eMedicine Specialties > Dermatology > Reactive & Inflammatory Dermatoses

Lichen Simplex Chronicus

Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), NOVA Southeastern University; Investigator, Hill Top Research, Florida Research Center
Stephen H Mason, MD, Assistant Professor of Dermatology, Medical College of Georgia; Siobahn M Bower, MD, Internal Medicine Resident, Creighton University

Updated: Oct 15, 2009

Introduction

Background

Lichen simplex chronicus (LSC) is thickening of the skin with variable scaling that arises secondary to repetitive scratching or rubbing. Lichen simplex chronicus is not a primary process. Rather, a person senses pruritus in a specific area of skin (with or without underlying pathology) and causes mechanical trauma to the point of lichenification.

A proposed variant of lichen simplex chronicus is lichen amyloidosis. Lichen amyloidosis is described as lichen simplex chronicus in which the keratinocytes have necrosed and formed keratinocytic-derived amyloid in the dermis. The initial insult is pruritus with resultant amyloid formation, rather than the reverse.^{[1,2 ]}

Pathophysiology

Lichen simplex chronicus is found on the skin in regions accessible to scratching. Pruritus provokes rubbing that produces clinical lesions, but the underlying pathophysiology is unknown. Some skin types are more prone to lichenification, such as skin that tends toward eczematous conditions (ie, atopic dermatitis, atopic diathesis). A relationship likely exists between central and peripheral neural tissue and inflammatory cell products in the perception of itch and ensuing changes in lichen simplex chronicus. The possible interplay among primary lesions, psychic factors, and the intensity of pruritus additively influence the extent and severity of lichen simplex chronicus.

A small study looking at lichen simplex chronicus and the use of P-phenylenediamine (PPD)–containing hair dye showed clinically relevant improvement in symptoms after discontinuation of PPD exposure, thus providing a basis for the role of sensitization and contact dermatitis in the etiology of lichen simplex chronicus.

Frequency

International

Exact frequency in the general population is unknown. In one study, 12% of aging patients with pruritic skin had lichen simplex chronicus.

Mortality/Morbidity

No mortality occurs as a result of lichen simplex chronicus. Overall, pruritus of lichen simplex chronicus is mild to moderate, but paroxysms may occur that are relieved by moderate-to-severe rubbing and scratching. Pruritus is usually described as much worse during periods of inactivity, usually at bedtime and during the night. Touch and emotional stress also may provoke pruritus, which is relieved by moderate-to-severe rubbing and scratching.

• Lesions cause little direct morbidity; however, occasionally patients report decreased or interrupted sleep, which affects motor and mental functioning.
• Lichen simplex chronicus SC may become secondarily infected after excoriation.
• Lichen simplex chronicus is often visible enough to cause patients to seek treatment.

Race

No differences are reported in frequency among races, although prior authors claimed lichen simplex chronicus was more common in Asians and African Americans. The appearance of lesions on darker skin sometimes shows follicular prominence. Secondary pigmentary alterations are also more severe in individuals with darker skin.

Sex

Lichen simplex chronicus is observed more commonly in females than in males. Lichen nuchae is a form of lichen simplex that occurs on the midposterior neck and is observed almost exclusively in women.

Age

Lichen simplex chronicus occurs mostly in mid-to-late adulthood, with highest prevalence in persons aged 30-50 years.

Clinical

History

• Patients with lichen simplex chronicus usually describe stable pruritic plaques on one or more areas; however, thickening of the skin occurs on any location that the patient can reach, including the following:
  • Scalp
  • Nape of neck
  • Extensor forearms and elbows
  • Vulva and scrotum^{[3,4 ]}
  • Upper medial thighs, knees, lower legs, and ankles
• Erythema is noted most in early lesions.
• Pruritus is described as worse when patients are still or quiet and as much less or nonexistent when patients are active.
• Pruritus is usually intermittent; the resultant scratching provides temporary relief.
• Patients may have a past medical history of a chronic skin condition or acute trauma. Patients with atopic dermatitis may have lichen simplex chronicus in areas of former atopic outbreaks. Sites of irritant or allergic contact dermatitis, insect bites, or other past minor skin trauma sometimes demonstrate pruritus and, subsequently, lichen simplex chronicus.
• Each palm-sized plaque may have 3 zones. A 2- to 3-cm wide peripheral zone that is barely thickened may have isolated papules. The middle zone has lenticular and hemispheric prurigo papules that may be excoriated. The central zone has the greatest thickening and pigmentary alteration.

