Trichotillomania (hair-pulling disorder) is characterized by the persistent and excessive pulling of one’s own hair, resulting in noticeable hair loss.[1, 2, 3] Hair pulling can occur in any area of the body where hair grows. The scalp is the most common area affected, followed by the eyelashes and eyebrows.[4] The alopecia that results from hair pulling can range from small undetectable areas of hair thinning to complete alopecia.
Trichotillomania most commonly presents in early adolescence, with the peak prevalence between ages 4 and 17 years.[5] The disorder has both physical and psychosocial implications. Affected patients may experience distress, moderate impairment in social or academic functioning, and impact to family relationships.[4]
Although trichotillomania is more often a focus of behavioral and psychiatric publications than dermatologic publications, patients are more likely to present to dermatologists than mental health professionals. Because of this, it is important for dermatologists to be familiar with the clinical features and treatment options for these patients.
Trichotillomania must be differentiated clinically from other alopecias (eg, alopecia areata, traction alopecia, androgenetic alopecia, pseudopelade, alopecia mucinosa) by careful physical examination and patient history. Dermatologists, psychologists, and psychiatrists should be familiar with the key features of the disorder as earlier treatment yields a better prognosis and can prevent complications such as trichobezoar and scarring.[6]
For patient education resources, see the Mental Health Center, as well as Anxiety, Panic Attacks, and Hyperventilation.
Diagnostic criteria (DSM-5)
The American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) places trichotillomania in the category of obsessive-compulsive and related disorders and notes that it is characterized by recurrent body-focused repetitive behavior (hair pulling) and repeated attempts to decrease or stop the behavior. The behavior can occur during both relaxed and stressful times, but there is often a mounting sense of tension before hair pulling occurs or when attempts are made to resist the behavior. Some authors have advocated for the distinction between “automatic” pulling occurring during sedentary activities with little awareness and “focused” pulling in response to negative or stressful emotions, as these different styles may respond to different treatment strategies.[7]
The specific DSM-5 criteria for trichotillomania (hair-pulling disorder) are as follows[8] :
Recurrent pulling out of one’s hair, resulting in hair loss
Repeated attempts to decrease or stop the hair-pulling behavior
The hair pulling causes clinically significant distress or impairment in social, occupational, or other important areas of functioning
The hair pulling or hair loss cannot be attributed to another medical condition (eg, a dermatologic condition)
The hair pulling cannot be better explained by the symptoms of another mental disorder (eg, attempts to improve a perceived defect or flaw in appearance, such as may be observed in body dysmorphic disorder)
From a dermatologic standpoint, trichotillomania is a form of traumatic alopecia. The trauma to the follicle occurs as a result of the patient’s repetitive hair-pulling behavior. The hair pulling may present in conjunction with other repetitive grooming behaviors, such as nail biting and skin picking.
Trichotillomania results in highly variable patterns of hair loss. The scalp is the most common area of hair pulling, followed by the eyebrows, eyelashes, pubic and perirectal areas, axillae, limbs, torso, and face. The resulting alopecia can range from thin unnoticeable areas of hair loss to total baldness in the area(s) being plucked.
In addition, trichophagia (ingestion of the hair) is common in persons who pull out their hair. This chewing or mouthing behavior can frequently lead to the formation of trichobezoars (ie, hair casts) in the stomach or small intestines. Trichobezoars can result in anemia, abdominal pain, hematemesis, nausea or vomiting, bowel obstruction, perforation, gastrointestinal (GI) bleeding, acute pancreatitis, and obstructive jaundice.
The etiology of trichotillomania is largely unknown, though both environmental and genetic causes have been suspected. Explanations that have been proposed for the onset and maintenance of the hair-pulling behavior include the following:
Coping mechanism for anxiety or stressful events
A benign habit that developed from a sensory event (eg, itchy eyelash) or another event and resulted in trichotillomania
Co-occurring with another habitual behavior (ie, thumbsucking) in young children
Serotonin deficiency: A link may exist between a deficiency of the neurotransmitter serotonin (5-hydroxytryptamine [5-HT]) and trichotillomania; the hypothesized connection between the two is based on the success of selective serotonin reuptake inhibitors (SSRIs) in treating some people with trichotillomania.
Structural brain abnormalities: Magnetic resonance imaging (MRI) studies have demonstrated that some individuals with trichotillomania have abnormalities of subcortical regions involved in habit generation, inhibitory control, and regulation of affect.[9]
Abnormal brain metabolism: Positron emission tomography (PET) scans have revealed that some individuals with trichotillomania have a high metabolic glucose rate in the global, bilateral, cerebellar, and right superior parietal areas.
