Diagnosis of Trichotillomania
Trichotillomania Diagnosis: Book Excerpts
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Alopecia [Hair loss]:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient isn’t receiving a chemotherapeutic drug or radiation therapy, begin by asking when he first noticed the hair loss or thinning. Does it affect the scalp alone, or does it occur elsewhere on the body? Is it accompanied by itching or rashes? Then carefully explore other signs and symptoms to help distinguish between normal and pathologic hair loss. Ask about recent weight change, anorexia, nausea, vomiting, excessive stress, and altered bowel habits. Also ask about urinary tract changes, such as hematuria or oliguria. Has the patient been especially tired or irritable? Does he have a cough or difficulty breathing? Ask about joint pain or stiffness and about heat or cold intolerance. Inquire about exposure to insecticides. If the patient is female, ask if she has had menstrual irregularities and note her pregnancy history. If the patient is male, ask about sexual dysfunction, such as decreased libido or impotence.
Next, ask about hair care. Does the patient frequently use a hot blow dryer or electric curlers? Does he periodically dye, bleach, or perm his hair? If the patient is black, ask if he uses a hot comb to straighten his hair or a long-toothed comb to achieve an Afro look. Does he ever braid the hair in cornrows? Check for a family history of alopecia, and ask what age relatives were when they started experiencing hair loss. Also ask about nervous habits, such as pulling the hair or twirling it around a finger.
Begin the physical examination by taking vital signs and then assessing the extent and pattern of scalp hair loss. Is it patchy or symmetrical? Is the hair surrounding a bald area brittle or lusterless? Is it a different color than other scalp hair? Does it fall out easily? Inspect the underlying skin for follicular openings, erythema, loss of pigment, scaling, induration, broken hair shafts, and hair regrowth.
Then examine the rest of the skin. Note the size, color, texture, and location of any lesions. Check for jaundice, edema, hyperpigmentation, pallor, or duskiness. Examine nails for vertical or horizontal pitting, thickening, brittleness, or whitening. As you do so, watch for fine tremors in the hands. Observe the patient for muscle weakness and ptosis. Palpate for lymphadenopathy, enlarged thyroid or salivary glands, and masses in the abdomen or chest.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Hair Loss:
Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Congenital Hair Loss
Localized
Nevus Sebaceous of Jadassohn
Appearson scalp as smooth, slightly raised, linear or oval, yellow or orange,waxy plaque, which is usually solitary.Because of possibility of developingsecondary tumors during puberty, excision is recommended beforepuberty. Aplasia Cutis Congenita
≥1 ovaldefects, 1–2 cm in diameter, appear as ulcerlike lesions,usually in midline of posterior scalp. Lesions sometimes have atrophicskin covering and generally heal in a scar without hair.Inheritance pattern is usually autosomaldominant but may be autosomal recessive. Congenital Triangular Alopecia
May go unnoticed until 2–3 yrs ofage. Triangular area of alopecia, which may be unilateral or bilateral,overlies frontotemporal suture and impinges on anterior hairline.Area remains unchanged throughout life.
Diffuse
Ectodermal Dysplasias
In X-linkedanhidrotic form of ectodermal dysplasia, affected boys have alopecia,hypotrichosis, lack of sweating due to absent sweat glands, andabnormal teeth (small pointed incisors or absence of teeth). Skinbiopsy that shows absence of sweat glands is confirmatory.Autosomal-dominant hidrotic form ischaracterized by variable focal alopecia or loss of all scalp hair,severe nail dystrophy (thick and brittle nails), normal sweating,and normal teeth. Gene locus has been mapped to chromosome 13q12.Rare type of ectodermal dysplasia iscartilage-hair hypoplasia, autosomal-recessive disorder of incompletepenetrance, in which individuals have fine, sparse hair; metaphysealdysplasia resulting in short stature; and immunodeficiency. See Chap. 53, Recurrent Infection. Hair Shaft Defects
Trichorrhexisnodosa produces hair that breaks easily, leaving broken stubs andareas of alopecia. Microscopic exam shows hair that looks like 2paint brushes pushed together. May be associated with argininosuccinicaciduria and Menkes disease.Pili torti refers to dry, lusterless,fragile hair, which can occur as autosomal-recessive disorder ormay be associated with Menkes disease. Microscopic exam revealsflattened hair shaft twisted on its own axis.Monilethrix is autosomal-dominant disordercharacterized by scalp hair breakage. Microscopic exam shows typicallybeaded hair.Scalp and body hair appears dry, lusterless,and fragile with trichorrhexis invaginata. Microscopic exam revealsbamboolike ball and cup joints. Can occur in Netherton disease,which is characterized by ichthyosis. Loose Anagen Hair Syndrome
Autosomal-dominant disorder with variableexpression in which hair is sparse, slow growing, usually fair colored,and easily pulled from scalp. Hair shafts have reduced caliber.Electron microscopy shows slight flattening and longitudinal groovingof hair.
