dermatitis – Atopic dermatitis is characterized by thickened skin, increased skin markings (lichenification), and excoriated and fibrotic papules (picture 2A-B). The diagnosis of atopic dermatitis is supported by a history or visible evidence of itchy dermatitis involving the flexural surfaces (picture 3), a history of symptoms beginning in infancy or childhood, and the presence of generally dry skin within the past year. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)
●Psoriasis – Psoriasis is often associated with pruritus. It is not restricted to the area of the psoriatic plaque, often being generalized and poorly responsive to antipruritics. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis".)
●Scabies – Scabies is caused by the mite Sarcoptes scabiei, which lays its eggs in the epidermal layer of human skin. The outstanding clinical feature of scabies is intense itching. It is often severe and usually worse in the evening and night. Lesions may appear as small, erythematous papules or nodules, often excoriated with hemorrhagic crust (picture 4). (See "Scabies: Epidemiology, clinical features, and diagnosis", section on 'Clinical manifestations' and "Scabies: Epidemiology, clinical features, and diagnosis", section on 'Differential diagnosis'.)
●Bullous pemphigoid – Bullous pemphigoid is an autoimmune subepidermal blistering disease occurring most frequently in older adult individuals. Bullous pemphigoid may present in a subgroup of patients with pruritus and an eruption similar to prurigo nodularis (pemphigoid nodularis) (picture 5) [40]. A skin biopsy for histologic examination and direct immunofluorescence and the measurement of circulating autoantibodies against bullous pemphigoid antigens confirm the diagnosis. (See "Clinical features and diagnosis of bullous pemphigoid and mucous membrane pemphigoid".)
●Trigeminal trophic syndrome – Trigeminal trophic syndrome happens as the result of trigeminal nerve or sensory nuclei damage. Altered sensation, most commonly around the nose and nasal alar areas, leads to repetitive, self-induced trauma causing ulceration and disfigurement (picture 6). It less commonly affects other areas on the head or neck. (See "Overview of craniofacial pain", section on 'Trigeminal trophic syndrome'.)
●Prurigo nodularis/chronic prurigo – Prurigo nodularis is a chronic skin disorder of unclear pathogenesis characterized by multiple firm, itchy nodules typically localized to the extensor surface of the extremities (picture 7A-B) [41]. Pruritus is always severe and distressing. Underlying causes of chronic pruritus and repetitive scratching may include atopic dermatitis (in nearly half of the patients), other dermatologic conditions, systemic disease, emotional stress, or psychiatric disorder (eg, anxiety, depression). (See "Prurigo nodularis".)
●Midface toddler excoriation syndrome – Midface toddler excoriation syndrome (MiTES) is a rare disorder caused by congenital insensitivity to pain presenting in young children with self-inflicted, severe, midfacial excoriations and scarring [42-44]. MiTES is associated with biallelic mutations in PRDM12, encoding a member of a family of transcriptional regulators involved in the development of sensory neurons into nociceptors [42].
Systemic diseases associated with chronic pruritus — Several systemic conditions may be associated with intense and persistent pruritus in the absence of primary skin disease [45]. (See "Pruritus: Etiology and patient evaluation", section on 'Systemic disorders'.)
Secondary skin changes, including nodular lesions similar to prurigo nodularis, eczematization, excoriation, and lichenification, can be observed in patients with:
●Uremia
●Cholestasis and primary biliary cholangitis
●Polycythemia vera
●Lymphoma
●Solid organ tumors
●Hyperthyroidism
●Iron deficiency
●HIV infection
●Advanced age
●Drug or alcohol dependence/abuse
Other psychocutaneous syndromes — Other psychocutaneous syndromes that should be differentiated from SPD include dermatitis artefacta, delusional infestation, and body dysmorphic disorders [46]:
●Dermatitis artefacta – Dermatitis artefacta is a psychocutaneous disorder in which patients intentionally induce skin lesions in order to simulate disease and assume the patient role [47,48]. The lesions of dermatitis artefacta usually appear at an identical stage of development; can be single or multiple; are often geometric, unilateral, or bilateral; and are generally within reach of the hands (picture 8A-C). The lesions can be created by the use of sharp instruments or by applying or injecting chemical substances into the skin. Characteristically, patients describe the sudden appearance of complete lesions, with little or no prodrome ("hollow history"), and usually deny taking part in the process, exhibiting a "belle indifference" and lack of frustration despite the recurrent nature of their symptomatology [49,50].
