## 4 Discussion  
AA occurs as a result of T-cell mediated autoimmune reaction against hair follicles. The main histopathologic feature of AA is a lymphocytic infiltrate surrounding the follicular bulbs with a peribulbar or intrabulbar \"swarm of bees\" pattern [4]. Affected hair follicles terminate their anagen phase prematurely and regress via the induction of massive apoptosis of the lower portion of the follicle (the catagen phase), which results in a resting hair follicle (the telogen phase) [29]. Genome-wide association studies (GWASs) have greatly facilitated our understanding of the immune pathways involved in AA. Some genes found in AA patients were related to autophagy/apoptosis, regulatory T-cells (T regs) and Janus kinase signaling [15].  
Anecdotal paradoxical hypertrichosis noted during laser epilation for hair removal has generated the interest in the use of laser to stimulate hair growth [30; 31; 32]. There is no study of the 1064 nm ps-Nd:YAG laser in inducing hair regrowth in AA. In our case report, 1064 nm ps-Nd:YAG laser provided beneficial effect for treatment of AT. The mechanism is unknown. It is proposed to be the induction of T-cell apoptosis and enhancement of hair growth. Similar to 308 nm excimer laser and LLLT reported in many studies, laser might promote hair growth by inducing T-cell apoptosis or decreasing inflammation [29]. Another possible mechanism may resemble the action of fractional laser, with a decrease in perifollicular lymphocytic infiltration through'scattering of perifollicular lymphocytes' [29]. The 1064 nm ps-Nd:YAG laser treatment may result in a laser-induced optic breakdown, which are microinjuries, with pockets of intraepidermal necrosis, created without damage to the dermis below or ablative wound to the tissue surface. This process induces cavitation bubbles in the skin, which expand and may generate shock waves to disrupt the tissue and create a healing process that includes lymphocyte infiltrations [28]. These phenomena may scatter perifollicular lymphocyte infiltration and halt disease progression by arresting the hair follicles in the telogen stage of the hair  
Figure 4: Total surface area and the percentage of hair growth on each side of the scalp after laser treatment. (Percentage of hair growth % = total surface area of hair growth on one side of the scalp/total surface area of the same side of scalp.)cycle and increasing the anagen stage. Besides, minor trauma and the wound healing process itself can drive hair growth by de novo hair follicle neogenesis in skin [33; 34].  
In our study, this patient demonstrated greater hair regrowth on the laser treatment plus topical and intralesional steroid use side of the scalp compared with the side with topical and intralesional steroid use alone. It means the picosecond laser may induce a different mechanism to hair regrowth other than the anti-inflammatory effect of steroid. Besides, picosecond laser treatment may have synergistic effect with steroid use. Whether the cytokines or signaling pathways involved in modifying the immunology of the scalp is related to Janus kinase signaling is less understood and needs more investigation. Besides, there is no optimal therapeutic parameter yet, because this is the first study to investigate the picosecond laser treatment for AA. According to many previous reports which were treated by other laser modalities to AA, we modified the treatment protocols with medium energy, once a month in frequency for more than six months. Further studies need to be undertaken to determine the optimal therapeutic parameters.