AssessmentsAlopecia: Clinical practice
USMLE® Step 1 style questions USMLE
USMLE® Step 2 style questions USMLE
Content Reviewers:Rishi Desai, MD, MPH
Assessment begins with obtaining a description of hair loss and the areas involved, as well as a medical history and family history.
Assessment of activity on the scalp may be done with a hair pull test, done by gripping about 20 hairs and gently pulling upward and away from the skin. Normally, about three hairs may fall out with each pull, while if more than 10 hairs are removed, the test is considered positive.
A noninvasive method of examining hair and scalp is trichoscopy, which is performed with the use of a dermatoscope. This traditionally consists of a magnifier, a non-polarised light source, a transparent plate and a liquid medium between the instrument and the skin.
In some cases, diagnostic techniques such as microscopic examination of cut or plucked hair fibers and scalp biopsies may provide additional information.
The pluck test is conducted by pulling hair out by the roots.
The root of the plucked hair is then examined under a microscope to determine the phase of growth, and is used to diagnose if there’s a defect of anagen or telogen.
Anagen hairs have sheaths attached to their roots, while telogen hairs have tiny bulbs without sheaths at their roots.
Finally, getting a scalp biopsy from the centre of the lesion gives confirmation of permanent hair loss, whereas a biopsy from the edge or an area of active inflammation may shed light on the underlying disease, and depending on the suspected diagnosis, additional laboratory studies may be performed.
Cicatricial alopecias are characterized by irreversible damage to the hair follicle that results in interruption of hair cycling and permanent hair loss if not treated in time.
A scalp biopsy is necessary to diagnose the type of cicatricial alopecia, to determine the degree of activity, and to select appropriate therapy.
Cicatricial alopecias may be primary or secondary.
Primary cicatricial alopecias are inflammatory disorders with unknown cause, which may be associated to inflammatory diseases like lupus or lichen planopilaris, and are subdivided by the type of predominant inflammatory infiltrate detected on scalp biopsy into lymphocytic, neutrophilic, and mixed primary cicatricial alopecias.
Treatment strategies are different for each subtype.
The goal in lymphocytic cicatricial alopecias is to decrease or eliminate the lymphocytic inflammatory cells that are attacking and destroying the hair follicle.
Individuals with more localized disease may be treated with high-potency topical corticosteroids.
On top of this, individuals with more extensive disease may also get oral antibiotics like doxycycline.
Finally, individuals who fail to respond to standard therapy with topical corticosteroids and antibiotics may be given oral anti-inflammatory medications like hydroxychloroquine, mycophenolate mofetil, or cyclosporine.
Now, the neutrophilic group of cicatricial alopecias may be associated to pathogenic microbes, even if their correlation isn’t well understood, so treatment is directed at eliminating them with oral antibiotics like doxycycline as initial therapy, and rifampin and clindamycin as second-line therapy.
Oral isotretinoin is an alternative second-line therapy for individuals who fail or who cannot receive clindamycin and rifampin therapy.
Finally, for the mixed group of cicatricial alopecias, mild to moderate inflammation areas get high-potency topical corticosteroid therapy, and may get a topical antibacterial agent or topical retinoid as adjunctive therapy.
On the other hand, individuals with more severe inflammation get initial treatment with oral antibiotic therapy, generally with doxycycline, and should be tested for secondary infection with cultures and sensitivity testing. If they turn out negative, topical corticosteroids may be given as well to help reduce inflammation.
On the other hand, secondary cicatricial alopecia always has a known cause. Causes include tinea capitis, radiation therapy, and surgical or injury scars.
Tinea capitis is a common fungal infection of the scalp caused by dermatophyte fungi of the Trichophyton and Microsporum species. The most common clinical findings are single or multiple scaly patches with alopecia.
Some individuals may present patches with black dots at follicular orifices that represent broken hairs.
In addition, often individuals have palpable cervical lymphadenopathy.
A severe manifestation of tinea capitis known as kerion results from an intense immune response to the infection.
Kerion is characterized by the development of an inflammatory plaque with pustules, thick crusting, and drainage, and it is often associated with tenderness or pain.
Biopsy of tinea capitis shows fungal elements within or surrounding hair shafts, and perifollicular mononuclear infiltrate in the dermis, as well as multinucleated giant cells in the dermis in cases where the hair follicle is disrupted.
Trichoscopy may help the diagnosis of tinea capitis, showing broken hairs and black dots.
Finally, fungal cultures are performed to confirm tinea capitis when the diagnosis is uncertain.
Adjunctive interventions for tinea capitis include using a shampoo with antifungal properties to reduce risk of spread of infection to other individuals.
Secondary cicatricial alopecia may also be secondary to radiation therapy administered to the head, most commonly used to treat cancerous growths within the brain, since hair follicles are very sensitive to radiation and enter the telogen phase. Hair shedding may start as soon as two weeks after the first dose of radiation and continue for a couple of weeks.
Finally, secondary cicatricial alopecia may occur in areas with surgical or injury scars. This occurs when the scar is so deep as to damage the hair follicle permanently.
Next up, non scarring alopecias are conditions in which the hair follicle is not permanently damaged, so hair regrowth is possible.
In non scarring alopecias, clinical signs of inflammation are usually mild or absent and destruction of the hair follicle does not occur.
This disease interferes with hair cycling by causing a follicle to prematurely leave the anagen phase and enter the telogen phase.
Most often, alopecia areata presents with smooth circular patches of complete hair loss that develop over a period of a few weeks.
The course of alopecia areata is unpredictable, as many individuals with limited patchy hair loss experience regrowth within one year, but recurrence is common, and a minority of individuals may progress to total loss of scalp hair, which is called alopecia totalis, or even loss of all hair, which is called alopecia universalis.
For diagnosis, close visual inspection may reveal exclamation point hairs, which are short broken off hairs that are narrower closer to the scalp and therefore look like an exclamation point.
Performing a hair pull test can help confirm active hair loss.
Trichoscopy findings include yellow dots, short vellus hairs, black dots, tapering hairs, and broken hairs.
In addition, individuals with alopecia areata should be assessed for associated conditions, such as autoimmune disorders or stress.