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Thomas J. Joly, MD, PhD · Mark L. Levine, MD
Duke-Elder's classic ophthalmology textbook classifies brow and lash abnormalities into three main categories1:
This tutorial will discuss the major clinical entities within each of these categories.
Hypertrichosis, abnormal increase in the number (polytrichosis) or length (trichomegaly) of hairs, can affect the lashes, brows, or lanugo hair of the lids (Slide 1). Ciliary polytrichosis is an acquired hypertrichosis in which irregularly arranged new lashes sprout as side-buds from preexisting cilia. These lashes are typically stunted, misdirected, and irregularly spaced within the normal rows of cilia. They are thought to arise in reaction to an inflammatory stimulus. The etiology of acquired hypertrichosis lanuginosa, abnormal increase in the fine lanugo hair, is unclear but the condition has been associated with serious illness, internal malignancies,2 and endocrine disorders. The disorder affects the lids and nose primarily, but can be generalized to the entire body. It can rarely be seen as a familial, congenital trait.1,3
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Congenital distichiasis is the abnormal development of meibomian glands into hair follicles. In this case, the lashes form an evenly spaced additional row in the location of the meibomian gland orifices. Acquired distichiasis can also occur in reaction to a noxious stimulus, whereby the normal meibomian sebaceous glands are transformed into hair follicles by mechanical or chemical stimuli.4 Synophrys is excessive hair growth over the glabella so that the two eyebrows are continuous. This condition is seen in a number of syndromes, including congenital hypothyroidism, Waardenburg syndrome, Down syndrome, kwashiorkor, and Brachmann-de Lange syndrome. Nevoid hypertrichosis is the association of bundles of coarse, elongated hairs with nevi. Ciliary trichomegaly is usually congenital and has been associated with a variety of ocular (retinal pigmentary degeneration, cataract) and systemic anomalies (dwarfism, mental retardation, spherocytosis, kwashiorkor, AIDS, and Brachmann-de Lange syndrome).1,3,5 Trichomegaly is also an adverse effect of topical latanoprost for the treatment of glaucoma.6
Hypotrichosis, abnormally sparse hair, is usually an acquired condition secondary to alopecia, or hair loss. Loss of lashes due to destruction of the follicles is termed madarosis. Alopecia areata, hair loss in a circumscribed area of the scalp, can include the brows and lashes, as does alopecia totalis, total hair loss of the head, and alopecia universalis, total hair loss of the body. An immunopathologic mechanism has been implicated for alopecia areata; the disorder has been associated with diabetes, vitiligo, atopy, pernicious anemia, Hashimoto thyroiditis, and AIDS. It has been associated with sympathetic nervous system disorders and can accompany Horner syndrome. Alopecia is associated with uveitis in sympathetic ophthalmia and Vogt-Koyanagi-Harada syndrome. Alopecia artefacta is the result of purposeful epilation of the brow to sculpt its contours, and trichotillomania is irresistible self-epilation as a manifestation of an underlying psychiatric condition.1,3,5
Hair loss in the lateral end of the brows (Hertoghe sign) is associated with a variety of systemic disorders. Syphilis, which can also cause madarosis, is the classic infectious disease causing lateral brow loss. Other infectious causes include leprosy, tuberculosis, severe acute bacterial infections such as scarlet fever, and viral infections such as smallpox, measles, and hepatitis. Endocrine disorders, including hypothyroidism and hyperthyroidism, as well as certain dermatoses such as keratosis pilaris atrophicans faciei and keratosis pilaris decalvans, can cause this pattern of brow alopecia. It has also been described in association with Meige syndrome.7 Total brow and lash loss can be secondary to acanthosis nigricans, hypopituitarism, malnutrition, and emotional shock.1,3
If scarring results in destruction of hair follicles, cicatricial madarosis results. This is common following trauma, ulcerative blepharitis, trachoma, and basal cell carcinoma. It can also occur in lupus erythematosus, scleroderma, irradiation, and, occasionally, chronic blepharitis or chalazion.