Physical

• One or more slightly erythematous, scaly, well-demarcated, lichenified, firm, rough plaques with exaggerated skin lines are noted.
• Pigmentary changes (especially hyperpigmentation) are seen variably as in any dermatitic lesion.
• Rubbing plays a key role in lesion formation and is visualized variably by white scratch marks, erosion, and ulceration from deeper scratching.
• Lichen simplex chronicus is one of the hyperkeratotic processes from which a cutaneous horn may grow.^{[5 ]}
• Patients may scratch lesions de novo when observed. Some patients may start scratching while discussing the itch or describing the lesions.

Plaque of lichen simplex chronicus demonstrating accentuated skin markings. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.

Area of lichen simplex chronicus originally believed to be chronic contact dermatitis. The true nature was revealed when the patient admitted to rubbing this area while watching television. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.

Causes

• Atopic dermatitis results in a higher probability of developing lichen simplex chronicus.
• Insect bites, scars (eg, traumatic, postherpetic/zoster^{[6 ]}), acne keloidalis nuchae,^{[7 ]}xerosis, venous insufficiency, and asteatotic eczema are common factors.
• Psychological factors appear to play a role in the development or exacerbation of lichen simplex chronicus.^{[8 ]}
  • Anxiety has been reported to be more prevalent in patients with lichen simplex chronicus.
  • Neurodermatitis is a term formerly used interchangeably with lichen simplex chronicus, suggesting a role of anxiety or obsession as part of the pathological process of developing lesions.
• Lithium has been linked to lichen simplex chronicus in one reported case. Lichen simplex chronicus was dependent on the administration of lithium as evidenced by the observation that the lichen simplex chronicus remitted when the medication was discontinued and recurred when it was restarted.^{[9 ]}
• A small study looking at lichen simplex chronicus and the use of PPD-containing hair dye showed clinically relevant improvement in symptoms after discontinuation of PPD exposure, thus providing a basis for the role of sensitization and contact dermatitis in the etiology of lichen simplex chronicus.^{[10 ]}
• Long-term exposure to street traffic exhaust has been associated with an increase in the frequency of childhood skin diseases, including lichen simplex chronicus.^{[11 ]}
• Some reserve the diagnosis of lichen simplex for patients who have no known predisposing skin disorder. The term secondary lichenification has been used if the eruption is initiated by a primary dermatosis.

Differential Diagnoses

Workup

Laboratory Studies

• An elevated serum immunoglobulin E level occasionally supports the diagnosis of an underlying atopic diathesis.
• Perform potassium hydroxide examination and fungal cultures to exclude tinea cruris or candidiasis in patients with genital lichen simplex chronicus.

Other Tests

• Patch testing helps exclude allergic contact dermatitis as an underlying primary dermatosis (eg, allergic contact dermatitis to nickel with secondary lichen simplex chronicus) or as a factor in chronicity (eg, allergic contact dermatitis to topical corticosteroids used to treat lichen simplex chronicus).

Procedures

• Frequently, skin biopsy is performed to exclude other disorders, particularly psoriasis or mycosis fungoides (cutaneous T-cell lymphoma) in elderly patients.^{[12 ]}

Histologic Findings

Histologic examination demonstrates hyperkeratosis, acanthosis, spongiosis, and patches of parakeratosis in the epidermis. Epidermal thickening of all layers is noted, with elongation of rete ridges and with pseudoepitheliomatous hyperplasia. Papillary dermal fibrosis with vertical streaking of collagen bundles is characteristic.

