SYMPOSIUM: DERMATOLOGY

Hair loss in infancy and conventionally divided into two regions: the upper permanent
part made up of the infundibulum and isthmus and the lower

childhood cycling (growing and then regressing) part consisting of the hair
bulb and suprabulbar region (Figure 1).
Hair follicle stem cells reside in the bulge region of the
Caroline Champagne isthmus. Evidence suggests that the lower part of the hair fol-
Noor Alwash licle is immunologically ‘privileged’ (a site that is not subject to
typical immune surveillance). The hair cycle is made up of an
Minal Patel anagen (growth) phase followed by a catagen (involution)
Nisha Arujuna phase and then a telogen (resting) phase. (Figures 2 and 3). The
Paul Farrant hair is eventually shed through an active process called
‘exogen’.
The hair passes through at least two hair cycles in utero in a
Abstract wave-like synchronised fashion from the frontal hair line.
Hair problems can cause considerable anxiety to both children and Lanugo downy hair is replaced by vellus hair and then vellus
their parents. This article discusses hair growth and cycling, the com- hair is replaced by thicker terminal hair. However, in the oc-
mon presentations of hair loss in infancy and childhood and an cipital area of the scalp, hair cycling is delayed until after birth,
approach to diagnosis. This information will help equip the reader to which can give rise to a patch of occipital hair loss in the
manage common types of hair loss in the paediatric setting. neonatal period. Hair cycling up to this stage is synchronised,
thereafter the hair follicles starts cycling independently.
Keywords alopecia; alopecia areata; aplasia cutis; hair loss; hair
Throughout childhood there is gradual transition from vellus
shaft disorders; telogen effluvium; tinea capitis; triangular alopecia;
(soft, short, unmedullated and usually non-pigmented) to in-
trichotillomania
termediate and then terminal hairs (longer, coarser, medullated
and pigmented).

Introduction
Evaluation of a child with hair loss
Hair problems in children are common and can cause consider-
able anxiety to both parents and children. Conditions such as History
alopecia areata and trichotillomania can present in adults as well It is important to establish whether the hair was normal at birth,
as in children, however, in children further consideration must when the hair loss began and whether this was a diffuse or
be given to rarer congenital and hereditary causes of hair loss patchy loss or failure to grow. Symptoms such as itch or
which can occasionally present as part of a multisystem syn- burning are often associated with infection or infestation (both
drome. A systematic approach to evaluating hair disorders in common) or inflammation (rare). History of teeth and nail
children is crucial to ensure that you make the correct diagnosis. development should be obtained as well as problems with heat
and sweating if an ectodermal dysplasia is suspected. Other
Normal hair growth important areas to ask about in the history include cutaneous
lesions and rashes, as well as the general health of the child and
At nine weeks of gestational age the first hair follicles start to achievement of developmental milestones. A family history of
appear and are fully established by 22 weeks. Hair follicles are hair problems is likely to be relevant in inherited conditions but
is also important when considering infective causes such as
tinea capitis.
Caroline Champagne MBChB MSc MRCP is a Consultant with the
Dermatology Department, The Churchill Hospital, Oxford University
Hospitals NHS Trust, Oxford, UK. Conflicts of interest: none Clinical examination
declared. Clinical examination should include an assessment of the pattern
Noor Alwash MBBS MRCP is Clinical fellow in the Dermatology and extent of hair loss. If a patchy alopecia is apparent, it is
Department, Brighton General Hospital, Brighton and Sussex important to determine whether there are patent follicular ostia
University Hospitals, Brighton, UK. Conflicts of interest: none (openings where hair usually comes out of) or whether these are
declared. lost, suggesting a scarring condition. Peri-follicular erythema
Minal Patel MBBS MRCP is Clinical fellow in the Dermatology (redness), follicular hyperkeratosis (scale around the base of
Department, Brighton General Hospital, Brighton and Sussex hairs), pustules or swelling are all signs that suggest an inflam-
University Hospitals, Brighton, UK. Conflicts of interest: none matory process. Abnormalities in the skin, nails and teeth should
declared. be noted as well as any syndromic features.
Nisha Arujuna (MBBS MRCP) is a Registrar in the Dermatology The hair pull technique can be used to assess hair shedding in
Department, Worthing Hospital, Worthing, UK. Conflicts of interest: generalised hair loss as well as disease activity in focal condi-
none declared. tions. An informal hair pull comprises of passing a hand with
splayed fingers through the hair and pulling up through the hair
Paul Farrant MBBS BSc FRCP is a Consultant Dermatologist in the
Dermatology Department, Brighton General Hospital, Brighton and to see if any hairs come away. A more formal test involves
Sussex University Hospitals, Brighton, UK. Conflicts of interest: none grasping a group of hairs (30e60) from a 1 cm  1 cm area,
declared. twisting loosely, then, holding at the base of the hairs between

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 SYMPOSIUM: DERMATOLOGY

Figure 3 Telogen hair with de-pigmented bulb and anagen hair

showing pigmented bulb enclosed within its root sheath.
Figure 1 Schematic diagram of basic components of the hair follicle.