Genetic susceptibility: DSM-5 notes that there is some evidence that genetic vulnerability plays a role[8] ; trichotillomania occurs more frequently in people with obsessive-compulsive disorder (OCD) and their first-degree relatives.
Psychological factors: Several psychological theories (eg, psychodynamic, behavioral, and ethologic) have attempted to explain trichotillomania in children; such theories have included stress reduction, emotional regulation, and sensory stimulation.[10, 11]
Disordered reward processing: Preliminary data suggest that trichotillomania may represent a disorder of altered reward processing within the central nervous system; a study by White et al regarding reward processing in trichotillomania patients demonstrated altered nucleus accumbens activations and a decreased functional connection between the dorsal anterior cingulate and nucleus accumbens and basolateral amygdala and reward network; input was through glutamatergic projections, identifying a possible intervention point with agents that modulate glutamate.[12]
Neurodegenerating disease associations: Reports also suggest a possible association between neurodegenerating diseases, such as Parkinson disease and dementia,[13] and trichotillomania in older populations.
Although US epidemiologic studies on the prevalence of trichotillomania are rare, estimates indicate that approximately 8 million people have trichotillomania. The overall frequency is probably underestimated, because only persons who present for treatment are counted; denial of the disorder is frequent, and many individuals with the disorder do not seek professional intervention. Further epidemiologic studies are needed.
In a study of college students, approximately 1%-2% had past or current symptoms of trichotillomania.[14] The rate fell to 0.6% when patients were restricted to the group having related mental tension and relief; without such restrictions, the rate of hair pulling resulting in visible hair loss was 1.5% for males and 3.4% for females. A survey at an African American university (n=248) showed that 6.3% of those surveyed had a history of pulling out their hair.[15]
In the authors’ experience, the number of patients with trichotillomania is approximately 5% of the number of patients with alopecia areata. The incidence of alopecia areata is approximately 50% of all patients presenting with alopecia, and the total number of hair-loss patients is approximately 2% of all dermatologic patients.
Age-, sex-, and race-related demographics
Trichotillomania is frequently a chronic disorder that lasts weeks to decades, with a variable age of onset. Hair-pulling sites may vary with the age of onset: Patients with a very early onset of trichotillomania are more likely to pull eyelashes, whereas those with a later onset are more likely to pull pubic hair.[16] In the study by Walther et all, it was reported that the 27 children in the preschool age group (0-5 y) only pulled from the scalp and over half of the 5- to 10-year-age group children pulled from other body areas in addition to the scalp.[17]
Although empirical data are not available, this condition appears to be substantially more common in children than in adults. In general, prognosis is related to patient age. Children typically have a time-limited disorder, with an excellent prognosis. Adolescents have more severe disease, with a guarded prognosis. Adults, many of whom were diagnosed before reaching adulthood, have a poor prognosis.
With regard to sex-related differences, the younger the patient, the more equal the sex distribution. However, a recent cross-sectional study of 110 young children (age 0-10 y) demonstrated that a female predominance still exists, even among younger patients.[17] In adult groups, most patients are women. In adolescents, girls are affected more often than boys. DSM-5 cites an overall female-to-male ratio of 10:1.[8]
No racial differences in prevalence have been reported; trichotillomania appears to be equally common in whites, blacks, and Asians.
In very young children, the prognosis is excellent; hair pulling that occurs in young children may be described more accurately as a short-term habit disorder. In late childhood and adolescence, the prognosis is usually good but should be considered guarded; the alopecia quite often continues for months or a couple of years and then recurs after a variable time. In adult patients, the prognosis is poor, and permanent recovery is uncommon.
Trichotillomania results in highly variable patterns of hair loss, ranging from small undetectable patches of hair loss to total baldness. Ingestion of the pulled hair can result in trichobezoar formation and subsequent anemia, abdominal pain, hematemesis, nausea or vomiting, bowel obstruction, perforation, GI bleeding, pancreatitis, and obstructive jaundice.
Trichotillomania can become a chronic and persistent condition of hair pulling. Specifically, symptoms of trichotillomania can persist for weeks to decades. Therefore, comprehensive treatment planning is critical and may require consultations with mental health professionals. Treating trichotillomania in children may be difficult because of the low reliability and validity of self-report.
Mortality is not reported with trichotillomania. Most patients with trichotillomania in dermatologic clinics are children and early adolescents. Patients may try to conceal the alopecic area and may have some restrictions in their school activities. In adult patients, trichotillomania may cause distress and impairment in occupational and social or marital relations.[18]
Trichotillomania can be difficult to diagnose. Reported symptoms may include the following:
Pulling hair: Patients may report hair loss related directly to hair pulling or plucking; however, they frequently complain of unexplainable alopecia or hair loss, because they typically conduct the pulling or plucking behavior in private and often deny engaging in it.