A characteristic finding of LSC that is noted on electron microscopy is frequent collagen fibers attached to and just above the lamina basalis.

Treatment

Medical Care

Treatment is aimed at reducing pruritus and minimizing existing lesions because rubbing and scratching cause lichen simplex chronicus.

• Topical steroids are the current treatment of choice because they decrease inflammation and itch while concurrently softening the hyperkeratosis.^{[13,14,15 ]}Because lesions are by nature chronic, treatment most likely is lifelong. On larger and more active lesions, a midpotency steroid may be used to treat acute inflammation. Occasionally, occlusion is used to increase potency and enhance delivery of the agent. Occlusion also provides a physical barrier to the scratching. Midpotency topical steroids are not recommended for thin skin (eg, vulva, scrotum, axilla, face). Direct long-term therapy more at daily use of low-potency nontrophogenic topical corticosteroids. High-potency topical corticosteroids may be used for 3-week courses on thicker-skinned areas.
• Oral antianxiety medications and sedation may be considered in certain patients. According to individual need, treatment can be scheduled throughout the day, at bedtime, or both. Antihistamines such as diphenhydramine (Benadryl) and hydroxyzine (Atarax) are common. Doxepin (Sinequan) and clonazepam (Klonopin) may be considered in appropriate cases.
• For infected lesions, a topical or oral antibiotic can be considered.
• Other topical medications reported to decrease pruritus include doxepin cream^{[16 ]}and capsaicin cream.^{[17 ]}
• One study suggests that topical aspirin/dichloromethane is effective in patients with lichen simplex chronicus who have not responded to topical corticosteroids.^{[18 ]}
• For topical corticosteroid unresponsive patients or those with lesions on thin skin, a few case reports and small studies have shown efficacy of topical immunomodulators tacrolimus and pimecrolimus.^{[19 ]}
• A more investigational treatment for patients who fail conventional therapy is local botulinum toxin injections.^{[20,21 ]}
• A clinical guideline summary from the American College of Obstetricians and Gynecologists, Diagnosis and management of vulvar skin disorders, may be helpful.^{[22 ]}

Consultations

• Consultation with a dermatologist may be considered for severe cases requiring more than topical treatments or to facilitate patch testing.
• Consultation with an allergist may be considered in individuals with multisystemic atopic symptoms.
• Consultation with a psychiatrist may be necessary for patients with severe stress or compulsive scratching.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify the body's immune response to diverse stimuli. Decrease pruritus, thin lichenification, and reduce inflammation.

Clobetasol (Temovate)

Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.

Dosing

Adult

Apply bid for up to 2 wk; not to exceed 50 g/wk

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, or bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in prolonged therapy over large body surface areas; may cause atrophy/striae with prolonged use or in intertriginous (skin fold) areas; in general, not recommended for face

Betamethasone dipropionate cream 0.05%(Diprolene, Betatrex)

For inflammatory dermatoses responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells.

Dosing

Adult

Apply thin film bid for up to 2 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, or bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in prolonged therapy over large body surface areas; may cause atrophy/striae with prolonged use or in intertriginous (skin fold) areas; in general, not recommended for face

Fluocinolone 0.01% or 0.025% cream (Synalar, Synalar HP, Fluonid)

Medium potency topical corticosteroid that inhibits cell proliferation; also is immunosuppressive, antiproliferative, and anti-inflammatory. Flurandrenolide tape (4 mcg/cm²; Cordran tape) combines this potent topical steroid with the benefits of occlusion.

Dosing

Adult

Apply sparingly bid

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, or bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in prolonged therapy over large body surface areas; may cause atrophy/striae with prolonged use or in intertriginous (skin fold) areas; in general, not recommended for face

Triamcinolone 0.025%, 0.1%, 0.5% cream or ointment (Perrigo)

For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Dosing

Adult

Apply thin film bid

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; fungal, viral, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in prolonged therapy over large body surface areas; may cause atrophy/striae with prolonged use or in intertriginous (skin fold) areas; in general, not recommended for face

Hydrocortisone valerate cream 0.2% (Westcort)

An adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. Has mineralocorticoid and glucocorticoid effects, resulting in anti-inflammatory activity.