Trichiasis is misdirection of the lashes so that they turn in toward the globe, often causing chronic corneal irritation. Scarring secondary to trauma often causes this condition. Trachoma, in which softening and thickening of the tarsal plate combines with distortion of the follicles by cicatrization, may also cause trichiasis. Other causes of trichiasis include cicatricial pemphigoid, Stevens-Johnson syndrome, chemical burns, chalazion, ulcerative blepharitis, and lid margin neoplasm. Entropion and distichiasis also result in cilia directed toward the globe.1,3,8
Cilia incarnata is an anomaly in which the lash grows obliquely out of the follicle so that it is incarcerated under the epithelium, causing local irritation, granulation, and papule formation. Treatment includes excision and epilation of the offending lash. In one variant, cilium incarnatum internum, the lash grows posteriorly under the tarsal conjunctiva until it pierces through into the cul-de-sac.1,3,9
Various trichoses can cause secondary misdirection of the lashes. Trichorrhexis nodosa is characterized by nodes of longitudinal splitting of the hair shaft resulting in stunted growth. Monilethrix is a genetic condition in which hair shafts have areas of swelling and areas of constriction resulting in a beaded appearance and fragile, brittle cilia. Pili torti is a spontaneous or inherited condition in which lashes as well as cilia elsewhere are overly curved, twisted, and fragile.1,3
Congenital lack of hair pigmentation, leukotrichia, occurs in conditions such as albinism. Acquired loss of pigmentation is termed canities if generalized or poliosis if localized. Senile canities often affects the brows and lashes as hair bulb melanocytes progressively lose tyrosinase activity with age. Premature poliosis can be associated with vitiligo. Of special ophthalmologic interest is the lash poliosis and lid vitiligo associated with diffuse uveitis, dysacusis, and alopecia composing the Vogt-Koyanagi-Harada syndrome. Lash poliosis has also been associated with sympathetic ophthalmia and with Alezzandrini syndrome of unilateral retinal degeneration, vitiligo, and poliosis. Poliosis can be an adverse effect of some medications, including chloroquine and topical thiotepa. Poliosis neurotica is poliosis secondary to extreme emotional stress or a nervous disturbance.1,3
Treatment of alopecia varies with the nature of the alopecia itself. Noncicatricial alopecia will often resolve spontaneously with resolution of the underlying condition. Local subcutaneous and systemic corticosteroids have been used to stimulate regrowth in alopecia areata.1,4 Recently, topical latanoprost has been reported to enhance the regrowth of lashes in noncicatricial alopecia.10 In more permanent forms of alopecia, eyebrows have been reconstructed using free scalp grafts, and various techniques have been described for grafting follicles into the lid margins to serve as lashes.1
Trichiasis and distichiasis must be treated on an individual case basis. Epilation can serve as a temporary measure for trichiasis or distichiasis involving one or a small number of lashes. But generally, the offending lashes quickly grow back. Epilation with cryotherapy of the follicles to prevent regrowth can produce longer-lasting results. Repeated freezing to -20° C results in optimum destruction of the hair follicle with minimum destruction of surrounding tissue. Destruction of individual follicles can be accomplished by inserting an electrolysis needle along an aberrant hair shaft to its base and passing current for approximately 15 seconds. Alternatively, argon laser energy can be applied coaxial to each hair follicle by everting the lid margin and burning to a depth of 2 mm. More extensive trichiasis, distichiasis, and entropion can be addressed surgically with various techniques that restructure or reposition the offending lid margin. Full thickness block resection can effectively treat a smaller area of cicatricial trichiasis. Retractor advancement and lateral tightening procedures will evert entropic lid margins. Lid-splitting procedures with cryotherapy to the posterior lamella can be used to treat distichiasis, while anterior lamella recession can redirect anterior trichiatic cilia.4