Available online at http://www.biij.

org/2012/1/e6
doi: 10.2349/biij.8.1.e6

biij
Biomedical Imaging and Intervention Journal
ORIGINAL ARTICLE

Precocious puberty in children: A review of imaging

findings
Faizah MZ1,*, Zuhanis AH1, Rahmah R2, Raja AA2, Wu LL2, Dayang AA3,
Zulfiqar MA1
1 Department of Radiology, Universiti Kebangsaan Malaysia Medical Centre (UKMMC), Kuala Lumpur, Malaysia
2 Department of Paediatrics, Universiti Kebangsaan Malaysia Medical Centre (UKMMC), Kuala Lumpur, Malaysia
3 Paediatric Surgical Unit, Department of Surgery, Universiti Kebangsaan Malaysia Medical Centre (UKMMC), Kuala Lumpur, Malaysia

Received 6 July 2011; received in revised form 20 October 2011; accepted 27 October 2011

ABSTRACT

Objectives: This review was aimed at determining the imaging findings in patients with precocious puberty.
Results: Within a period of 8 years (from 2002 to 2010) there were 53 patients diagnosed with precocious puberty.
Out of the 53 patients, 37 had undergone diagnostic imaging to detect the possible organic causes of precocious puberty.
Imaging findings were positive in 31 patients and out of that, 3 patients had 2 findings each (34 abnormalities). Of the
patients with positive imaging findings, central precocious puberty (gonadotrophin-dependent) was more common (81%;
25/31) and the causes included: tuber cinereum hamartoma (n = 10), glioma (n = 6), pineal gland tumour (n = 4),
hydrocephalous (n = 3), arachnoid cyst (n = 2) and others (n = 3). Peripheral precocious puberty (gonadotrophin-
independent) causes included: testicular adrenal rest tumour (n = 3), adrenal carcinoma (n = 1), ovarian granulosa thecal
cell tumour (n = 1), and tuberous sclerosis (n = 1).
Conclusion: Positive imaging findings were observed in 84% (31/37) of the subjects. Hypothalamic hamartoma
was the most common imaging finding in central precocious puberty while testicular adrenal rest tumour was the most
common imaging finding in peripheral precocious puberty. © 2012 Biomedical Imaging and Intervention Journal. All
rights reserved.

Keywords: precocious puberty, imaging.

INTRODUCTION puberty (CPP) and peripheral precocious puberty (PPP)

[1–3].
Precocious puberty is defined as the development of In order to understand the two types of precocious
secondary sexual characteristics before the age of 8 years puberty, basic knowledge of normal puberty pertaining
in girls and 9 years in boys [1–3]. Two types of to the hypothalamus-pituitary-gonadal (HPG) axis is
precocious puberty are recognised, central precocious necessary [2, 3]. The gonadotrophin-releasing hormone
(GnRH) that is produced by the brain’s hypothalamus
leads to activation of the anterior pituitary to produce
* Corresponding author. Present address: Department of Radiology, and release gonadotrophins, luteinising hormone (LH),
Universiti Kebangsaan Malaysia Medical Centre (UKMMC), Jalan and follicle-stimulating hormone (FSH). These
Yaacob Latiff, 56000 Cheras, Kuala Lumpur, Malaysia. E-mail:
hormones will then activate the gonads (testes in boys
[email protected] (Faizah Mohd. Zaki).
and ovaries in girls) to produce the male sex hormone
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Table 1 Causes of precocious puberty

Causes of CPP Girls Boys Total

1 idiopathic 16 1 17
2 hamartoma 6 4 10
3 astro/glioma 3 3 6
4 pineal gland tumour 2 2 4
5 hydrocephalus## 1## 2## 3##
6 arachnoid cyst 1 1 2
7 intra-cranial germinoma 0 1 1
8 pituitary macroadenoma 1 0 1
9 neurofibromatosis Type 1 0 1 1
Total number of patients with CPP 29 13 42
Causes of PPP
1 congenital adrenal hyperplasia 4 1 5
2 testicular adrenal rest tumour 0 3 3
3 adrenal carcinoma 0 1 1
4 ovarian granulosa cell tumour 1 0 1
5 tuberous sclerosis 1 0 1
Total number of patients with PPP 6 5 11
Total with PP 35 18 53
Key: ## Hydrocephalus was an associated finding in patients with intracranial tumour

Figure 1 Imaging algorithm for precocious puberty.

