Lichen striatus often appears as a sudden eruption of small papules on an extremity. The papules are usually asymptomatic, reaching maximum involvement within several days to weeks. When lichen striatus patients are symptomatic, the most common complaint is pruritus. Lichen striatus is self-limited, but it may resolve with postinflammatory hyper or hypopigmentation.
Lichen striatus appears as a continuous or interrupted, linear band consisting of small (1- to 3-mm) pink, tan, or skin-colored lichenoid papules. The papules may be smooth, scaly, or flat topped. Occasionally, a vesicular component is present. The band may range from a few millimeters to 1-2 cm wide and extends from a few centimeters to the full length an extremity. The lesions are usually unilateral and single on an extremity along the lines of Blaschko. [21, 15] In rare cases, they may be bilateral or occur in multiple parallel bands. [25, 26, 27] The lesions are most commonly located on a proximal extremity and less commonly on the trunk, head, neck, or buttock. A recent study suggests that facial lichen striatus is underreported and may represent up to 15% of all cases.  In darkly pigmented individuals, eruptions may appear as a bandlike area of hypopigmentation. Note the images below.
Nail involvement is uncommon in lichen striatus, with approximately 40 reported cases worldwide. [28, 3, 29] Nail lesions may occur before, after, or concurrently with the skin lesions. They may also be the only area of involvement. Often, only the medial or lateral portions are involved, and involvement is almost always restricted to one single nail. Nail changes may include longitudinal ridging, splitting, onycholysis, nail loss, hyperkeratosis of the nail bed, thinning or thickening of the nail plate, nail pitting, onychodystrophy, punctuate and striate leukonychia, and overcurvature of the nail plate. [30, 31] Dermoscopic examination may reveal sharply marginated, deep-white structures resembling Wickham striae and brown, keratotic, cerebriform structures with pinpoint red dots surrounded by a pale halo. 
The etiology of lichen striatus is unknown. Many etiologic or predisposing factors are suggested for lichen striatus. The most commonly accepted hypothesis is the combination of genetic predisposition with environmental stimuli.
Atopy may be a predisposing factor. One group reported that 85% of patients with lichen striatus have a family history of atopic dermatitis, asthma, or allergic rhinitis. However, another report disputes this claim, stating that the incidence of atopy is no greater than that of the general population.
An autoimmune response may also be involved in lichen striatus. A case of lichen striatus has been reported during pregnancy, and it has been postulated that the pregnancy may have triggered an autoimmune response leading to the appearance of the eruption.  Lichen striatus has also been reported concurrently with vitiligo  and after adalimumab  and etanercept.  Some reports simply suggest that lichen striatus is an inflammatory skin disease mediated by T cells. It has been reported 17 months after allogenic peripheral blood stem cell transplantation. 
An environmental (infectious or trauma  ) etiology has also been suggested. Familial cases, [13, 14] outbreaks among unrelated children in a shared living environment, and a possible seasonal variation suggest an environmental agent, such as a virus. Support of infectious involvement includes elevations of interleukin 1-beta in lichen striatus biopsy specimens.  However, results of viral testing have not conclusively proven this association. In addition, familial episodes of lichen striatus are not always simultaneous, signifying a possible genetic predisposition as a second explanation. Lichen striatus has been reported to occur shortly following immunization with BCG and hepatitis B vaccination, after UV exposure from a tanning bed,  following a prick from a pineapple leaf, after a bite by a bumblebee,  and after varicella and influenza infection. [18, 19]
One group of authors has suggested that epigenetic mosaicism may be involved. They hypothesize that lichen striatus is triggered by an immunologic reaction to an infection, which triggers methylation or demethylation of a partially silenced genomic element in predisposed patients.  A report of concurrent pityriasis rosea and lichen striatus may lend support to this theory. Human herpes viruses 6 and 7 have been implicated in the etiology of pityriasis rosea. The concurrent lichen striatus eruption may have manifested after being triggered by this viral infection. 
Lesions of lichen striatus follow the lines of Blaschko. [21, 15, 22, 23, 24] Blaschko lines are thought to be embryologic in origin. They are believed to be the result of the segmental growth of clones of cutaneous cells or the mutation-induced mosaicism of cutaneous cells. In lichen striatus, an acquired event (eg, viral infection) may allow an aberrant clone of cutaneous cells to express a new antigen, resulting in the phenotypic skin changes.
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