Clinical Reference / Clinical Atlas / Atopic Dermatitis and Its Analogues (lichen simplex chronicus, prurigo nodularis, picker’s nodules, and erosions and ulcerations secondary to excoriation) | Chondrodermatitis Nodularis Helicis

Atopic Dermatitis and Its Analogues (lichen simplex chronicus, prurigo nodularis, picker’s nodules, and erosions and ulcerations secondary to excoriation) | Chondrodermatitis Nodularis Helicis


A condition of persons of any age, but particularly children with a genetic proclivity for allergic rhinitis and conjunctivitis, and allergic asthma. Intense pruritus induces patients to rub the skin intensely and to scratch furiously, the resultant factitious lesions being erythematous, often scaly, macules, patches, papules, and plaques that tend to become lichenified, eroded, ulcerated, and crusted.


Because in so-called atopic dermatitis none of the skin lesions are primary in the sense that they develop de novo, no statement can be made about chronological sequence, either of the lesions themselves or of the disease itself. For example, if a patient scratches lightly, only reddish discoloration may result, but if scratching is more animated, erosions may come into being. If scratching is furious, ulcerations may be produced. If rubbing is done very lightly, there may be no morphologic manifestations of it. If, however, rubbing is to and fro vigorously for a long period of time, a plaque of lichen simplex chronicus may be formed. If only a discrete site is rubbed persistently with the ball of a finger, a papule or nodule of prurigo nodularis may be brought into being. If a discrete focus is both rubbed and scratched, an eroded or ulcerated papule of picker’s nodule may be brought forth.

Atopic dermatitis, because it results entirely from the effects of rubbing and scratching, may be reversed completely by cessation of external irritation. It may develop transiently if there are paroxysms of rubbing and scratching, and it may be sustained if there is nearly continuous rubbing and scratching.

Integration: Unifying Concept

Atopic dermatitis is factitious dermatitis that occurs in persons who are atopic, to wit, those with a personal or family history of allergic rhinitis, allergic conjunctivitis, or allergic asthma. Such people also have a predilection for allergic urticaria. The state of atopy is determined genetically, and one of the cardinal symptoms of it is pruritus.

Persons who are atopic itch easily and in response to many causes. For example, a person who is not atopic has no difficulty wearing mohair, but on an atopic person a mohair sweater causes extraordinary pruritus, which is greeted by bouts of intense scratching. When an atopic person, whether child or adult, becomes unhinged emotionally at a particular moment, frenzied scratching of wildly pruritic skin may ensue, and, in minutes the entire integument may be transformed by the effects of fingernails. Those effects may range everywhere and into an erythroderma. If, however, the hands of an atopic could be shackled, the skin would be free of signs of rubbing and scratching that have come to be known, erroneously, as atopic dermatitis. This fact was demonstrated experimentally more than 100 years ago.

Lichen simplex chronicus appears in the skin of people who may or may not be atopic, and always as a consequence of mechanical trauma, such as in a variety of circumstances where trauma occurs expectedly. It might, for example, appear beneath the chin where a violin “rests” and on the elbows of a microscopist who “reads” sections of tissue for many hours daily. Lichen simplex chronicus, therefore, is not at all contingent on whether or not a person is atopic; vigorous rubbing of skin over the course of months or years is the common denominator.

The same principle applies to prurigo nodularis. When that condition occurs on the knees of surfers, it is called “surfers nodules,” on the nose or behind the ear as a consequence of the pressure applied to the skin by parts of eyeglasses “granuloma fissuratum,” and as a consequence of a prosthesis utilized because of amputation of a leg, “pressure papule.” When pressure is applied to the helix or the antehelix of an ear damaged by the effects of ultraviolet light, the analogue of prurigo nodularis that develops is called “chondrodermatitis nodularis helicis,” a misnomer. It is not truly a chondrodermatitis, but rather a papule that results from pressure against the cartilage, even pressure as light as is caused by sleeping on an ear.

Adjunctive Diagnostic Test

Detection of elevated serum IgE levels and serum IgE antibodies directed against various inhalant allergens can be accomplished by skin (“prick”) tests.


Click here for an up-to-date discussion of therapeutic management presented in Therapeutic Strategies in Dermatology.


Fig. 8-1

Periorbital erythematous, slightly scaly patches and plaques consequent to vigorous rubbing.

Fig. 8-2

Hemorrhagic crusts atop excoriated papules, and periorbital dusky erythema (“allergic shiners”).

Fig. 8-3

Red patches and plaques, erosions, hemorrhagic and yellow crusts, and scales. Note spared zones are untouched.

Fig. 8-4

Erythematous scaly patches and plaques. Paranasal folds, tip of the nose, and skin below the lower lip are unaffected.

Fig. 8-5

Erythematous papules, many excoriated.

Fig. 8-6

Erythematous, slightly scaly patches and plaques eroded secondary to excoriation.

Fig. 8-7

Erythematous scaly patches and plaques on cheeks. Sites spared are protected from rubbing and scratching.