Dosing

Adult

Apply sparingly to affected areas bid

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in prolonged therapy over large body surface areas

Fluocinonide cream 0.1% or 0.05% (Lidex)

High-potency topical corticosteroid that inhibits cell proliferation. Has immunosuppressive and anti-inflammatory properties.

Dosing

Adult

Apply sparingly bid for up to 2 wk

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, or bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May suppress adrenal function in prolonged therapy over large body surface areas; may cause atrophy/striae with prolonged use or in intertriginous (skin fold) areas; in general, not recommended for face

Antipruritic agents

Oral agents may control itching by blocking effects of endogenously released histamine. Decrease sense of pruritus, sedate/calm patients, and induce sleep. Topical agents stabilize neuronal membrane and prevent the initiation and transmission of nerve impulses, thereby producing local anesthetic action.

Diphenhydramine (Benadryl, Benylin, Diphen, AllerMax)

For symptomatic relief of pruritus caused by release of histamine.

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 400 mg/d
10-50 mg IV/IM q6-8h prn; not to exceed 400 mg/d

Pediatric

12.5-25 mg PO tid/qid or 5 mg/kg/d or 150 mg/m²/d divided tid/qid; not to exceed 300 mg/d
5 mg/kg/d IV/IM or 150 mg/m²/d divided qid; not to exceed 300 mg/d

Interactions

Potentiates effects of CNS depressants; because of alcohol content, do not administer syr to patients taking medications that can cause disulfiramlike reactions

Contraindications

Documented hypersensitivity; MAOIs

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer disease, and urinary tract obstruction; xerostomia may occur

Chlorpheniramine (Chlor-Trimeton)

Competes with histamine or H1-receptor sites on effector cells in blood vessels and respiratory tract.

Dosing

Adult

4 mg PO q4-6h or 8-12 mg SR q8-12h; not to exceed 24 mg/d

Pediatric

<2 years: Not recommended
2-6 years: 1 mg PO divided q4-6h; not to exceed 6 mg/d
6-12 years: 2 mg PO q4-6h or 8 mg SR PO hs; not to exceed 12 mg/d
>12 years: 4 mg q4-6h SR PO hs; not to exceed 24 mg/d

Interactions

CNS toxicity increases with coadministration of other CNS depressants, TCAs, MAOIs, and phenothiazines

Contraindications

Documented hypersensitivity; asthma attacks; narrow-angle glaucoma; symptomatic prostate hypertrophy; bladder-neck obstruction; stenosing peptic ulcer

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause significant confusional symptoms; not for administration in premature or full-term neonates

Hydroxyzine (Atarax, Vistaril)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS.

Dosing

Adult

25-100 mg PO qd/qid

Pediatric

0.6 mg/kg/dose PO q6h

Interactions

CNS depression may increase with alcohol or other CNS depressants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated with clinical exacerbations of porphyria (may not be safe for patients with porphyria); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness

Clonazepam (Klonopin)

For anxiety associated with pruritus. Binds receptors at several sites within the CNS, including the limbic system and reticular formation. Effects may be mediated through GABA receptor system.

Dosing

Adult

0.25-0.75 mg PO bid

Pediatric

Not recommended

Interactions

Phenytoin and barbiturates may reduce effects; coadministration of CNS depressants increase toxicity

Contraindications

Documented hypersensitivity; severe liver disease; acute narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in chronic respiratory disease or impaired renal function; withdrawal symptoms can result from abrupt discontinuation

Pramoxine (Itch-X)

Blocks nerve conduction and impulses by inhibiting depolarization of neurons. Hypoallergenic topical anesthetic. Contains 0.5% menthol and 0.5% camphor, which are nonstaining agents that provide a subjective cooling effect to the skin and are much preferred to rubbing or scratching the skin.