●Delusional infestation – Delusional infestation is a rare disorder in which affected individuals have the fixed, false belief (delusion) that their skin is infested by parasites. No obvious skin disease may be present, but excoriations frequently result from the patient's attempt to extract the imaginary parasites. Patients often bring in specimens that they have picked from their skin for examination; these may include scales, scabs, or cloth fibers but do not include parasites. (See "Delusional infestation: Epidemiology, clinical presentation, assessment, and diagnosis".)
●Body dysmorphic disorder – Body dysmorphic disorder, or dysmorphophobia, is a disturbance of the body image manifesting as a preoccupation with an imagined or exaggerated defect in physical appearance. Skin picking is common among patients with body dysmorphic disorder. Approximately one-third of patients compulsively pick at their skin, trying to remove minor blemishes or otherwise clear or perfect their skin [51]. Patients often report multiple dermatologic consultations and express dissatisfaction with previous treatments. (See "Body dysmorphic disorder: Clinical features".)
●Factitious disorder (Munchausen syndrome) – Factitious disorder, which was previously known as Munchausen syndrome, is the falsification of disease even without an obvious reward. This can manifest in cutaneous symptoms. This is different from factitious disorder imposed on another (most commonly a child). (See "Factitious disorder imposed on self (Munchausen syndrome)".)
●Malingering – Malingering involves the falsification of illness in order to gain an external reward. (See "Factitious disorder imposed on self (Munchausen syndrome)", section on 'Malingering'.)
MANAGEMENT
General considerations — The management of SPD is notoriously difficult [52]. Treatment involves three elements [53]:
●Optimization of the patient's mental state in terms of insight, motivation, and awareness
●Pharmacologic therapies
●Nonpharmacologic therapies
Patients with SPD should be managed by clinicians who have expertise in the use of psychotropic medications as well as topical medications. This may require a multidisciplinary approach with psychiatry and dermatology or management by a specialist who has experience in both psychiatric and dermatologic disorders.
The treatment plan should be based upon a thorough discussion with the patient and should include close monitoring for both clinical efficacy and adverse effects. Standardized assessment tools for disease severity may be helpful to assess SPD severity at the beginning of treatment and monitor treatment effects over time. (See 'Severity assessment tools' above.)
Treatment of skin lesions — Complications of SPD, including skin infection or disfigurement, may require medical, surgical, or cosmetic intervention. Topical and/or systemic antibiotics may be prescribed to treat secondarily infected excoriations or ulcerations. Semiocclusive dressings may be useful to limit further skin damage and promote healing.
In patients with SPD and associated pruritus, potent topical corticosteroids (groups 1 to 3 (table 1)) or intralesional glucocorticoids, such as triamcinolone acetonide, are commonly used and appear to provide benefit. However, there are no published studies of efficacy of topical or intralesional corticosteroids for SPD, and their use is mainly based on clinical experience. We typically initiate therapy with a high-potency corticosteroid for nonfacial lesions and taper the potency of the topical steroid as response is observed.
Phototherapy with narrowband ultraviolet B (UVB) has been reported as beneficial in reducing pruritus and skin picking behaviors in a small series of patients [54]. (See "UVB phototherapy (broadband and narrowband)".)
For patients with acne excoriée, appropriate treatment of the underlying acne should be initiated, depending on acne severity and type. Laser treatment for scars has been used in case reports [55]. (See "Acne vulgaris: Overview of management" and "Management of acne scars".)
Behavioral therapies — Cognitive-behavioral therapies may be beneficial for patients accepting psychiatric referral. Data from observational studies and a few randomized trials examining nonpharmacologic therapeutic options for SPD, including cognitive-behavioral therapy, habit reversal therapy, and acceptance-enhanced behavior/acceptance and commitment therapy, have shown improvement of SPD with the interventions [52,56-59]. Preliminary data on clinician-guided self-help therapy using internet-based programs for SPD have shown promising results [60] (see "Obsessive-compulsive disorder in adults: Psychotherapy"):
●In a randomized trial, 34 college students were randomly assigned to treatment with a four-session course of cognitive-behavioral treatment or a waiting list control group [59]. Skin picking severity measures (skin picking scale, skin picking impact scale, and self-control cognition questionnaire) decreased more in the treatment group compared with the no intervention group. Treatment effects were maintained at two months after the end of treatment.