Potential hair pull findings

Condition Positive hair pull findings

Telogen effluvium Increased telogen hairs extracted from all

areas, hairs are often normal length
Alopecia areata Increased telogen hairs or dystrophic
hairs from affected areas
Primary scarring Increased anagen hairs extracted
alopecias
Loose anagen Painless extraction of dysplastic anagen
syndrome hairs (may lack root sheath and have
a hockey stick appearance)
Short anagen Increase in telogen hairs;
syndrome hairs are often short

Table 1

Microscopy and scalp biopsies

Light microscopy of hairs trimmed at their base should be used
for the investigation of possible hair shaft disorders. Scanning
electron microscopy will provide even more detailed images of
Figure 2 Stages of the hair cycle. hair shafts but expertise and availability limits its use. Scalp bi-
opsies sent for both horizontal and vertical sectioning may give
useful clues to the underlying cause but requires at least two skin
finger and thumb, gently applying a tractional force at 90 degrees
biopsies and it should be avoided in children if possible.
from the scalp. For focal conditions, it can be informative to
grasp a few hairs from the patch of hair loss and pull gently at 90
Hair disorders in infancy
degrees from the scalp. The number and type of hairs extracted
may give clues to the underlying diagnosis (see Table 1). Anagen Aplasia cutis congenita (ACC)
hairs have a pigmented bulb enclosed within its root sheath An uncommon condition characterised by areas of absent or
whereas telogen hairs have a de-pigmented club shaped bulb scarred skin at birth. It reflects disruption of intrauterine skin
(Figure 3). A modified hair pull test can be used to assess hair development, and potential causes include vascular compromise,
breakage. trauma, intrauterine infection or teratogenic medication. It may

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 SYMPOSIUM: DERMATOLOGY

be incorrectly attributed to obstetric trauma such as forceps de-

livery or fetal scalp electrodes application. It is typically an iso-
lated abnormality, but can be associated with developmental
anomalies or disorders such as Bart’s syndrome, Adams-Oliver
syndrome or Seitles syndrome.
The most common presentation is usually a solitary erosion,
deep ulceration or scar affecting the scalp. The lesion is usually
located on the vertex of the scalp lateral to the midline and varies
in size from 1 to 10 cm in diameter. Distorted hair growth around
the lesion is known as the hair collar sign which might be
associated with an underlying neural tube defect. The abnor-
mality in ACC is usually limited to the epidermis, dermis and/or
fat. Most lesions heal spontaneously within a few months leaving Figure 5 Triangular alopecia.
hairless scars which generally become less noticeable as the child
grows.

Temporal triangular alopecia

Temporal triangular alopecia is a relatively common condition of
localised non-scarring hair loss. The majority of patients present
between 2 and 6 years of age with a well circumscribed trian-
gular, lancet or oval patch of alopecia in the fronto-temporal
region (Figures 4 and 5). Most lesions are unilateral with the
base of the triangle orientated forwards. On closer examination,
the patches contain fine vellus hairs. Due to the location and
typical lancet shape the diagnosis of triangular alopecia is usually
made clinically, with alopecia areata being the main differential.