Dosing

Adult

Apply to affected area q3-4h

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; do not apply over large areas; avoid contact with eyes and nose

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with trauma in area to be treated

Doxepin (Sinequan, Zonalon)

Inhibits histamine and acetylcholine activity. Widespread use produces sedation, as does its use in areas of high percutaneous absorption (eg, genitals). Many individuals develop allergy to topical doxepin.

Dosing

Adult

PO: 25-150 mg qhs
Topical: Apply to affected area bid/qid

Pediatric

Not recommended

Interactions

Decreases antihypertensive effects of clonidine but increases effects of sympathomimetics and benzodiazepines; effects of desipramine increase with phenytoin, carbamazepine, and barbiturates

Contraindications

Documented hypersensitivity; urinary retention; acute recovery phase following MI; glaucoma

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease, conduction disturbances, seizure disorders, urinary retention, hyperthyroidism, and patients receiving thyroid replacement; topical preparation may be associated with drowsiness; oral medicine may cause drowsiness lasting until morning, with difficulty arising, even in low doses and particularly in elderly persons; topical medicine may also cause drowsiness

Immunosuppressant Agent

Tacrolimus (Protopic)

Mechanism of action in LSC unknown. Reduces itching and inflammation by suppressing release of cytokines from T cells. Also inhibits transcription for genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, may inhibit release of preformed mediators from skin mast cells and basophils and down-regulate expression of FCeRI on Langerhans cells. Can be used in patients as young as 2 y. Drugs of this class are more expensive than topical corticosteroids. Available as ointment in concentrations of 0.03 and 0.1%. Indicated only after other treatment options have failed.

Dosing

Adult

Apply thin layer to affected skin areas bid and rub in gently and completely; continue treatment for 1 wk after clearing of signs and symptoms
Short-term and intermittent use only

Pediatric

<2 years: Not recommended
2-15 years: Apply 0.03% ointment bid to affected area(s)
>15 years: Administer as adults
Short-term and intermittent use only

Interactions

None reported

Contraindications

Documented hypersensitivity to tacrolimus or components of ointment

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use with occlusive dressings; may be associated with an increased risk of folliculitis in adults; may cause local burning sensation, stinging, soreness, or pruritus (typically improve as lesions heal); for external use only; minimize exposure to natural or artificial sunlight (eg, tanning beds or UVA/B treatment); be sure skin is completely dry before application
Product insert revised in January 2006 and contains a boxed warning stating long-term safety of calcineurin inhibitors has not been established; although a causal relationship has not been established, rare cases of malignancy (eg, skin, lymphoma) have been reported; only the 0.03% ointment is indicated for use in children aged 2-15 y

Immune Modulator

Pimecrolimus (Elidel)

Derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus. Selectively inhibits production and release of inflammatory cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. Resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy not observed in clinical trials, a potential advantage over topical corticosteroids. Indicated only after other treatment options have failed.

Dosing

Adult

Apply topically to affected areas bid
Short-term and intermittent use only

Pediatric

<2 years: Not established
>2 years: Administer as in adults
Short-term and intermittent use only

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Potential exacerbation of existing infection at site of application; may cause burning and irritation; caution with conditions that suppress the immune system (eg, AIDS, cancer)
Product insert revised in January 2006 and contains a boxed warning stating long-term safety of calcineurin inhibitors has not been established; although a causal relationship has not been established, rare cases of malignancy (eg, skin, lymphoma) have been reported; only the 0.03% ointment is indicated for use in children aged 2-15 y

Neuromuscular Blocker Agent, Toxin

Botulinum toxin type A (BOTOX ®)