Fig. 8-8

Erythroderma with erosions covered by hemorrhagic crusts.

Fig. 8-9

Lichenified dusky red plaques interrupted by fissures and covered by scales.

Fig. 8-10

Erythematous patches, plaques, and papules, many eroded and covered by crust. Some plaques are lichenified.

Fig. 8-11

Keratotic papules and plaques.

Fig. 8-12

The lateral aspect of the eyebrows is missing as a consequence of prolonged rubbing (“Herthoge sign”).

Fig. 8-13

Scales and fissures in the retroauricular region.

Individual Lesions

Fig. 8-14

Scale-crusts interrupted by fissures on cheeks (“eczemacraquelé”) and yellow crusts on scalp (“crusta lactea”).

Fig. 8-15

Excoriations covered by crusts in company with lichenification, erythema, and scaling.

Fig. 8-16

Erythematous scaly plaques. The paranasal folds are largely spared because they are indented.

Fig. 8-17

Erosions and hemorrhagic crusts atop lichenified plaques. Signs of scratching are the excoriations.

Fig. 8-18

Erythroderma, erosions covered by hemorrhagic crusts, and lichenification in an obviously atopic person.

Fig. 8-19

Diffuse erythema traversed by linear excoriations and covered by subtle scale-crusts.

Fig. 8-20

Lichenification covered by scales and associated with erosions and ulcerations.

Fig. 8-21

Lichenification surmounted by scales and traversed by fissures.

Fig. 8-22

Erythematous scaly plaques with indistinct borders.

Fig. 8-23

Reticulated hyperpigmentation and lichenification (“dirtyneck”).

Fig. 8-24

Hyperpigmentation and lichenification.

Fig. 8-25

Lichenification and fissures at the angles of the mouth and lichenification of the upper lip.

Fig. 8-26

Erythema, scales, and a fissure of the tip of a toe whose nail is dystrophic.

Fig. 8-27

Dusky erythema, lichenification, and scales on wrinkled skin (juvenile plantar dermatosis). Arches are spared.

Fig. 8-28

Shiny nails result from buffing them by longstanding intense rubbing.

Fig. 8-29

Accentuation of palmar creases (hyperlinearity of palms).

Fig. 8-30

Lichenification of the scrotum.

Fig. 8-31

Linear zones of pallor after a recent scratch of erythematous skin (“white dermographism”).

Fig. 8-32

“White dermographism” induced artifactually by strokes of a blunt-tipped object against erythematous skin.

Fig. 8-33

Hypopigmented scaly patches in an atopic child (“pityriasis alba”).

Fig. 8-34

Hypopigmented scaly patches of pityriasis alba in an atopic child.

Fig. 8-35

Monomorphous nonkeratotic follicular papules.

Lichen Simplex Chronicus

Fig. 8-36

Ill-defined lichenified plaque.

Fig. 8-37

Zones of lichenification.

Fig. 8-38

Lichenified hyperpigmented lesions secondary to rubbing.

Fig. 8-39

Lichenified plaque.

Fig. 8-40

Lichenified plaque.

Prurigo Nodularis

Fig. 8-41

Papules consequent to persistent forceful rubbing of each discrete site.

Fig. 8-42

Hyperpigmented, hypopigmented, and depigmented papules have resulted from the effects of rubbing and scratching.

Fig. 8-43 A

Hyperpigmented and hyperkeratotic papules, and hyperpigmented lichenified plaques consequent to rubbing. The chalky appearance of linear lesions derives from scratching the keratotic surface of papules.

Fig. 8-43 B

Hyperpigmented and hyperkeratotic papules, and hyperpigmented lichenified plaques consequent to rubbing. The chalky appearance of linear lesions derives from scratching the keratotic surface of papules.

Picker's Nodules

Fig. 8-44 A

Papules, many of which are ulcerated and hyperpigmented.

Fig. 8-44 B

Papules, many of which are ulcerated and hyperpigmented.

Fig. 8-45

Ulcers covered by purulence and surrounded by redness and lichenification.

Fig. 8-46

Hyperpigmented ulcerated papules.

New! Additional Images

Fig. 8-50

All of the lesions pictured, namely, macules, papules, erosions, and crusts, resulted from external trauma, to wit, excoriation, the condition being factitious entirely.

Fig. 8-51

The blotchy patches and plaques shown here are secondary to rubbing vigorously.

Fig. 8-52

Ill-defined zone of lichenification, evidenced by thickening of skin whose markings are accentuated, resulted from persistent, firm rubbing; the hemorrhagic crusts derived from animated scratching.

Fig. 8-53

All of the changes depicted, i.e., hemorrhagic crusts atop papules and scale-crusts that cover ill-defined plaques punctuated by fissures, result from scratching and rubbing.

Fig. 8-54

The constellation of shininess, scaliness, accentuation of skin markings, and incipient fissures, known colloquially as “juvenile plantar dermatitis,” is a manifestation of “atopic dermatitis,” resulting as it does, in large measure, from rubbing.