●In another trial, 25 adults were randomly assigned to a habit reversal treatment (one-hour treatment session followed by two 30-minute booster sessions over the next three weeks) or a waiting list and were followed up for three months [57]. The number of skin picking episodes decreased significantly over time in the treatment group compared with the waiting list group. Benefits were maintained at three-month follow-up.
●An internet-based self-help program of cognitive-behavioral therapy for the treatment of SPD was evaluated in a 12-week, randomized trial including 133 participants (93 percent female) [60]. Compared with the waiting list control group, participants in the intervention group showed substantial improvements in skin picking severity from baseline, as assessed by the Skin Picking Scale-Revised, and were generally satisfied with the intervention.
Pharmacologic therapies
Antidepressants — When pharmacotherapy is selected for the treatment of SPD, we suggest initial treatment with selective serotonin reuptake inhibitor (SSRI) antidepressants, which include fluoxetine, paroxetine, citalopram, escitalopram, fluvoxamine, and sertraline. SSRIs have been shown to be efficacious in the treatment of obsessive-compulsive disorder [61]. However, SSRIs for SPD have been evaluated only in a limited number of small clinical trials, some with significant dropout rates and wide confidence intervals, and their efficacy for SPD remains uncertain [62-66].
A meta-analysis of two randomized trials and three uncontrolled studies found that SPD patients on SSRIs experienced improvement over time [67]. However, the analysis limited to the two randomized trials did not show any benefit of SSRIs compared with placebo.
SSRIs should generally be started at their minimal effective dose: fluoxetine 20 mg, paroxetine 20 mg, citalopram 20 mg, escitalopram 10 mg, fluvoxamine 25 to 50 mg, and sertraline 25 to 50 mg. The dose can be increased every week or every other week, as tolerated. The clinical response to the SSRI antidepressant is gradual. Patients showing no response at six to eight weeks may be switched to another class of antidepressants.
Common SSRI side effects include sexual dysfunction, drowsiness, weight gain, insomnia, anxiety, dizziness, headache, and dry mouth. When discontinuing an SSRI, a slow taper is advised due to withdrawal symptoms, such as nausea, diaphoresis, agitation, anxiety, dizziness, and sensory problems. (See "Selective serotonin reuptake inhibitors: Pharmacology, administration, and side effects", section on 'Prescribing SSRIs' and "Selective serotonin reuptake inhibitors: Pharmacology, administration, and side effects", section on 'Side effects'.)
Antipsychotics — Atypical antipsychotics, such as olanzapine or risperidone, may be helpful in selected patients with SPD, particularly in delusional patients. (See "Treatment of delusional infestation".)
Olanzapine 2.5 to 5 mg per day and paliperidone 3 to 6 mg per day, either alone or with an antidepressant, have been shown to reduce SPD behaviors in case reports [68-70].
Glutamate-modulating drugs
N-acetylcysteine — N-acetylcysteine (an amino acid derivative that has glutamate-modulating properties) has been used alone or in combination with SSRI for the treatment of obsessive-compulsive disorders in adults and children with promising results [71-74]. (See "Management of obsessive-compulsive disorder in adults" and "Obsessive-compulsive disorder in children and adolescents: Treatment overview", section on 'Glutamate modulators'.)
Data from a few case series and single case reports suggest that N-acetylcysteine reduced the symptom severity in patients with SPD [75-77]. The efficacy of N-acetylcysteine for the treatment of SPD has been evaluated in a randomized trial in which 66 participants with SPD received N-acetylcysteine at a dose of up to 3000 mg per day or placebo for 12 weeks [78]. The main outcome measures were changes in the modified Yale-Brown Obsessive-Compulsive Scale score and in the Clinical Global Impression severity scale score. At the end of the study, participants in the N-acetylcysteine group showed a significantly greater improvement in both scores compared with participants in the placebo group. The treatment was generally well tolerated. However, given the chronic nature of SPD, further studies are needed to evaluate the long-term efficacy and safety of N-acetylcysteine for the treatment of this disorder.
Memantine — Memantine is an antagonist of the N-methyl-D-aspartate receptor that is activated by glutamate. Memantine is approved by the US Food and Drug Administration for the treatment of moderate to severe Alzheimer disease. (See "Treatment of Alzheimer disease", section on 'Memantine'.)