(testosterone) and the female sex hormone (oestrogen), brain tumours, brain infections, congenital brain defects,
respectively. The hormones produced by the gonads lead radiation or injury to the brain or spinal cord, and brain
to the physical and sexual changes of puberty [2, 3]. ischaemia. The most common cause of CPP is
CPP, which is also called GnRH-dependent hypothalamic tumour, in particular the tuber cinereum
precocious puberty, is caused by early activation of the hamartoma followed by hydrocephalus and previous
HPG axis [1, 3]. It is more common in girls, and is central nervous system (CNS) injury [1].
usually idiopathic. Secondary causes of CPP includes:
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PPP, which is also called GnRH-independent

precocious puberty, does not involve the HPG axis. It is
caused by release of oestrogen or testosterone into the
body from abnormal organs and causes include adrenal
hyperplasia, adrenal tumour, and gonadal tumour [1].
This review was aimed at determining the imaging
findings in patients with precocious puberty.

MATERIALS AND METHODS

This was a retrospective review of the radiological

findings of patients diagnosed with precocious puberty.
The list of patients with precocious puberty from 2002
until 2010 was obtained from the paediatric
endocrinologist at the medical centre where this study
Figure 2 One year-old boy who presented with penile
was carried out. Based on this list, the radiological enlargement. Coronal T1WI MRI of the brain shows
reports of patients who had undergone radiological mass in hypothalamus (arrow) representing tuber
investigations were reviewed. These reports were cinerium hamartoma.
retrieved from the Integrated Radiology Information
System (IRIS). The radiological images were reviewed
from the Picture Archiving and Communication System
(PACS) (Medweb®) for patients imaged after September
2007. Hardcopy images were reviewed for patients
imaged prior to September 2007.
The diagnosis of precocious puberty was made
based on clinical evaluation, plasma hormonal
investigations (LH, FSH and testosterone/ oestradiol
levels), and assessment of bone age by the paediatric
endocrinologist. Radiological investigations were
performed when indicated (Figure 1). The decision to
perform radiological investigations was made by the
paediatric endocrinologist based on several factors which
included: very young age (below 3 years old), rapid
progression of puberty, presence of neurological signs
and symptoms, and biochemical investigations that point Figure 3 A girl with global developmental delay who presented
towards pathological precocious puberty. The senior with bilateral breast enlargement. T1WI Sagittal MRI
medical officer or radiologist performed the ultrasound of the brain (post-gadolinium dynamic protocol) shows
scans (USG) using ultrasound machine (HD11 or IU22, an intrasellar lesion representing pituitary
microadenoma (arrow).
Philips, Eindhoven,The Netherlands). Computed
tomography (CT) with contrast was performed in axial
plane with multi-planar reconstruction (Siemens
SOMATOM 64-slices, Erlangen, Germany). The MRI
was performed using two different machines; prior to
year 2006 (Siemens MAGNETOM 1.5T, Erlangen,
Germany) and after year 2006 (Siemens AVANTO 1.5T,
Erlangen, Germany).
Data were recorded in Microsoft Excel and were
analysed using the statistical packages SPSS (version 16)
for its descriptive statistics. Statistical analysis was not
performed, as this is a descriptive evaluation.