One of several toxins produced by Clostridium botulinum. Blocks neuromuscular transmission through a 3-step process, as follows: (1) blockade of neuromuscular transmission; botulinum toxin type A (BTA) binds to the motor nerve terminal. The binding domain of the type A molecule appears to be the heavy chain, which is selective for cholinergic nerve terminals. (2) BTA is internalized via receptor-mediated endocytosis, a process in which the plasma membrane of the nerve cell invaginates around the toxin-receptor complex, forming a toxin-containing vesicle inside the nerve terminal. After internalization, the light chain of the toxin molecule, which has been demonstrated to contain the transmission-blocking domain, is released into the cytoplasm of the nerve terminal. (3) BTA blocks acetylcholine release by cleaving SNAP-25, a cytoplasmic protein that is located on the cell membrane and that is required for the release of this transmitter. The affected terminals are inhibited from stimulating muscle contraction. Toxin does not affect synthesis or storage of acetylcholine or conduction of electrical signals along the nerve fiber. Prevents calcium-dependent release of acetylcholine and produces a state of denervation at the neuromuscular junction and postganglionic sympathetic cholinergic nerves in the sweat glands.
Typically, a 24-72 h delay between administration of toxin and onset of clinical effects exists, which terminate in 2-6 mo.
This purified neurotoxin complex is a vacuum-dried form of purified BTA, which contains 5 ng of neurotoxin complex protein per 100 U.
BTA has to be reconstituted with 2 mL of 0.9% sodium chloride diluent. With this solution, each 0.1 mL results in 5 U dose. Patient should receive 5-10 injections per visit.
Must be reconstituted from vacuum-dried toxin into 0.9% sterile saline without preservative using manufacturer's instructions to provide injection volume of 0.1 mL; must be used within 4 h of storage in refrigerator at 2-8°C.
Preconstituted dry powder must be stored in freezer at <5°C.
Injections of BTA must be repeated at varying intervals to maintain long-term results.

Dosing

Adult

Varies by size of lesion; injections should be evenly distributed into multiple sites (10-15), administered in 0.1- to 0.2-mL aliquots, ~1-2 cm apart

Pediatric

Not established

Interactions

Aminoglycosides or drugs that interfere with neuromuscular transmission may potentiate effects

Contraindications

Documented hypersensitivity; infection at injection site

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not exceed recommended dosages and frequencies of administration; presence of antibodies to BTA may reduce effects of therapy; when used for cervical dystonia may cause dysphagia, upper respiratory tract infection, neck pain, or headache; ptosis may occur when used for blepharism or strabismus; weakness of hand muscles and blepharoptosis may occur when used for palmar or facial hyperhidrosis, respectively
When used cosmetically for glabellar lines may cause headache, respiratory tract infection, flu syndrome, blepharoptosis, or nausea

Follow-up

Further Outpatient Care

• Periodically examine patients with lichen simplex chronicus in an outpatient dermatology clinic to evaluate lesions for changes. Perform follow-up examinations more frequently in patients being treated with potent class I topical corticosteroids or oral agents.

Deterrence/Prevention

• Direct patients to stop scratching. Lichen simplex chronicus is worsened or improved depending on the patient's ability to stop scratching.
• Extremes of temperature and/or humidity, psychic stress, and exposure of previously affected or predisposed areas to cutaneous irritants and allergens provoke relapse.
• Discussing individual ways to change habitual scratching is helpful.

Prognosis

• Lesions may clear completely.
• Pruritus may resolve, but some mild scarring and pigmentary changes remain after successful treatment.
• Relapse is more likely in periods of psychic stress or if previously affected skin is stressed by extremes of heat or humidity or by skin irritants or allergens.
• In patients who do not comply with the treatment regimen and scratching cessation, lesions will not improve.

Patient Education

• Direct patients to stop scratching. Lichen simplex chronicus is worsened or improved depending on the patient's ability to stop scratching.
• Discussing individual ways to change habitual scratching is helpful.

Miscellaneous

Medicolegal Pitfalls

• Lichen simplex chronicus may complicate occupational irritant contact dermatitis and allergic contact dermatitis.
• Lichen simplex chronicus may interfere with normal wound healing following surgery in an affected area.
• The Medscape Medical Malpractice and Legal Issues Resource Center may be of interest.

