## 1 Introduction  
Alopecia areata (AA) is a polygenic autoimmune disease causing nonscarring hair loss mediated through chronic hair follicle inflammation. The lifetime risk of this condition is about 2.1% of the world population [1; 2]. Although patchy AA (patchy hair loss involving <40% of the scalp) is the most common presentation, it can progress to complete loss of scalp hairs (alopecia totalis (AT)), or the entire body hairs (alopecia universalis (AU)) [1; 3]. Although spontaneous remission may occur in patchy AA within one year, patients with more extensive hair loss, including AT and AU, do not commonly experience remission and are difficult to treat [1; 4; 5].  
Traditionally, the first-line treatments for mild patchy AA include topical and intralesional steroids [6; 7; 8], but both increase the risk of skin atrophy over the treated sites [9]. Systemic steroids are used in moderate to severe AA [10]. Arguments against the use of systemic steroids include relapses, adverse side effects, and ineffectiveness in the case of AT or AU [11; 12; 8; 13]. Topical immunotherapy with use of sensitizing agent, such as diphenylcyclopropenone (DPCP) or squaric acid dibutylester (SADBE),is the treatment option for severe AA (>50% scalp involvement) or chronic relapsing AA [8; 14]. Dermatitis, blistering, urticaria, and depigmentation are potential adverse effects [1]. Oral Janus kinase inhibitors (tofacitinib, ruxolitinib) are being popularly investigated as potential treatment for AA in recent years. The response rate revealed in one meta-analysis was impressive (72.4%), with mean time to initial and complete hair growth about 2.2 and 6.7 months [8; 15; 16]. Various response rates of phototherapy for treatment of AA, including narrow-band ultraviolet (UV) B [17; 18], topical psorlaen-UVA [19; 20], and UVA-1 [21], have been reported. However, the long-term potential oncogenic effect on treated areas is a limiting factor of phototherapy [22].  
Due to the side effects and high relapse rates of traditional medical treatment and phototherapy, numerous types of lasers have been explored for alternative treatment of AA [4], including the 308 nm excimer laser or light, low-level laser therapy (LLLT) or photomodulation therapy and fractional lasers. Each of these lasers/lights has different mechanisms and variable effects on hair growth.  
Recently, novel picosecond duration lasers (ps-lasers) have been developed for the treatment of unwanted tattoos [23; 24; 25; 26; 27]. The picosecond pulse duration is 10 times shorter than the traditional q-switched nanosecond devices. This shorter pulse delivery creates more photomechanical shock than the nanosecond duration, with greater possibility of shattering ink or pigment, and thus requires less treatments to remove tattoos than the longer-nanosecond devices [28]. Since 2013, ps-lasers have become commercially available [23]. The most popular ones for clinical use are picosecond 755 nm alexandrite laser (ps-Alex laser) and picosecond 1064/532 nm Nd:YAG laser (ps-Nd:YAG laser).  
To date, no studies have evaluated the effects of the novel 1064 nm picosecond Nd:YAG laser (ps-Nd:YAG) for the treatment of AA. The objective of this study was to evaluate the efficacy of 1064 nm ps-Nd:YAG laser on hair growth of one patient with AT.