RESULTS

From 2002 until 2010, there was a total of 53

patients (35 girls and18 boys) aged between 1 and 15
Figure 4 Seven year-old boy with neurofibromatosis Type 1 (NF-
years (mean age of 6.9 years) with a diagnosis of 1) who presented with hirsutism. T2-FLAIR MRI of the
precocious puberty. Some had been diagnosed before the brain shows multiple foci of high signal intensity in the
study period (before 2002) and therefore children older basal ganglia and cerebelli (arrows) consistent with
than age 8 and 9 years were included in the sample. myelin vacuolation.
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8% (1/13) had idiopathic CPP (Table 1). The GnRH-

dependent causes seen on imaging included:
hypothalamic hamartoma (n = 10), hydrocephalus (n = 3),
astrocytoma/glioma (n = 6), pineal gland tumour (n = 4),
arachnoid cyst (n = 2) and 1 case each for pituitary
microadenoma, myelin vacuolation in neurofibromatosis
Type 1 (NF-1) and suprasellar germ cell tumour with
cerebral metastases (Figures 2–5).

Figure 5 Five year-old boy who presented with penile

enlargement. T1WI post-gadolinium MRI of the brain
in sagittal and coronal views demonstrates multiple
enhancing lesions in the hypothalamus and right basal
ganglia (arrows). Histology showed intracranial germ
cell tumour.

Figure 7 Eight year-old boy who presented with signs of increased

intracranial pressure and hirsutism. MRI shows
heterogenously enhancing suprasellar tumour (arrows)
with hydrocephalus. Histology showed low-grade
astrocytoma.

Figure 6 Four year-old boy who presented with impaired vision

and acne. T1WI post-gadolinium sagittal MRI of the
brain shows heterogenously enhancing suprasellar
tumour (arrows) with hydrocephalus. Histology revealed
pilomyxoid astrocytoma.

Out of 53 patients reviewed, 70% (37/53) had

undergone some form of radiological investigation: MRI
of the brain, ultrasound of the pelvis/testes or CT of the
abdomen. Out of the 37 patients who underwent Figure 8 Seven years-old girl who presented with bilateral breast
radiological investigations, 84% (31/37) had abnormal enlargement. T2-FLAIR axial MRI of the brain shows
brainstem glioma (arrows).
findings. Three of the patients had 2 findings each. These
were concomitant intracranial tumour with
hydrocephalus. This resulted in a total of 34 The most common cause of intracranial tumour in
abnormalities. Six patients had normal MRI of the brain CPP was hypothalamic hamartoma, which was true in
and were therefore diagnosed with idiopathic CPP. This both male and female populations. In 4 out of 6 patients
was more common in girls (n = 5) compared to boys with astrocytoma/glioma cases, the location of the
(n = 1). Of the 16 patients who were not imaged, 11 were tumour was in the supratentorial region. Two of these
girls diagnosed with idiopathic CPP, while 4 girls and 1 cases had concomitant hydrocephalus (Figures 6 and 7).
boy were diagnosed with congenital adrenal hyperplasia. The other 2 glioma cases occurred in girls and were
There were 82% (28/34) GnRH-dependent causes found in the brainstem (Figure 8). Both did not have
detected on imaging as compared to 18% (6/34) GnRH- neurofibromatosis. One of the two arachnoid cysts was
independent causes. Among the girls with CPP, 45% located in the suprasellar region and complicated with
(13/29) had intracranial pathology and 55% (16/29) were hydrocephalus (Figure 9) while the other was located in
diagnosed as idiopathic CPP (Table 1). Among the boys the left middle cranial fossa. There were 4 pineal gland
with CPP, 92% (12/13) had intracranial pathology while tumours which consisted of pineal gland germinoma
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(n = 2) (Figure 10), pineocytoma (n = 1) and pineal cyst There were 8 patients with congenital adrenal
(n = 1). hyperplasia (CAH) in our review. Three had imaging
studies performed because they were resistant to steroid
therapy. All 3 cases showed testicular adrenal rest
tumour (TART) (Figure 11). Other GnRH-independent
PP were adrenocortical carcinoma (n = 1) (Figure 12),
ovarian granulosa thecal cell tumour (n = 1) (Figure 13)
and tuberous sclerosis (n = 1). The CT abdomen of the
child with tuberous sclerosis showed bilateral
angiomyolipoma.