In a randomized trial, 100 patients with trichotillomania, SPD, or both were assigned to treatment with memantine 10 mg/day for two weeks and then 20 mg/day for six weeks or placebo [79]. The rates of psychiatric comorbidities and current use of therapeutic doses of antidepressants were similar in the two groups. The primary outcome measure was change from baseline to week 8 in total symptom score on the modified National Institute of Mental Health Trichotillomania Symptom Severity Scale (range 0 to 20). At week 8, the average National Institute of Mental Health Trichotillomania Symptom Severity Scale score decrease from baseline was -6.98 in the memantine group versus -1.19 in the placebo group. Moreover, at week 8, more participants in the memantine group achieved a Clinical Global Impressions improvement scale score of "much or very much improved" than participants in the placebo group (60.5 versus 8.3 percent, respectively). Treatment was generally well tolerated. Adverse effects occurred with similar frequency in both groups and included fatigue/drowsiness, nausea, constipation, and dizziness.
Anxiolytics — Anxiolytics may be used when the underlying cause of SPD is an anxiety disorder, although there are no specific studies of the use of anxiolytic drugs in the treatment of SPD. Lorazepam is a shorter-acting benzodiazepine that can be dosed at 0.5 to 1 mg four times daily, as needed, depending on the severity of symptoms [80]. Treatment duration should be short-term due to the risk of dependency. The most common side effect is sedation. If the anxiety disorder is chronic, buspirone at doses of 10 to 30 mg twice daily may be helpful. (See "Generalized anxiety disorder in adults: Management".)
Neuromodulation procedures — Repetitive transcranial magnetic stimulation, a neuromodulation procedure used for the treatment of unipolar depression in adults who do not respond to standard treatment, was used in a small, preliminary, randomized study including 15 patients with SPD [81]. Treatment response, as assessed by the Yale-Brown Obsessive-Compulsive Scale Modified for Neurotic Excoriation, was achieved by five of eight patients in the active treatment group versus two of six in the sham group. Relapse occurred in one to three months after completing the study. (See "Unipolar depression in adults: Overview of neuromodulation procedures", section on 'Repetitive transcranial magnetic stimulation'.)
Supplementary therapies — There are very limited data on the use of alternative treatments for SPD (eg, yoga, aerobic exercise, hypnosis, acupuncture, and biofeedback) as possible adjuncts to standard treatments in SPD [82].
RELATED DISORDERS
Trichotillomania
Definition and classification — Trichotillomania (TTM), or hair pulling disorder, is a repetitive body-focused disorder frequently associated with skin picking [83]. TTM, previously classified as an impulse control disorder, is included in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) as a separate diagnosis in the group of the obsessive-compulsive and related disorders, along with SPD and body dysmorphic disorder [2]. Whether SPD, TTM, and nail picking disorder are separate entities or different manifestations of the same disorder (pathologic grooming) remains unclear [84].
Etiology and pathogenesis — The precise etiology of TTM is unknown. A twin study suggests that genetic factors may be important [85]. There is limited evidence that abnormalities in neurotransmitter systems (eg, serotonin, dopamine, norepinephrine, glutamate) may be involved in the pathogenesis of TTM. Neuroimaging studies have found increased resting cerebral glucose metabolic rates in TTM patients compared with healthy controls and an increase in gray matter density in several brain regions involved in affect regulation, motor habits, and top-down behavioral inhibition or white matter tract abnormalities [86-88].
Epidemiology — The exact prevalence of TTM in the general population is unknown. One study found a 0.6 percent lifetime prevalence of TTM among college students [89]. Another study found a 1 percent lifetime prevalence of TTM among 17-year-old teenagers [90]. The estimated lifetime prevalence ranges between 0.6 percent and 4 percent, with the highest incidence observed in childhood. However, estimates may change due to different diagnostic criteria used.
Clinical features — Patients with TTM may present with bald spots in various body sites, including the scalp, face, arms, legs, and pubic areas. However, the scalp is the most common pulling site in both children and adults (picture 9A-B), but eyelashes and eyebrows are often involved (picture 10A-B). The scalp typically shows diffuse or bizarre-shaped patches of alopecia (picture 11) [91]. The hair shafts are typically of different length due to different points of breakage or pulling at different times (picture 9A).