Denial of hair pulling: Children are particularly likely to deny hair pulling; because the behavior is usually not conducted in the presence of adults or others, it is often difficult to diagnose as self-inflicted hair loss.
Pulling hairs from other objects or people: Occasionally, patients engage in hair pulling or plucking from other people, pets, dolls, or other fibrous materials (eg, carpets).[19]
Avoidance of social situations: Some individuals with trichotillomania tend to avoid social situations so that they can maintain the privacy to engage in hair-pulling behavior and escape the embarrassment such behavior may bring.
Increased levels of stress or anxiety: Although hair pulling can occur during periods of relaxation, increased stress frequently precipitates or exacerbates trichotillomania; furthermore, patients may present with anxiety (which they may not report) associated with their hair-pulling behavior.
Gastrointestinal (GI) complaints: Trichobezoar (hair cast) formation can lead to complaints of abdominal pain, nausea and vomiting, constipation or other symptoms of bowel obstruction, and GI bleeding.
To obtain an effective history, a high index of suspicion for the diagnosis is essential. Many cases erroneously diagnosed as alopecia areata are thus misdiagnosed because of the physicians’ lack of suspicion about the possibility of trichotillomania. It is important to keep in mind that trichotillomania can occur in all types of people from all walks of life.
Conditions that may increase suspicion of trichotillomania based on the reported associations include psychiatric disorders such as anxiety disorder, attention-deficit disorder, obsessive-compulsive disorder, mood disorder, tic disorder, and body-focused repetitive behaviors such as skin picking, nail biting, or lip/check bitting. They have been reported to increase with the age of the patient.
Patients with sharply defined alopecic lesions with broken stumps tend to confess their manual hair manipulations if asked about them by a physician, whereas patients with poorly circumscribed alopecic lesions tend to give very ambiguous answers. During the interview, the latter patients’ answers may confuse an inexperienced physician, leading to potential confusion with malingering.
It should be kept in mind that hair manipulations frequently occur while patients are engaged in sedentary activities, such as reading, writing, watching television, or driving a car, and that their daily time allotted to physical exercise is scant. A sleep-isolated variant has been recognized.[20]
In many cases, patients or their parents claim that the hair does not grow longer than approximately 1.5 cm; these patients or parents believe the hairs are suffering from periodic loss. Some patients may report pruritus of the scalp without visible dermatoses or may confess that they tried to remove nits or had a curiosity about hair roots and wanted to make an observation of the roots.
In the authors’ experience, trichotillomania does not always occur in isolation and can coexist with inflammatory alopecias. The authors have encountered patients with lichen planopilaris and alopecia areata with repetitive hair pulling triggered by discomfort from the underlying inflammatory disorder. In our experience, patients with a concurrent inflammatory disorder are more forthcoming about hair-pulling behaviors when queried. A high index of clinical suspicion based on clinical morphology with histologic confirmation is important for diagnosis in these cases, and management of both conditions is critical for optimal treatment response.
Physical signs of trichotillomania may include the following:
Alopecia: This can range from barely noticeable areas of hair loss to total baldness; the scalp is the most common area, though hairs may also be pulled from the eyebrows, eyelashes, pubic and perirectal areas, axilla, limbs, torso, and face; the absence of eyebrows and eyelashes can indicate a more serious form of trichotillomania.
Friar Tuck sign: This common presentation consists of areas of hair loss with twisted and broken hairs of varying lengths arranged in a circular pattern, with unaffected hairs surrounding the area of hair loss. In contrast with inflammatory alopecias such as alopecia areata, the affected areas are “irregularly irregular” with areas of sparing.
Hair regrowth: Hairs of varying lengths may be noted during the regrowing phase.
Absence of skin abnormalities or inflammation: The signs of excoriation or other dermatologic pathology that may be common in individuals with tinea capitis are typically absent in people with trichotillomania.
Hair abnormalities: These may include empty and/or damaged hair follicles; twisted or broken hairs of varying length, and wavy, wrinkled, or corkscrew-shaped hair shafts
Trichobezoars: These are typically found in the stomach and intestines of patients who chew or mouth their pulled hairs and may give rise to anemia, abdominal pain, hematemesis, nausea and vomiting, bowel obstruction, perforation, GI bleeding, pancreatitis, or obstructive jaundice.
For dermatologists who pay close attention to morphology, diagnosing trichotillomania usually is not difficult. The general morphology of an individual lesion, showing a geometric shape and incomplete nonscarring alopecia of the involved area, typically identifies the condition (see the images below). In longstanding cases, scarring may occur.[21]
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Geometric patch of incomplete alopecia in teenage boy.