Occipital neonatal alopecia Figure 6 Occipital alopecia courtesy of Professor Andrew Messenger,
Royal Hallamshire Hospital.
A type of localised non-scarring alopecia, develops in the oc-
cipital region during the first few months of life (Figure 6). It
occurs due to alterations in the hair cycle. Unlike hairs at other atrichia with papular Lesions where children develop small
sites the occipital hairs don’t move into the telogen phase until papules on the face, neck and scalp.
after birth and therefore shedding in this area commonly occurs 2
e3 months after birth. Friction between the pillow and the scalp Ectodermal dysplasia (ED)
may contribute to the shedding. This alopecia will resolve These are a group of inherited developmental syndromes with
spontaneously. The important differential diagnoses to be abnormalities in at least two of the major ectoderm derived
considered are pressure alopecia and alopecia areata. structures. Infants usually present with abnormalities in hair,
nails, skin, teeth and eccrine glands. ED can be associated with
Atrichia congenita and atrichia with papular lesions other abnormalities such as deafness, intellectual developmental
Atrichia congenita is a rare condition characterised by total and disorder, skeletal abnormalities and distinctive facies.
permanent scalp hair loss. It may begin at birth or hair can start The alopecia can be due to hypotrichosis or hair shaft defects
shedding in infancy leading to total hair loss. Autosomal domi- with increased fragility. Eyebrows and eyelashes may be
nant and recessive variants have been described. It can be an involved. Nails may be absent (anonychia), thickened or
isolated phenomenon or associated with other defects such as dystrophic and teeth can have enamel defects causing hypo-
dontia, adontia or peg-shaped incisors. Abnormalities of the
eccrine glands can result in defective sweating and impaired
thermoregulation.

My child’s hair won’t grow

Hypotrichosis
Hypotrichosis is a common feature of many inherited syndromes
with gradual development of sparse hair. It is common for hair to
be present at birth or in infancy and then thin with age. Hypo-
trichosis simplex is an autosomal dominant condition charac-
terized by a hair defect confined to the scalp, with no other
ectodermal or systemic abnormalities. Hair may be normal at
birth with gradual progressive thinning of scalp hair with age.
Marie Unna hypotrichosis is an autosomal dominant disorder
Figure 4 Triangular alopecia. characterized by sparse or absent hair at birth followed by

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 SYMPOSIUM: DERMATOLOGY

regrowth of coarse, wiry twisted hair during childhood, and Congenital TN may be present at birth or appears later in the first
finally a progressive non scarring hair loss at puberty, often in a 1e2 years of life. The breakage of hair occurs at the proximal and
pattern resembling androgenetic alopecia. Other body hair is distal shaft. Beard, moustache, eyebrow, eyelashes, axillary and
typically absent. Autosomal recessive hereditary hypotrichosis is pubic hairs can be affected as well. Acquired TN occurs in
characterised by sparse woolly hair associated with skin fragility structurally normal hair exposed to excessive trauma (heat,
and palmoplantar keratoderma. straightening, chemicals, sunlight etc). The hair can be dry, dull
or brittle with whitish nodules at the ends. It affects the scalp hair
Loose anagen syndrome only, with distal shaft breakage. Excessive physical and chemical
Loose anagen is a condition effecting the anchorage of growing trauma must be avoided.
anagen hairs. Hair can be easily and painlessly plucked from the
scalp. It classically occurs between 2 and 7 years of age and is more Monilethrix: an autosomal dominant disorder caused by muta-
common in girls with fair skin and blond hair. Hair is normal at tions of the genes encoding hair keratins. It results in beading
birth but fails to grow long. A gentle hair pull will painlessly (wide and narrow zones in the hair shaft) with increased fragility
remove anagen hairs. Light microscopy of extracted hairs will and breakage in the narrow zones (Figure 8). This leads to a
reveal dysplastic anagen hairs, often resembling a hockey stick. stubble appearance with dry and brittle hair. Topical minoxidil
This condition may resolve spontaneously with age. and oral retinoids may help and avoidance of behaviours causing
excessive weathering is important. There tends to be some
Short anagen syndrome improvement with age.
Short anagen syndrome is a hair cycle disorder where the hair
does not grow long or need cutting due to short duration of the Pili torti: a rare, congenital or acquired condition, in which the
anagen phase. It is usually first noticed by parents around the age hair shaft is flattened at irregular intervals and twisted 180 along
of 2e4 years. The hair shaft is normal without signs of breakage its axis. (Figure 8). Not all hairs are affected. It is characterized
but the anagen phase is shortened and subsequently there are by fragile, brittle, unruly and lusterless hairs, due to uneven light
overall more telogen hairs (Figure 7). Short anagen syndrome reflection on the twisted hair surface. In the classic form, hair is
tends to improve after puberty. normal at birth and is then gradually replaced by spangled blond
hair. At puberty the hair darkens and becomes less fragile. Pili
Hair shaft abnormalities torti can also be a feature of other syndromes such as Menke’s
Abnormal hair fibre production can produce unruly hair due to syndrome and several ectodermal dysplasias. There is no specific
hairs being irregularly shaped, spangled hair where hair twists
reflect light at variable angles and fragile hair. Hair fragility can
lead to localised or diffuse areas of hair loss occur due to
breakage of structurally weak hair. Hair shaft disorders are
divided into those with or without increased fragility.