Additional behaviors associated with TTM include hair biting and hair ingestion (trichophagy). The latter can lead to the rare, serious complication of trichobezoar ("hair ball"). (See "Gastric bezoars".)
Comorbidities — Among patients with TTM, there is a high prevalence of a number of conditions from different DSM-4 groups, including tic disorders, alcohol dependence, mood disorders, anxiety disorders, impulse control disorders, and bulimia nervosa. In a study of 131 individuals with lifetime TTM (median age of onset 13 years), obsessive-compulsive disorder was present in 87 percent, mood disorder in 64 percent, generalized anxiety disorder in 52 percent, and SPD in 44 percent [26].
Diagnosis — The diagnosis of TTM is based upon history, a clinic interview, and a number of diagnostic criteria defined in the DSM-5.
DSM-5 criteria — The diagnostic criteria for TTM proposed in the DSM-5 are as follows:
●Recurrent pulling out of one's hair, resulting in hair loss.
●Repeated attempts to decrease or stop hair pulling.
●The hair pulling causes significant distress and impairment in at least one important area of functioning.
●The hair pulling or hair loss is not attributable to another medical condition.
●The hair pulling is not better explained by the symptoms of another mental disorder (eg, attempts to improve a perceived defect or flaw in appearance in body dysmorphic disorder).
Disease severity can be assessed by using several validated instruments, including:
●The Massachusetts General Hospital Hairpulling Scale [92]
●The Yale-Brown Obsessive-Compulsive Scale [93]
●The Psychiatric Institute Trichotillomania Scale [94]
●The Trichotillomania Scale for Children [95]
●The Milwaukee Inventory for Styles of Trichotillomania-Child Version [96]
Other diagnostic tests — A skin biopsy may be useful to confirm the diagnosis and exclude other types of hair loss. In TTM, histology shows a noninflammatory, nonscarring alopecia with morphologic changes of follicular damage (trichomalacia) secondary to the external insult, including distortion of the hair follicle anatomy and perifollicular and intrafollicular hemorrhage [97]. The number of hair follicles is normal, with an increased number of catagen/telogen hair follicles without significant inflammation.
Differential diagnosis — The differential diagnosis of TTM includes:
●Tinea capitis – Tinea capitis is a common fungal infection of the scalp and hair that most commonly occurs in children. The most common manifestations are scaly patches with alopecia (picture 12) and patches of alopecia with black dots at follicular orifices that represent broken hairs (picture 13). Potassium hydroxide examination and fungal culture confirm the diagnosis. (See "Tinea capitis".)
●Alopecia areata – Alopecia areata is a chronic, relapsing disorder characterized by nonscarring hair loss. Patients typically present with smooth, circular, discrete areas of complete hair loss that develop over a period of a few weeks (picture 14A-B). (See "Alopecia areata: Clinical manifestations and diagnosis".)
●Monilethrix – Monilethrix (MIM #158000) is an autosomal dominant disorder characterized by hair shaft abnormalities and hair fragility (picture 15). Microscopic examination of the hair shaft reveals elliptical nodes, resulting in a beaded appearance (picture 16). (See "Evaluation and diagnosis of hair loss", section on 'Inherited and acquired structural hair disorders'.)
Treatment — Psychiatric referral is appropriate for patients with TTM. For patients accepting mental health professional referral, we suggest cognitive-behavioral psychotherapy and, in particular, habit reversal therapy, rather than pharmacologic therapy. (See "Body dysmorphic disorder: Choosing treatment and prognosis", section on 'Cognitive-behavioral therapy'.)
The management of TTM in children requires strong clinician-patient and clinician-parent/caregiver relationships [98]. For children in whom a trigger can be identified (eg, birth of a new sibling, new school), brief counseling and parental/caregiver support and reassurance may be sufficient to reverse the habit [99].
The efficacy of behavioral therapy and pharmacotherapy for TTM has been evaluated in a small number of randomized trials and meta-analyses, as summarized below:
●The benefit of behavioral therapy was confirmed in a 2020 meta-analysis of 24 trials that included 857 participants [100]. This study demonstrated a large effect size for cognitive-behavioral therapy with habit reversal training components, compared with control treatments or no treatments, using the Massachusetts General Hospital Hairpulling Scale or the National Institute of Mental Health Trichotillomania Symptom Severity Scale (standardized mean difference [SMD] -1.66, 95% CI -2.31 to 1.02).