Multimedia

Media file 1: Plaque of lichen simplex chronicus demonstrating accentuated skin markings. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.

Media file 2: Area of lichen simplex chronicus originally believed to be chronic contact dermatitis. The true nature was revealed when the patient admitted to rubbing this area while watching television. Courtesy of San Antonio Uniformed Services Health Education Consortium Dermatology Program.

References

1. Weyers W, Weyers I, Bonczkowitz M, Diaz-Cascajo C, Schill WB. Lichen amyloidosus: a consequence of scratching. J Am Acad Dermatol. Dec 1997;37(6):923-8. [Medline].

2. Weyers W. [Lichen amyloidosus--disease entity or the effect of scratching]. Hautarzt. Mar 1995;46(3):165-72. [Medline].

3. Ball SB, Wojnarowska F. Vulvar dermatoses: lichen sclerosus, lichen planus, and vulval dermatitis/lichen simplex chronicus. Semin Cutan Med Surg. Sep 1998;17(3):182-8. [Medline].

4. Pleimes M, Wiedemeyer K, Hartschuh W. [Lichen simplex chronicus of the anal region and its differential diagnoses : A case series.]. Hautarzt. Mar 7 2009;[Medline].

5. Khaitan BK, Sood A, Singh MK. Lichen simplex chronicus with a cutaneous horn. Acta Derm Venereol. May 1999;79(3):243. [Medline].

6. Gerritsen MJ, Gruintjes FW, Andreissen MA, van der Valk PG, van de Kerkhof PC. Lichen simplex chronicus as a complication of herpes zoster. Br J Dermatol. May 1998;138(5):921-2. [Medline].

7. Burkhart CG, Burkhart CN. Acne keloidalis is lichen simplex chronicus with fibrotic keloidal scarring. J Am Acad Dermatol. Oct 1998;39(4 Pt 1):661. [Medline].

8. Woodruff PW, Higgins EM, du Vivier AW, Wessely S. Psychiatric illness in patients referred to a dermatology-psychiatry clinic. Gen Hosp Psychiatry. Jan 1997;19(1):29-35. [Medline].

9. Shukla S, Mukherjee S. Lichen simplex chronicus during lithium treatment. Am J Psychiatry. Jul 1984;141(7):909-10. [Medline].

10. Chey WY, Kim KL, Yoo TY, Lee AY. Allergic contact dermatitis from hair dye and development of lichen simplex chronicus. Contact Dermatitis. Jul 2004;51(1):5-8. [Medline].

11. Ising H, Lange-Asschenfeldt H, Lieber GF, Weinhold H, Eilts M. [Effects of long-term exposure to street traffic exhaust on the development of skin and respiratory tract diseases in children]. Schriftenr Ver Wasser Boden Lufthyg. 2003;81-99. [Medline].

12. Thaipisuttikul Y. Pruritic skin diseases in the elderly. J Dermatol. Mar 1998;25(3):153-7. [Medline].

13. Brunner N, Yawalkar S. A double-blind, multicenter, parallel-group trial with 0.05% halobetasol propionate ointment versus 0.1% diflucortolone valerate ointment in patients with severe, chronic atopic dermatitis or lichen simplex chronicus. J Am Acad Dermatol. Dec 1991;25(6 Pt 2):1160-3. [Medline].

14. Datz B, Yawalkar S. A double-blind, multicenter trial of 0.05% halobetasol propionate ointment and 0.05% clobetasol 17-propionate ointment in the treatment of patients with chronic, localized atopic dermatitis or lichen simplex chronicus. J Am Acad Dermatol. Dec 1991;25(6 Pt 2):1157-60. [Medline].

15. Geraldez MC, Carreon-Gavino M, Hoppe G, Costales A. Diflucortolone valerate ointment with and without occlusion in lichen simplex chronicus. Int J Dermatol. Nov 1989;28(9):603-4. [Medline].

