Neonatal Occipital Alopecia (NOA) is a type of non-scarring, localized alopecia, which occurs temporarily on the occiput of babies between the ages of two and three months.
In a band-like shape or oval alopecic patch, its lower margin is sharp and consists of a band of hair extending to the nape, but the upper limit is merged with the hair of the vertex in a less marked manner. The cause of this entity is thought to be a combination of physiologic telogen effluvium and, possibly, localized pressure owing to the neonate’s sleeping position
What causes NOA?
For many years, the etiology of NOA has been thought to be friction. Recently it was found that NOA is related to the physiological hair shedding.
It was not associated with the baby’s sleeping position, but was significantly associated with the maternal parturition age, the delivery method, and the gestation. Pregnancy-related factors, such as non-elderly gravida, non-Caesarean-section delivery, and enough gestational age, are also associated with NOA.
It rarely shows severe symptoms that need treatment, and it improves spontaneously. Therefore, many physicians do not pay attention to this disease.
This could occur if:
- There are cases with a history of obstetric diseases, such as caput succedaneum or cephalhematoma
- Cases in which the hair loss occurred in areas other than the occiput
- Cases in which alopecia was persistently present for more than one year after birth are seen besides
Experts also state that that there was no significant correlation between the sleeping position of infants and the occurrence of NOA
Studies and conclusions
The hair development on the fetal scalp begins about after nine or twelve weeks of the gestation and the whole scalp is covered with anagen hair by 18-20 weeks of gestation.
Although the hair roots go through the catagen and then the telogen phases in a progressive manner, i.e. from frontal to parietal areas at 26-28 weeks of gestation, those in the occipital area are not involved in this process and remain in the anagen phase due to an operative signal, delaying the onset of telogen until close to term.
Later, these hairs abruptly go into the telogen phase and are inevitably shed 8-12 weeks after birth. If the pregnant process does not progress properly, we suggest that the signal may be interrupted, leading to the absence of NOA. Based on the changes in different phases of the follicular cycle, Headington recently classified the telogen effluvium into five functional types. Of them, he proposed the “delayed anagen release”.
What is it?
According to this, some follicles remain in prolonged anagen until they abruptly enter telogen. He also suggested that the telogen effluvium of the postpartum woman is the most notable alopecia associated with delayed anagen release. In the current study, there was no significant correlation between NOA and the maternal telogen effluvium. Therefore, despite having a similar mechanism for hair loss and a tendency to occur around the same time, these conditions are presumed to develop independently, i.e. without a common operative signal.
A sufficient amount of anagen hair might replace the alopecia site after some telogen hair shedding occurs in some infants. Moreover, since there are mild symptoms and can be resolved spontaneously in most cases of NOA, it is assumed that parents are not aware of this disease.
As mentioned earlier, the NOA has been reported to be relatively higher in fair-complexioned neonates. The important diagnoses of NOA to be considered are pressure alopecia, the halo scalp ring, and alopecia areata. Diagnosis of telogen effluvium is made based on the personal history or clinical manifestation and may be assisted through several tests, such as the hair pulling test, trichogram, and scalp biopsy.
Originally posted 2019-03-21 12:17:37.
Tagged with: Baby hair