●A 2021 Cochrane review of 12 small, randomized trials found insufficient evidence from meta-analysis to confirm or refute the efficacy of any agent or class of medication, including antipsychotics, N-acetylcysteine, naltrexone, selective serotonin reuptake inhibitors (SSRIs), and tricyclic antidepressants, for the treatment of TTM in adults, adolescents, and children [101]. Low-quality evidence from two small included trials indicated probable benefit (reduction of hair pulling symptoms) of olanzapine and N-acetylcysteine treatment in adults [102,103]. A separate trial in children and adolescents did not find any beneficial effect of N-acetylcysteine compared with placebo [104].
●A 2023 eight-week, randomized trial that included 100 patients with trichotillomania, SPD, or both showed that memantine, an antagonist of the N-methyl-D-aspartate, was more effective than placebo in reducing the total symptom score on the modified National Institute of Mental Health Trichotillomania Symptom Severity Scale from baseline (average reduction -6.98 versus -1.19, respectively) [79]. Moreover, more participants in the memantine group achieved a Clinical Global Impressions improvement scale score of "much or very much improved" than participants in the placebo group (60.5 versus 8.3 percent, respectively). (See 'Memantine' above.)
●A 2014 meta-analysis of 11 randomized trials examined the efficacy of SSRI and behavioral therapy for the treatment of TTM; the SMD of change in hair pulling severity was the outcome measure [105]. This meta-analysis found a large effect size for behavioral therapy compared with no interventions (SMD 1.56, 95% CI 0.99-2.14) and only a moderate effect size for SSRI compared with placebo (SMD 0.46, 95% CI 0.06-0.86).
Nail picking disorder — Nail picking disorder, or onychotillomania, is an uncommon condition in the spectrum of obsessive-compulsive disorder characterized by recurrent picking or pulling of fingernails or toenails, leading to shortening or destruction of the nails [106]. Habit-tic disorder is a variant of onychotillomania. It typically presents with a midline furrow in the nail plate; absence of the cuticle; and erythema, edema, and scaling of the proximal and lateral nail folds and periungual area (picture 17). The abnormality results from repeated, self-inflicted nail matrix trauma due to conscious or unconscious manipulation of the cuticle. Some patients may develop longitudinal melanonychia secondary to nail manipulation [107].
Treatments that have been used for onychotillomania include occlusive dressings, cognitive-behavioral therapy, and SSRIs.
Associated syndromes — Onychotillomania may be one aspect of the behavioral abnormalities seen in Lesch-Nyhan syndrome and Smith-Magenis syndrome [108]. Lesch-Nyhan syndrome is an X-linked disorder caused by defects in the enzyme hypoxanthine-guanine phosphoribosyltransferase 1, resulting in alterations in purine metabolism and accumulation of uric acid. Patients present with motor dysfunction, intellectual disability, and self-injurious behavior, including chewing the fingers and biting the lips [109]. Smith-Magenis syndrome is a rare, multisystemic disorder caused by the deletion of 17p11.2 [110]. The syndrome is characterized by brachycephaly, midface hypoplasia, prognathism, hoarse voice, speech delay, psychomotor and growth retardation, cutaneous features, and self-injurious behavior. (See "Microdeletion syndromes (chromosomes 12 to 22)", section on '17p11.2 deletion syndrome (Smith-Magenis syndrome)'.)
Pachydermodactyly — Pachydermodactyly (PDD) is a rare, benign form of superficial digital fibromatosis characterized by symmetrical, periarticular soft tissue swelling of the proximal interphalangeal joints (picture 18) [111]. The disorder is caused by repetitive local trauma or compulsive habits of interlacing the fingers or rubbing the fingers and predominantly affects young males. PDD has been reported in patients with generalized anxiety disorders and obsessive-compulsive disorder [112,113].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Skin picking disorder".)
SUMMARY AND RECOMMENDATIONS
●Definition and classification – Skin picking disorder (SPD) is the repetitive manipulation of the skin, with or without instrumentation, resulting in visible tissue damage and impairment in social functioning. Patients with SPD may present with features of impulse control disorder, obsessive-compulsive disorder, or both (table 2). SPD is included in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) as a separate diagnosis in the group of the obsessive-compulsive and related disorders. (See 'Definition and classification' above.)