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Bizarre-patterned lesion covered with short hairs in 11-year-old girl.
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Typical geometric shape trichotillomania in a 7-year-old boy. Smooth baldness of scalp surface at this age is rare.
However, if the lesion is limited to an eyebrow or eyelash, the characteristic geometric shape may not develop; this lack of a geometric pattern sometimes draws suspicion away from a diagnosis of traumatic alopecia (see the image below).[22]
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In eyebrow involvement, the characteristic geometric shape is not made.
Occasionally, the hair-thinning pattern is not circumscribed and shows only a somewhat deficient volume of hair (see the image below).
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Sometimes, alopecia is not circumscribed but simply shows deficient hair volume, as in this 9-year-old girl.
Involvement of the entire scalp also occurs, in which a characteristic geometrical shape is also not recognized. At first glance, this type of trichotillomania resembles a hereditary disorder of keratinization such as monilethrix or pili torti (see the image below).
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When entire scalp is involved, trichotillomania resembles keratinization disorder of hairs (eg, monilethrix).
The patches may be single or multiple. The degree of involvement may range from a few square centimeters to the entire scalp. An extensive involvement of the scalp, sparing only marginal areas, is termed tonsure trichotillomania because of its resemblance to the tonsuring practiced by monks in the Middle Ages (see the image below).
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Tonsure trichotillomania (so named because of its similarity to medieval monks' tonsures). In this patient, hair is preserved only in posterior margin....
Examination of the lesions with a magnifying glass or dermatoscope (see the image below) reveals various combinations of the following:
Newly growing short hairs with tapered ends
Broken short terminal hairs
Vellus or indeterminate hairs
Comedolike black dots
Empty follicular orifices
A 2015 article reviewed the role of dermoscopy in adult and childhood hair disorders and noted fraying of ends, breakage at different lengths, and scratching and hemorrhaging as possible signs of trichotillomania. Black dots, yellow dots, coiled hair, and exclamation-mark hairs are nonspecific since they are present in alopecia areata.[23]
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Close-up picture of lesion of usual trichotillomania shows combination of newly growing young hair, broken shafts, comedolike black dots, empty orific....
Positioning an appropriate contrast card (eg, a white card for black hair) at an involved area is helpful for detecting both the broken shafts and the newly growing hairs with tapered tips (see the image below).
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Contrast card examination helps demonstrate nature of the alopecia to parents of children with trichotillomania. It shows broken hairs and newly growi....
In severe long-standing lesions, the hairs are regressed to vellus type hairs, and the lesional surface is almost smooth, similar to that seen a scarring alopecia (see the images below).
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Woman with severe long-standing lesions from trichotillomania.
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Close-up picture of severe long-standing lesion in which hairs are regressed to vellus or intermediate-type hairs and scalp is rather smooth.
In addition to scalp lesions, other hairy areas (eg, eyebrows, eyelashes, or the pubic area) may be involved. Additionally, extremely short fingernails (from nail biting or onychophagia) frequently accompany trichotillomania, especially in children. Knuckle pads caused by frequent cracking or rubbing of the digits may also be found.
The Trichotillomania Scale for Children (TSC) is a child and parent report that may be used to assess symptom severity and impairment.[24]
Trichography (ie, microscopic examination of plucked hairs) can help verify the diagnosis of trichotillomania. Findings vary according to the area examined. Where the hairs are all short with tapered tips (regrowing hairs), the trichogram may show all anagen roots (telogen count, 0). In other areas, especially those showing broken shafts of various lengths, an increased number of club hairs (>20%), and even exclamation-mark hairs typical of alopecia areata,[25] can be seen.
Creation of a “hair growth window” by shaving an involved area weekly and observing for growth can help to confirm a diagnosis of trichotillomania. The area demonstrates normal, dense regrowth as hairs are too short to be manipulated or pulled.
Ultrasonography and computed tomography (CT) may be useful in detecting trichobezoar formation that can result from swallowing or ingesting plucked hairs in children with trichotillomania.
Histologic procedures may aid in the diagnosis of suspected trichotillomania in children. Punch biopsy may be used to verify a suspected diagnosis of trichotillomania. Melanin pigment casts and granules in the upper hair follicles and infundibulum of hair shaft are characteristic (see Histologic Findings).
In most cases, a clinical diagnosis, based on an inspection of the lesion and an appropriate patient history, is sufficient. Hairs collected by the patient can be examined. Trichotillomania demonstrates anagen hairs, telogen effluvium demonstrates catagen hairs, and alopecia areata demonstrates tapered fractures.