Congenital Hypothyroidism
Scalp hair may be sparse and brittle. See Chap. 23, Growth Deficiency: Weight and Height.
Acquired Hair Loss
Localized
Traction Alopecia
Excessivetension on hair shafts can cause hair loss, and most cases are relatedto hair care. Broken hairs of various sizes are seen in areas ofalopecia.Friction alopecia occurs from repeatedrubbing of scalp and is seen in infants who lie for prolonged timeon their backs or who repetitively rub back of their heads as dailyritual. Trichotillomania
Compulsivepulling of scalp hair, eyebrows, or eyelashes. Habitual, possiblyrelated to underlying anxiety.Irregular patches of hair loss occur,while residual hairs of varying length remain.Psychologic treatment is sometimesnecessary. Tinea Capitis
T. tonsuransis most common cause of tinea capitis in North America. M. canisacquired from kittens or puppies may also cause tinea capitis. Severalpresentations may occur:Circumscribed areas of hair loss with hairsbroken off at follicular orifice (black dot sign) and no other scalpchangeDiffuse fine scaling in dandruff-likepattern without obvious broken off hairsMultiple patches of hair loss withindistinct margins accompanied by kerion (boggy, erythematous nodulewith superficial pustules)Multiple kerions Diagnosis may be confirmed by KOH preparationor fungal culture. Injury
Physical trauma or burns severe enough tocause scarring can produce localized alopecia.
Alopecia Areata
Autosomal-dominantdisorder in which complete or almost complete hair loss occurs incircumscribed areas. Autoimmune mechanism is thought to be responsible.Loss of body hair, eyebrows, and eyelashesalso may be seen. Patches of hair loss do not have any hair exceptperhaps some loose ones at margins. In most cases of incompletehair loss, regrowth of hair usually occurs within 1 yr. With extensivehair loss, prognosis is uncertain.Diagnosis can be confirmed by biopsy. Other
Localizedscalp lesions sometimes occur with varicella, pyoderma, lichen planus,discoid lupus erythematosus, secondary syphilis, and psoriasis.See Chap. 60, Skin Lesions andRashes.Morphea is scleroderma localized toskin. Scalp lesions are linear or oval and often extend from foreheadinto frontal scalp, producing scarring hair loss. Skin is immobile,shiny, hypopigmented, and often surrounded by purplish border. Skinbiopsy is diagnostic. Diffuse
Telogen Effluvium
Characterizedby hair loss resulting from various stresses that cause cessationof hair growth. Such stresses include febrile or chronic illness,general anesthesia, severe injury, drugs (propranolol, coumadin,heparin, valproic acid), and psychologic disturbances. Time betweenstress and hair loss is 2–4 mos.Telogen hairs have absent or fragmentedexternal root sheaths, which often lack pigment. Root of hair isnarrower than shaft and is often curved.Presence of >25% oftelogen hairs in sample of plucked hairs is diagnostic. Anagen Effluvium
Temporaryarrest of follicular activity produced by a substance or physicalmodality that is toxic to hair follicle. Onset of increased sheddingand hair loss usually occurs 1–2 wks after exposure.Anagen hair has pigmented core andbulbous root, which is larger in diameter than hair shaft.Most common causes of anagen hair lossare chemotherapeutic agents that interfere with hair growth (methotrexate,5-fluorouracil, nitrogen mustard, chlorambucil, vincristine, cyclophosphamide,actinomycin D, vinblastine) and radiation that damages growing hair.History and microscopic observationthat most of the lost hairs are in anagen phase confirm diagnosis. Androgenetic Alopecia
In boys, there is thinning over vertex andbifrontal areas of scalp, whereas in girls the crown thins. Geneticallydetermined and potentiated by androgens.
Diagnostic Approach
Diagnosisof hair loss in children can often be made by history and physicalexam.About 90–95% of casesinvolve acquired localized hair loss with tinea capitis, traction alopecia,trichotillomania, or alopecia areata.Diagnosis of tinea capitis is usuallyclinical, but if diagnosis is uncertain, KOH preparation can beperformed. If results are negative, fungal culture should be performed.Most diffuse hair loss is acquired,and most common causes are anagen effluvium (usually chemotherapeuticagents) and telogen effluvium. History and microscopic exam of hairis usually diagnostic of anagen or telogen effluvium.Hair shaft defects also can cause diffusehair loss, but they are rare. Diagnosis is made by microscopic examof hair.Skin biopsy is often necessary in diagnosisof unusual lesions (e.g., aplasia cutis congenita, lichen planus,discoid lupus erythematosus, and morphea).
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
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