●Psychiatric comorbidities – Multiple psychiatric comorbidities are associated with SPD, including depression, bipolar disorder, obsessive-compulsive disorder, alcohol abuse or dependence, and trichotillomania (TTM). (See 'Comorbid conditions' above.)
●Clinical presentation – SPD appears as excoriated, polymorphic lesions of variable size in all stages of evolution, localized most frequently on the face (picture 1A-D). (See 'Clinical manifestations' above.)
●Diagnosis – The diagnosis of SPD is supported by a list of DSM-5 diagnostic criteria. SPD should be differentiated from the excoriations seen in subgroups of patients with primary pruritic skin conditions, chronic pruritus associated with systemic diseases, or other psychocutaneous diseases. (See 'Patient evaluation and diagnosis' above and 'Differential diagnosis' above.)
●Management:
•Psychiatric referral – Psychiatric referral is appropriate for patients with SPD, although many patients will not accept it. Patients with SPD should either be comanaged by a mental health specialist and dermatologist or managed by a specialist who has experience in both psychiatric and dermatologic disorders. (See 'General considerations' above.)
•Behavioral therapies – For patients with SPD accepting mental health professional referral, we suggest cognitive-behavioral therapy or habit reversal therapy, rather than pharmacologic therapy (Grade 2C). (See 'Behavioral therapies' above.)
•Pharmacologic therapies – Pharmacotherapy may be appropriate for patients with SPD in the following scenarios (see 'Pharmacologic therapies' above):
-For patients with severe SPD that is not responsive to behavioral therapy or interferes with daily functioning, we suggest a selective serotonin reuptake inhibitor (SSRI) antidepressant (Grade 2C). Evidence is limited, but we typically initiate treatment with fluoxetine 20 mg per day, titrating the dose up every two to four weeks as needed and tolerated.
-In patients presenting with features of delusional disorder, antipsychotic medications may be indicated. Atypical antipsychotics, such as olanzapine and risperidone, are options, but their use has only been described in case reports. (See 'Antidepressants' above and 'Antipsychotics' above and "Treatment of delusional infestation".)
•Treatment of skin lesions – Complications of SPD, including skin infection or disfigurement, may require medical, surgical, or cosmetic intervention. Topical and/or systemic antibiotics may be prescribed to treat secondarily infected excoriations or ulcerations. Semiocclusive dressings may be useful to limit further skin damage and promote healing. Potent topical (table 1) or intralesional corticosteroids or narrowband ultraviolet B phototherapy are options for patients with skin lesions associated with intense pruritus. In patients with acne excoriée, aggressive treatment of the underlying acne should be initiated. (See 'Treatment of skin lesions' above.)
●Disorders related to skin picking disorder:
•Trichotillomania – Trichotillomania (TTM), or hair pulling disorder, is a repetitive body-focused disorder frequently associated with skin picking and included in the DSM-5 as a separate diagnosis in the group of the obsessive-compulsive and related disorders. Patients with TTM present with bald spots in various body sites, including the scalp (picture 9A), face (picture 10B), arms, legs, and pubic areas. (See 'Definition and classification' above and 'Clinical features' above.)
The diagnosis of TTM is supported by a list of DSM-5 diagnostic criteria. A skin biopsy may be useful to confirm the diagnosis and exclude other causes of hair loss. (See 'Diagnosis' above.)
Psychiatric referral is appropriate for patients with TTM. For patients with TTM accepting mental health professional referral, we suggest cognitive-behavioral therapy, rather than pharmacologic therapy (Grade 2C). (See 'Trichotillomania' above and 'Treatment' above.)
•Nail picking disorder – Nail picking disorder, or onychotillomania, is an uncommon condition in the spectrum of obsessive-compulsive disorder characterized by recurrent picking or pulling of fingernails or toenails, leading to shortening or destruction of the nail plates (picture 17). (See 'Nail picking disorder' above.)
•Pachydermodactyly – Pachydermodactyly is a rare, benign form of superficial digital fibromatosis characterized by symmetrical, periarticular soft tissue swelling of the proximal interphalangeal joints (picture 18) caused by repetitive local trauma or compulsive habits of interlacing the fingers or rubbing the fingers. (See 'Pachydermodactyly' above.)
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