Occasionally, however, biopsy is needed to differentiate trichotillomania from alopecia areata. Biopsy findings of trichotillomania overlap significantly with those of alopecia areata and syphilis. Scalp biopsy specimens are best interpreted by someone with considerable expertise.
Multiple sections, either vertically or transversely oriented, are recommended to observe characteristic findings, especially because both may show numerous catagen hairs and pigment casts. In general, the biopsy specimen should be taken from a new lesion. The most frequent findings are empty anagen follicles (especially in transverse sections), increased numbers of noninflamed catagen follicles, and pigment casts in hair canals, with the latter two findings also present in alopecia areata. The presence of twisted linear pigment in the cortex (zip sign) or circular, central aggregation of pigment surrounded by the inner root sheath (button sign) demonstrate a traumatic cause and can help differentiate the two conditions.[26] There may be hemorrhage in the surrounding dermis from trauma with plucking and scarring over the long term.
Trichomalacia (incompletely keratinized, soft, distorted, and pigmented hair shafts) and bizarre fractured hair shafts are fairly specific for trichotillomania (see the image below).
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Histopathologically, trichomalacia (twisted pigmented soft cortex) with catagen follicles is characteristic of trichotillomania with empty follicles.
It should be kept in mind that increased numbers of catagen hairs and pigment casts within hair canals may also be seen in persons with alopecia areata or syphilis, as well as in those with trichotillomania. Care should be taken to search for clues to the diagnosis of alopecia areata or syphilis, such as peribulbar lymphoid infiltrate or peribulbar eosinophils.
Lymphocytes, pigment, and eosinophils within fibrous tract remnants are also associated with alopecia areata and syphilis and may be helpful clues to the correct diagnosis. Plasma cells are a common sign of syphilis, but are not specific. In biopsy specimens from the occipital scalp, plasma cells are common, regardless of the etiology of the hair loss.
Because both trichotillomania and chronic traction alopecia are the result of applied external force, the resulting histopathologic pictures are similar and sometimes identical.
The diagnosis of trichotillomania should be confirmed through a workup.
Determine whether symptoms represent a short-term childhood habit rather than true trichotillomania.
Distinguish whether the patient engages in inattentive automatic pulling or focused pulling in response to stressful emotions, as these pulling styles affect therapy selection.
Determine whether the symptoms indicate a more serious psychological problem through consultation and collaboration with a psychiatrist, developmental-behavioral pediatrician, or licensed clinical psychologist; consultation is recommended and may be required for choosing various treatment options.[27]
Recognize that children with presenting symptoms of trichobezoars may require further evaluation via ultrasonography, magnetic resonance imaging (MRI), or computed tomography (CT).
Currently available evidence suggests that the first line of treatment for trichotillomania is behavioral treatment and intervention, with a focus on affective regulation.[28] No medication has been approved for the treatment of trichotillomania. Drug therapy has largely been disappointing, although some studies have yielded encouraging results.[29, 30, 31]
N-acetyl cysteine may be of benefit, as may behavior modification techniques and psychotherapy.[32, 33]
A psychiatrist should be consulted when a serious psychiatric disorder is suspected. Consultations with other specialists (eg, a psychologist or a developmental-behavioral pediatrics specialist) should be obtained as indicated. A surgeon may be consulted if removal of trichobezoars in the stomach and intestines is under consideration.
In current practice, behavioral treatment seems to be the most powerful intervention, even for patients older than 16 years.[34] Effective behavioral strategies in the treatment of trichotillomania in children include the following:
Habit reversal: This is a set of procedures taught to a child that includes the following components: increasing awareness of the habit; teaching a competing response to practice when the child feels the urge to engage in the habit, in situations in which the habit historically occurs, or for 1 minute after the occurrence of the habit; practicing stress and anxiety reduction procedures daily; and support and encouragement from parents.[35] Studies suggest that traditional habit-reversal therapy is most beneficial in patients with automatic pulling.[7]
Self-monitoring: This involves systematically observing and discriminating when the behavior occurs, recording the responses, and evaluating one’s own behavior.
Competing reaction training: This is a component of habit reversal that is occasionally used alone; a child is taught a socially appropriate alternative behavior or response and is encouraged to practice it on daily when he or she feels the urge to engage in the habit, in situations in which the habit historically occurs, or for 1 minute after the occurrence of the habit. Recommended behaviors should be inconspicuous and able to be performed in public for 60-90 seconds (eg, holding a clenched fist with both hands).
Relaxation training: This involves helping children identify their own bodily sensations associated with tension and then using procedures designed to induce relaxation; typically, it is individualized and may include such procedures as deep-breathing strategies and systematic muscle tensing and relaxation. Targeting anxiety and tension is of particular importance in patients with more focused pulling behavior.[7]
Psychotherapy: This process involves direct communication (mainly talking) between a therapist and a child and makes use of various techniques to help solve behavioral and other psychological problems; one of its most popular forms is cognitive-behavioral therapy (CBT).