16. Drake LA, Millikan LE. The antipruritic effect of 5% doxepin cream in patients with eczematous dermatitis. Doxepin Study Group. Arch Dermatol. Dec 1995;131(12):1403-8. [Medline].

17. Kantor GR, Resnik KS. Treatment of lichen simplex chronicus with topical capsaicin cream. Acta Derm Venereol. Mar 1996;76(2):161. [Medline].

18. Yosipovitch G, Sugeng MW, Chan YH, Goon A, Ngim S, Goh CL. The effect of topically applied aspirin on localized circumscribed neurodermatitis. J Am Acad Dermatol. Dec 2001;45(6):910-3. [Medline].

19. Kelekci HK, Uncu HG, Yilmaz B, Ozdemir O, Sut N, Kelekci S. Pimecrolimus 1% cream for pruritus in postmenopausal diabetic women with vulvar lichen simplex chronicus: A prospective non-controlled case series. J Dermatolog Treat. Apr 11 2008;1-5. [Medline].

20. Heckmann M, Heyer G, Brunner B, Plewig G. Botulinum toxin type A injection in the treatment of lichen simplex: an open pilot study. J Am Acad Dermatol. Apr 2002;46(4):617-9. [Medline].

21. Messikh R, Atallah L, Aubin F, Humbert P. [Botulinum toxin in disabling dermatological diseases]. Ann Dermatol Venereol. May 2009;136 Suppl 4:S129-36. [Medline].

22. [Guideline] American College of Obstetricians and Gynecologists. Diagnosis and management of vulvar skin disorders. National Guideline Clearinghouse. May 2008.

23. Ferry AP, Kaltreider SA. Lichen simplex chronicus of the eyelid. Arch Ophthalmol. Jun 1999;117(6):829-31. [Medline].

24. Frithz A, Lagerholm B. Lichen simplex chronicus Vidal: comparative submicroscopic aspects of acanthotic disorders. Acta Derm Venereol. 1977;57(2):103-11. [Medline].

25. Inoko M, Konishi T, Matsusue S, Kobashi Y. Midmural fibrosis of left ventricle due to selenium deficiency. Circulation. Dec 8 1998;98(23):2638-9. [Medline].

26. Jacob CI, Patten SF. Strongyloides stercoralis infection presenting as generalized prurigo nodularis and lichen simplex chronicus. J Am Acad Dermatol. Aug 1999;41(2 Pt 2):357-61. [Medline].

27. Kinsella LJ, Carney-Godley K, Feldmann E. Lichen simplex chronicus as the initial manifestation of intramedullary neoplasm and syringomyelia. Neurosurgery. Mar 1992;30(3):418-21. [Medline].

28. O'Keefe RJ, Scurry JP, Dennerstein G, Sfameni S, Brenan J. Audit of 114 non-neoplastic vulvar biopsies. Br J Obstet Gynaecol. Oct 1995;102(10):780-6. [Medline].

Keywords

lichen simplex chronicus, neurodermatitis circumscripta, circumscribed neurodermatitis, lichen simplex chronicus of Vidal, LSC, lichen amyloidosis, atopic dermatitis, lichen simplex, secondary lichenification, atopic diathesis, lichen simplex, cutaneous horn, lichenification

Contributor Information and Disclosures

Author

Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), NOVA Southeastern University; Investigator, Hill Top Research, Florida Research Center
Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, and Canadian Dermatology Association
Disclosure: Nothing to disclose.

Coauthor(s)

Stephen H Mason, MD, Assistant Professor of Dermatology, Medical College of Georgia
Stephen H Mason, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American Society for Dermatologic Surgery, Skin Cancer Foundation, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Siobahn M Bower, MD, Internal Medicine Resident, Creighton University
Siobahn M Bower, MD is a member of the following medical societies: American College of Physicians and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

James J Nordlund, MD, Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine
James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-San Antonio
Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)