Hair shaft abnormalities with increased fragility

Trichorrhexis nodosa (TN): TN is the commonest hair shaft
disorder. The cuticular cells are disrupted causing the cortical
cells to fray forming a fragile node which breaks leaving a paint-
brush like tip (Figure 8). It may be congenital or acquired.

Figure 7 Short anagen syndrome. Figure 8 Hair shaft abnormalities with increased fragility.

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 SYMPOSIUM: DERMATOLOGY

treatment for this condition, but it may improve spontaneously

after puberty.

Trichorrhexis invaginata: Trichorrhexis invaginata (bamboo

hair e Figure 8) is a specific hair shaft abnormality seen in pa-
tients with Netherton’s syndrome and is usually associated with
a distinctive rash, ichthyosis linearis circumflexa, and atopy.
Netherton’s syndrome is an autosomal recessive condition with
variable expression that affects girls more than boys. It results
from mutations in the SPINK5 gene which encodes the serum
protease inhibitor protein LEKTI. The hair abnormality usually
becomes noticeable in infancy with the development of short,
sparse, brittle and fragile hair. The eyebrows and eyelashes are Figure 10 Uncombable hair syndrome.
usually sparse or absent. Light microscopy will show areas
where the distal hair shaft invaginates into the proximal hair
shaft. The hair may improve with age as the follicles thicken but become less marked and the hair more manageable with age with
defects in eyebrow and body hair tend to persist. affected patients in adolescence often having completely normal
or normal textured hair.
My child has unruly hair
Hair shaft abnormalities without increased fragility Woolly hair: this is tightly coiled “Afro” textured hair covering
Pili anulati: this condition is characterised by hair shafts that all or part of the scalp occurring in non-African individuals
have alternating light and dark bands caused by air cavities in (Figure 11). Some patients present with a circumscribed patch of
the cortex. Patches of hair have an attractive spangled woolly hair (woolly hair naevus).
appearance with patients often describing their hair as stripy. Generalised woolly hair can be autosomal dominant heredi-
20e80% of the hair can be affected and is usually visible on tary disorder or an autosomal recessive trait. The triad of woolly
clinical examination, however the diagnosis is confirmed on hair, palmar-plantar keratoderma and cardiomyopathy may
electron microscopy. indicate either Naxos or Carvajal disease.
The condition can be inherited as an autosomal dominant or
sporadic with patients presenting anytime from infancy to Telogen effluvium: scalp hair loss due to increased telogen hair
adulthood. shedding can be acute, occurring after a triggering event with
spontaneous complete regrowth, or chronic, if the insult is pro-
Uncombable hair (Cheveux incoiffables, pili trianguli et longed or repeated. There is usually a two to three month delay
canaliculi, spun glass hair): this disorder is inherited in either between insult and the start of hair shedding. Common triggers
an autosomal recessive or an autosomal dominant pattern, in children include high fever/infections, physical and emotional
characterised by triangular hairs only affecting the scalp (Figures stress, a period of anorexia/starving and certain medications. In
9 and 10). a third of cases no trigger can be identified. Unless the trigger is
The abnormality may first present between 3 months and 12 repeated the shedding stops and regrowth occurs by 3e6
years of age. While normal in quantity and length the hair is months. A hair pull test reveals hairs in telogen phase throughout
unruly with a disordered appearance and resists being combed the scalp.
flat; the hair does not grow downward but in all directions from Hair shedding may be more chronic in children with thyroid
the scalp. The hair is often silvery blond in colour and typically disorders, iron deficiency anaemia, acrodermatitis enteropathica
more than 50% of the scalp hairs are affected. (zinc deficiency), malnutrition, malignancy, drugs and autoim-
On light microscopy the hairs have a triangular shape on cross mune disorders such as systemic lupus erythematosus and der-
section with a longitudinal groove. The appearance tends to matomyositis. The history may identify a known trigger but

Figure 9 Uncombable hair showing triangular hairs on microscopy and unruly “spun glass” hair.