Hypnosis: This is a process of controlling physiologic responses by focusing attention on specific mental images for therapeutic purposes, typically to gain more control over behavior, emotions, or physical well-being; in a hypnotized state, the subject is more open than usual to suggestions (provided by the hypnotist) for subsequent changes in behavior.
Elimination of a comorbid behavior: When two seemingly different behaviors occur together (eg, trichotillomania and thumb sucking), a treatment to reduce or change one of them may also reduce or change the other.
In a broad sense, the commonsense approach to stopping the bad habit that makes use of parental involvement is a primitive form of behavioral therapy. It is worth trying first. To achieve the level of parental involvement necessary to aid in treatment, the physician should ensure that parents fully understand the entire nature of the alopecia. Some parents who have not witnessed episodes of hair pulling by their child refuse to believe that the condition is self-inflicted.[36]
In infant patients, provision of loving care with enough maternal skin contact, in conjunction with available transitional objects such as dolls or other toys, would work well. For this purpose, parent-infant psychotherapy in combination with behavioral guidance may be needed.[7]
Parental involvement should include enough support to ensure that their children grow well not only intellectually but also physically and socially. In many cases, patients’ extracurricular activities are almost solely of an intellectual nature (eg, drawing, mathematics, language lessons) and are not well balanced with social and physical activities.
Shaving or clipping hair close to the scalp may be helpful both for stopping the behavior and for educating the parents regarding the nature of the alopecia. Shaving a circumscribed area weekly (the “hair growth window”) can yield benefits both for diagnosis and for reassurance. It should be kept in mind that the shaved (clipped) hairs are not all in the actively growing anagen stage and that a couple of months may be required before total regrowth is noted.
If these initial approaches do not work, CBT should be instituted. Trichotillomania is a kind of unwanted automated repetition of hair manipulations, and the awareness gained through CBT can help overcome such unwanted automated activity. Dermatologists who treat these patients should, therefore, be familiar with at least a few of the various CBT methods. Therapeutic success may depend on a firm understanding of the illness and on the cooperation of the family. Several courses of CBT may be needed; each course usually lasts 2 months.
In the authors’ experience, patients referred for psychoanalytical treatment often show disappointing results. However, patients whose trichotillomania is largely of the focused type should be referred for psychiatric evaluation because this type shows comorbidity with systemic psychiatric disorders.
Support groups
Support groups would be very helpful. At present, however, setting up and maintaining a support group for patients with trichotillomania is only a remote possibility in most countries because of the general lack of understanding of the disorder and because patients themselves are usually secretive about their behavior. An abundant amount of helpful information and educational tools can be found through the Trichotillomania Learning Center.
Few drug studies on trichotillomania in children and adults exist. The majority of studies to date have investigated the efficacy of selective serotonin reuptake inhibitors (SSRIs) because of their role in other obsessive-compulsive disorders.[37] These agents have demonstrated a degree of effectiveness in some patients with trichotillomania, but a positive treatment response is not consistent.[37] In children, SSRIs (eg, fluoxetine, sertraline, fluvoxamine) may be more advantageous as a medication choice than tricyclic antidepressants (TCAs) because of their milder adverse effects.
Although at present, no pharmacotherapy for trichotillomania is consistently effective, several studies show promise. The most compelling data to date are focused on N-acetylcysteine (NAC) and olanzapine.[37]
In a double-blind, placebo-controlled trial, Grant et al assessed whether N -acetylcysteine (1200-2400 mg/day) improved trichotillomania in adults with compulsive behavior.[29] Improvement was measured on the Massachusetts General Hospital Hair Pulling Scale (MGH-HPS), the Clinical Global Impression-Improvement (CGI-I) scale, and the Psychiatric Institute Trichotillomania Scale (PITS). After 9 weeks, significantly greater reduction in hair-pulling symptoms on both the MGH-HPS and the PITS was noted in patients taking N-acetylcysteine. Other authors also have had success.[38]
A study by Bloch et al, however, failed to document a significant improvement with N -acetylcysteine in children with trichotillomania.[39] Their 12-week randomized, double-blinded, placebo-controlled trial was conducted using N -acetylcysteine in children and adolescents aged 8-17 years (N=39) with trichotillomania. The trial did not show a benefit for treatment with N -acetylcysteine when compared with placebo. The authors did note that both groups improved with time, which could be attributed to the patients receiving education and support while being in the study.
