Halo Scalp Ring: An Annular Alopecia Associated with Birth Injury

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A 24-month-old boy presented with an annular hairless patch on his left occiput. His parents recalled that he had shown the round hairless patch at birth, which spontaneously and partially recovered from the central area, although the annular hairless patch has remained (Fig. 1A, B). He was a full-term infant with 3.1 kg birth weight and was delivered by vagina. Induction delivery was performed due to the labor that lasted more than 17 hours. Additionally, forceps or other instruments was not used during delivery. Furthermore, the boy had no history of caput succedaneum at birth, and his skull X-ray showed no gross bony abnormalities. Skin biopsy was performed from the hairless patch and normal scalp; compared to the normal patch, the histopathologic findings from the hairless patch showed miniaturized hair follicles and necrosis of the fat layer. Perifollicular fibrosis was not observed on the hairless patch (Fig. 2). Therefore, the patient’s hairless patch was diagnosed as halo scalp ring (HSR), which was treated with 3% topical minoxidil solution for 10 months and resulted in almost complete recovery (Fig. 1C). We received the patient’s consent form about publishing all photographic materials.

Fig. 1
An annular hairless patch was observed on the left occiput at first visit (A, B). The hairless patch almost recovered after 10 months (C).

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Fig. 2
The miniaturized hair follicles without perifollicular fibrosis, and the necrosis of the fat layer were observed on the hairless patch (A), but not in the normal scalp (B). Inlet: High-power view of the subcutaneous layer (H&E, ×20, Inlet: H&E, ×100).

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HSR, which was first described in 1984, is an annular scalp alopecia that arises during the neonatal period1. It is also frequently attributed to caput succedaneum, in addition to prolonged labor, premature rupture of amniotic membranes, vaginal or instrumental delivery, vertex presentation, and first delivery. HSR is believed to be caused by the ischemic damage resulting from prolonged periods of pressure on the fetal scalp during delivery2. In the current case, after the rupture of the amniotic membrane, the fetal scalp immediately received pressure from the cervix, and might have acquired a ring-shaped ischemic zone over time. The location of HSR is variable, which may be associated with the variation in fetal presentation. In our case, ischemic damage might have occurred in the area dominated by the occipital and posterior auricular arteries. HSR usually presents as a temporary and non-scarring alopecia, but may also appear as a permanent scarring depending on the degree of hypoxic damage to the fetal scalp3. The histopathologic findings of the patient suggest of a non-scarring alopecia, and the lesion showed recovery clinically. HSR is a benign condition with no systemic involvement, which requires no further work-up for the central nervous system4. Differential diagnoses include aplasia cutis congenita, neonatal occipital alopecia, pressure alopecia, and alopecia areata. Among them, aplasia cutis congenita presenting as scarring alopecia in infants, may require further evaluation5.

We believe that HSR should be considered as a birth injury-related alopecia, which is a benign condition that has no systemic associations. This case reports an HSR that clinically showed recovery after topical minoxidil treatment and histologically showed miniaturized hair follicle.