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 SYMPOSIUM: DERMATOLOGY

with AA have a family history of the disease. The inflammatory

process targets anagen hairs causing dystrophic anagen hairs and
their transition into the telogen phase. The disorder can occur at
any age.
In patchy alopecia spontaneous recovery can occur in up to
80% within one year. 14e25% progress to total loss of scalp hair
(alopecia totalis, AT) or loss of entire body hair (alopecia uni-
versalis, AU). Poor prognostic features include onset of AA pre-
puberty, severe disease at presentation, ophiasis pattern of alo-
pecia (band like loss over the occipital scalp, see Figure 12), nail
involvement and associated atopic disease.
The characteristic presentation of AA is the development of
well-circumscribed, totally bald, smooth patch of alopecia on the
scalp (Figure 13). Other presentations include AT, AU, ophiasis
Figure 11 Woolly hair.
pattern and rarely a diffuse variant with widespread thinning.
The eyebrows and eyelashes are lost in many cases and may be
the only sites affected. Regrowth can be fine and depigmented at
investigations should include full blood count, electrolytes, liver first. Often exclamation-mark hairs (dystrophic hairs with frac-
function, thyroid function, ferritin/iron studies, B12, Folate, tured tips) are present as well as cadaverised hairs (hairs frac-
serum zinc levels, vitamin D and antinuclear antibodies. If a drug tured before passing through the scalp). A hair pull can reveal
is thought to be the culprit, this should be stopped for a mini- telogen or dystrophic anagen hairs.
mum of 3 months. The management of AA is dependent on the extent of the
disease and on the psychological impact it is having on the child
My child has developed new patches of hair loss and the family. Referral to a paediatric psychologist may be
needed to develop a coping mechanism and prevent social and
Alopecia areata (AA) educational disruption. Leaving AA untreated is a legitimate
AA is a non-scarring form of alopecia that is considered to be a option, especially when spontaneous remission is possible or
chronic inflammatory disorder in which a T-cell autoimmune when effective treatments are unlikely to be tolerated well. In
mediated attack on hair follicles and occasionally nails occurs. A such situations a wig, headscarf and semi-permanent tattoos can
genetic predisposition is also suggested as about 20% of people be helpful.

Figure 12 Alopecia areata ophiasis pattern.

Figure 13 Patchy alopecia areata.

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 SYMPOSIUM: DERMATOLOGY

In limited patchy hair loss, potent topical steroids with or

without occlusion and intralesional steroid injections may induce
hair growth, but can cause skin atrophy. Discomfort from in-
jections restricts their use in young children under 10 years of
age.
For more extensive patchy hair loss or AT/AU, systemic
corticosteroids can produce regrowth but this is often not sus-
tained and the risks may outweigh the benefits. Pulsed oral ste-
roids have been favourable due to fewer significant systemic side
effects.
Contact immunotherapy has been shown to be effective but
is not widely available and can be difficult and disruptive in
young children as it needs to be repeated frequently (weekly).
Contact dermatitis, eczema and urticaria are common following
treatment.

Trichotillomania
A behavioural disorder characterised by compulsive hair pulling
or plucking. It occurs in two main forms. In infants and young
children it represents as a habit, similar to thumb sucking. It is
more common in boys and usually resolves spontaneously.
In older children and adolescents it is seen predominantly in
females often with evidence of psychological or behavioural
stress. This form is characterised by the American Psychiatric
Association as an impulse control disorder where irresistible hair
pulling results in release of tension and distress. Hair is most
commonly plucked from the fronto-temporal regions of the scalp
and results in patches of hair loss with irregular borders con- Figure 14 Tinea capitis.
taining hairs of variable length. The extent of alopecia can vary
but it is unusual for hair to be lost completely.
An accurate clinical diagnosis is essential but may not always Scalp scrapings or hair brushings sent for microscopy and
be easy and might require observation overtime. In young chil- culture are essential to confirm the diagnosis.
dren it is usually self-limiting. Management in adolescents can be Oral antifungal agents are needed to ensure eradication but
more challenging; those with insight should be referred to a combined use with topical treatment such as ketaconazole
psychologist for cognitive behavioural therapy, including habit shampoo may reduce the risk of transmission. Although not
reversal, and potentially pharmacological therapy. A combina- licensed in children, oral terbinafine is generally recommended
tion of both is more likely to reduce the chance of relapse. as it is particularly effective for the Trichophyton species. It is
fungicidal and the duration of treatment (2e4 weeks) is shorter
Tinea capitis than griseofulvin, a fungistatic agent. For infection with Micro-
Tinea capitis is a common dermatophyte infection of the scalp in sporum species, griseofulvin remains the treatment of choice.
children (Figure 14). The causative organisms are the Tricho- Combs, brushes, hats etc should be disinfected or discarded
phyton and Microsporum species. Currently Trichophyton ton- and family members must also be examined, screened and
surans is the commonest pathogen in the UK especially in urban treated accordingly to prevent re-infection. Both clinical and
areas but the epidemiology varies worldwide. mycological clearance should be confirmed once the standard
The Trichophyton species cause an endothrix infection, with course of treatment is completed.
fungal spores within the hair shaft. This does not fluoresce under
UV light but hair shaft damage causes hairs to break off close to Scarring alopecia
the scalp surface creating a “black dot” appearance. Scarring or cicatricial alopecia implies permanent hair loss
Microsporum canis, another common pathogen, causes an associated with destruction of hair follicles and scarring of the
ectothrix pattern with fungal spores formed around the hair pilosebaceous unit. This can result from a disease that affects the
shaft. This causes the hair shaft to fluoresce bright green with UV follicles primarily or a secondary external process.
light. Examples of secondary causes include burns, radio-
The clinical features may vary from a relatively non- dermatitis, morphoea and infections such as the favus form of
inflammatory patchy alopecia, with or without scale, to an tinea capitis. Primary scarring alopecia in children is extremely
inflamed boggy lesion with pustules and abscess formation, rare.
known as a kerion. Discrete patches are the commonest pre- In African American girls traction alopecia can result in a
sentation. Many children have associated lymphadenopathy. permanent alopecia if traction from hair styling is excessive and