Grant et al also assessed the efficacy of the cannabinoid dronabinol for treating trichotillomania in a small open-label treatment study in female subjects, finding that a dosage of 11.6±4.1 mg/day led to a decrease in the mean MGH-HPS from 16.5±4.4 at baseline to 8.7±5.5 at study endpoint.[30] In all, 64.3% of the subjects showed both a decrease in MGH-HPS and a rating of “much or very much” improved on the CGI-I scale, with no adverse effects on cognition.
Van Ameringen et al studied the efficacy of flexible-dose olanzapine for the treatment of trichotillomania in a randomized, double-blind, placebo-controlled trial.[31] A dosage of 10.8±5.7 mg/day showed a significant decrease in the Yale-Brown Obsessive Compulsive Scale for Trichotillomania and the CGI-Severity of Illness scale, with 85% of the subjects who received olanzapine showing improvement on the CGI-I scale. The drug appears to be both safe and effective.
In a study by Golubchik et al, methylphenidate showed limited efficacy in trichotillomania patients with comorbid attention deficit-hyperactivity disorder (ADHD) and a low rate of stressful life events (SLEs).[40]
Case studies suggest that both oxcarbazepine and aripiprazole warrant further study as possible treatments for trichotillomania.[41, 42]
The use of bimatoprost in the treatment of madarosis due to trichotillomania has been described. A 55-year-old woman with trichotillomania was started on bimatoprost 0.03% solution daily. At 2 months, the number and length of eyelashes had doubled compared with the baseline. The medication was stopped at 6 months, and no adverse effects were reported. The patient continued to take amitriptyline to control the urge to pull and fluoxetine for anxiety during the 6 months of treatment.[43]
Whereas drug monotherapy is generally not effective, combination therapy and the addition of other treatment modalities may be helpful.
Antidepressants in pediatric patients
Physicians are advised to be aware of the following information and to use appropriate caution when considering treatment with antidepressants in the pediatric population.
In December 2003, the UK Medicines and Healthcare Products Regulatory Agency (MHRA) issued an advisory stating that most SSRIs are not suitable for use by persons younger than 18 years for treatment of “depressive illness.” After review, this agency decided that the risks SSRIs pose to pediatric patients outweigh the benefits of treatment, except in the case of fluoxetine, which appears to have a positive risk-benefit ratio in the treatment of depressive illness in patients younger than 18 years.
In October 2003, the US Food and Drug Administration (FDA) issued a public health advisory regarding reports of suicidality in pediatric patients treated with antidepressant medications. This advisory reported suicidality (both ideation and attempts) in clinical trials of various antidepressant drugs in pediatric patients. The FDA asked that additional studies be performed, because suicidality occurred in both treated and untreated patients with major depression and thus could not be definitively linked to drug treatment.
However, a subsequent study of more than 65,000 children and adults treated for depression between 1992 and 2002 by the Group Health Cooperative in Seattle found that suicide risk declined, rather than rose, with the use of antidepressants. To date, this is the largest study to address this issue.
Currently, there is insufficient evidence to associate obsessive-compulsive disorder (OCD) and other anxiety disorders treated with SSRIs with an increased risk of suicide.
No special diet is required. No activity limitations are suggested. Physical exercise can provide a healthier outlet for stress. In the authors’ experience, many children and adolescents with trichotillomania spend too much time on activities involving little physical exertion (eg, studying at a desk) and not enough on physical activities. If the hair-pulling behavior is associated with a specific activity, however, that activity may require close monitoring. Activities during which patients may engage in hair pulling include the following:
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.
Clinical Context:
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.
Clinical Context:
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).
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Escitalopram is the S-enantiomer of citalopram. It may have a faster onset of depression relief (1-2 wk) compared with other antidepressants.
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.
Clinical Context:
Clomipramine inhibits reuptake of norepinephrine or serotonin at the presynaptic neuron. It is approved for OCD in children aged 10-17 years.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Amitriptyline inhibits the reuptake of serotonin and/or norepinephrine at the presynaptic neuronal membrane, thus increasing the concentration of these neurotransmitters in the CNS.
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.
Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Carly A Elston, The Commonwealth Medical College
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Additional Contributors
Connie J Schnoes, MA, PhD, Director, National Behavioral Health Dissemination, Supervising Practitioner, Boys Town Center for Behavioral Health, Father Flanagan’s Boys’ Home, Boys Town
Disclosure: Nothing to disclose.
Cynthia R Ellis, MD, Director of Developmental Medicine, Associate Professor, Department of Pediatrics and Psychiatry, Munroe Meyer Institute for Genetics and Rehabilitation, University of Nebraska Medical Center
Disclosure: Nothing to disclose.
Holly Jean Roberts, PhD, Assistant Professor, Department of Pediatrics, Munroe-Meyer Institute, University of Nebraska Medical Center
Disclosure: Nothing to disclose.
Megha Patel, The Commonwealth Medical College
Disclosure: Nothing to disclose.
Acknowledgements
David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Edward F Chan, MD Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine
Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Cynthia R Ellis, MD Director of Developmental Medicine, Associate Professor, Department of Pediatrics and Psychiatry, Munroe Meyer Institute for Genetics and Rehabilitation, University of Nebraska Medical Center
Cynthia R Ellis, MD is a member of the following medical societies: Nebraska Medical Association
Disclosure: Nothing to disclose.
Chull-Wan Ihm, MD Professor, Department of Dermatology, Chonbuk National University, Korea
Chull-Wan Ihm is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology
Disclosure: Nothing to disclose.
Chet Johnson, MD Professor and Chair of Pediatrics, Associate Director, Developmental Pediatrician, Center for Child Health and Development, Shiefelbusch Institute for Life Span Studies, University of Kansas School of Medicine; LEND Director, University of Kansas Medical Center
Chet Johnson, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.
Caroly Pataki, MD Clinical Professor of Psychiatry and Pediatrics, Keck School of Medicine of the University of Southern California
Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
CH Rhee, MD
Disclosure: Nothing to disclose.
Holly Jean Roberts, PhD Assistant Professor, Department of Pediatrics, Munroe-Meyer Institute, University of Nebraska Medical Center
Holly Jean Roberts, PhD is a member of the following medical societies: Autism Society of America, National Association of School Psychologists, and Psi Chi
Disclosure: Nothing to disclose.
Connie J Schnoes, MA, PhD Psychologist, Director of Training, Supervising Practitioner, Father Flanagan's Boys' Home, Boys Town
Disclosure: Nothing to disclose.
Leonard Sperling, MD Chair, Professor, Department of Dermatology, Uniformed Services University of the Health Sciences
Leonard Sperling, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Mansueto CS, Thomas AM, Brice AL. Hair pulling and its afftective correlates in an African-American university sample. J Anxiety Disord. 4/2007. 21:590-9.
Geometric patch of incomplete alopecia in teenage boy.
Bizarre-patterned lesion covered with short hairs in 11-year-old girl.
Typical geometric shape trichotillomania in a 7-year-old boy. Smooth baldness of scalp surface at this age is rare.
In eyebrow involvement, the characteristic geometric shape is not made.
Sometimes, alopecia is not circumscribed but simply shows deficient hair volume, as in this 9-year-old girl.
When entire scalp is involved, trichotillomania resembles keratinization disorder of hairs (eg, monilethrix).
Tonsure trichotillomania (so named because of its similarity to medieval monks' tonsures). In this patient, hair is preserved only in posterior margin of her scalp.
Close-up picture of lesion of usual trichotillomania shows combination of newly growing young hair, broken shafts, comedolike black dots, empty orifices, and vellus or intermediate hairs.
Contrast card examination helps demonstrate nature of the alopecia to parents of children with trichotillomania. It shows broken hairs and newly growing hairs with slender tips among long intact hairs.
Woman with severe long-standing lesions from trichotillomania.
Close-up picture of severe long-standing lesion in which hairs are regressed to vellus or intermediate-type hairs and scalp is rather smooth.
Histopathologically, trichomalacia (twisted pigmented soft cortex) with catagen follicles is characteristic of trichotillomania with empty follicles.
Geometric patch of incomplete alopecia in teenage boy.
Bizarre-patterned lesion covered with short hairs in 11-year-old girl.
Typical geometric shape trichotillomania in a 7-year-old boy. Smooth baldness of scalp surface at this age is rare.
In eyebrow involvement, the characteristic geometric shape is not made.
Sometimes, alopecia is not circumscribed but simply shows deficient hair volume, as in this 9-year-old girl.
When entire scalp is involved, trichotillomania resembles keratinization disorder of hairs (eg, monilethrix).
Tonsure trichotillomania (so named because of its similarity to medieval monks' tonsures). In this patient, hair is preserved only in posterior margin of her scalp.
Close-up picture of lesion of usual trichotillomania shows combination of newly growing young hair, broken shafts, comedolike black dots, empty orifices, and vellus or intermediate hairs.
Contrast card examination helps demonstrate nature of the alopecia to parents of children with trichotillomania. It shows broken hairs and newly growing hairs with slender tips among long intact hairs.
Woman with severe long-standing lesions from trichotillomania.
Close-up picture of severe long-standing lesion in which hairs are regressed to vellus or intermediate-type hairs and scalp is rather smooth.
Histopathologically, trichomalacia (twisted pigmented soft cortex) with catagen follicles is characteristic of trichotillomania with empty follicles.
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