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 SYMPOSIUM: DERMATOLOGY

prolonged. Initially the hair loss is temporary and behaves like a Messenger AG, McKillop J, Farrant P, et al. British Association of
non-scarring alopecia. Dermatologists’ guidelines for the management of alopecia areata
2012. Br J Dermatol 2012; 166: 916e26.
Conclusion Sperling L. Alopecias. In: Bolognia JL, Jorizzo JL, Rapini R, et al., eds.
Dermatology. 2nd edn. Elsevier Limited, 2008; 987e1005.
Understanding the basic hair biology improves the clinical
assessment of a child with hair problems and helps to explain
why some congenital disorders do not present until later in
childhood. Approaching a hair disorder in children according to Practice points
the principle complaint, be it patches of hair loss, hair shedding,
poor growth or hair breakage, is more likely to lead to a diag- C Establish the principle complaint: diffuse or patchy hair
nosis. An ability to recognise both the common and rarer hair loss, hair shedding, poor growth or breakage
conditions will ensure early access to correct management for C Determine whether there are signs of inflammation or
these distressing conditions. A scarring
C A dermatologist may use the hair pull technique, light mi-
croscopy and occasionally scalp biopsies to aid the diag-
FURTHER READING
nosis of more complex cases
Farrell A, Sinclair R, Dawber R. Disorders of the hair and scalp. Fast
C Abnormalities in hair shaft production can produce fragile
facts. Health Press Limited, 2000.
hair where breakage may cause either localised or diffuse
Franklin M, Zagrabbe K, Benavides K. Trichotillomania and its treat-
areas of hair loss
ment: a review and recommendations. Expert Rev Neurother 2011
C A common cause of hair shedding is acute telogen efflu-
Aug; 11: 1165e74.
vium, which occurs two to three months after a triggering
Fuller LC, Barton RC, Mohd Mustapa MF, et al. British Association of
event
Dermatologists’ guidelines for the management of tinea capitis
C Alopecia areata characteristically produces well-
2013. Draft update from: Higgins EM, Fuller LC, Smith CH.
circumscribed non-scarred patches of hair loss
Guidelines for the management of tinea capitis. Br J Dermatol
C The features of tinea capitis vary from scaly patches of al-
2000; 143: 53e8.
opecia to a boggy swelling or kerion formation and oral
Messenger AG, de Berker DAR, Sinclair RD. Disorders of hair. In:
antifungal agents are required after diagnostic hair sam-
Burns T, Breathnach S, Cox N, Griffiths C, eds. Rook’s textbook of
ples/skin scrapes are taken
dermatology. 8th edn., 4. Wiley- Blackwell, 2010; 66.1e6675.

PAEDIATRICS AND CHILD HEALTH xxx:xxx 8 Ó 2018 Elsevier Ltd. All rights reserved.

Please cite this article as: Champagne C et al., Hair loss in infancy and childhood, Paediatrics and Child Health, https://doi.org/10.1016/
j.paed.2018.12.005