Figure 9 Eight year-old girl who presented with bilateral breast

enlargement. T2WI sagittal MRI of the brain shows
suprasellar arachnoid cyst (arrows) with hydrocephalus.

Figure 12 Two year-old boy who presented with hirsutism and

acne. An ultrasound and subsequent CT (sagittal
reconstruction of contrast-enhanced CT abdomen)
shows a heterogenous mass in the right suprarenal
region (arrows). There is no calcification within the
mass. The tumour was surgically removed and
histology revealed adrenocortical carcinoma. The child
responded well to chemotherapy.

Figure 10 Three year-old boy with increased penile size. T1WI

post-gadolinium sagittal MRI of the brain shows an
enhancing pineal gland tumour (arrow). Histology was
consistent with germinoma.

Figure 13 Four year-old girl who presented with per-vaginal

bleeding. Transverse view of the pelvic ultrasound
shows a right ovarian cyst with thickened walls
(arrows). She underwent laparoscopic removal of the
ovarian cyst and the histology revealed a granulosa
thecal cell tumour.

DISCUSSION
Figure 11 Twelve year-old boy who was diagnosed earlier with
congenital adrenal hyperplasia at the age of 2 and was
on steroid treatment. An ultrasound of the testis was Precocious puberty is caused by a heterogeneous
performed because of resistance to steroid therapy. It group of disorders, which ranges from idiopathic to
shows multiple hypoechoic lesions within the testis
(arrows) representing testicular adrenal rest tumour.
malignant tumours [1]. There are several causes of
premature sexual development which can be divided
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into: i) premature activation of the hypothalamic- findings (29%). The aim of treatment is to preserve final
pituitary-gonadal (HPG) axis (central PP); ii) abnormal height and reverse physical changes to pre-pubertal stage
patterns of gonadotrophin secretion (premature thelarche, congruous to chronological age. For these patients, the
thelarche variant); iii) excess adrenal androgens left hand and wrist radiograph was used to monitor bone
(adrenarche, congenital adrenal hyperplasia (CAH), age. Of the 10 cases of hamartoma detected in this series,
adrenal tumours); and iv) gonadotrophin independent PP the indications for imaging included: 8 with early onset
(secretion of sex steroids is independent of the HPG axis) of precocious puberty before the age of 3 years, and 4
[2]. The patients reviewed in this series were mostly in male patients.
the first and fourth category. Precocious puberty and amenorrhoea have been
Premature thelarche or thelarche variant is associated with hydrocephalus. The exact pathway by
characterised by isolated premature breast development which hydrocephalus disrupts the hypothalamic GnRH
and is associated with normal growth velocity and bone system is unknown. However, previous reports
age advancement within two standard deviations of postulated that compressive forces, ischaemia, and
normal. It is thought to be a self-limiting condition likely impairment of the neurotransmitter feedback loop might
to resolve within 6 months to 6 years after diagnosis [2]. be the explanation [1]. We had 3 cases of CPP due to
hydrocephalus, which occurred as a complication of
Central precocious puberty (CPP) suprasellar tumour.
Most tumours of the chiasm and hypothalamus in
Central precocious puberty or GnRH-dependent
children are gliomas and the majority are low grade at
precocious puberty is more common by far in girls than
histology [11]. The authors noted that most of the non-
in boys, where in girls it is usually idiopathic. Central
hypothalamic intracranial tumours causing CPP were
nervous system disorders account for a higher percentage located in the suprasellar region with the pineal gland
of cases in boys but must also be excluded in girls [2, 4]. being the second most common location. All of the
Approximately 95% of girls with CPP have idiopathic
patients in this study with astrocytoma had the tumour in
CPP and only 5% have a secondary cause. Whereas more
the suprasellar region.
than 50% of boys have an identifiable aetiology and
Brainstem gliomas are the second most frequent
idiopathic CPP is a diagnosis of exclusion [2] . We tumour in NF-1 after optic tract tumour [12]. Brainstem
observed a much higher percentage for a secondary glioma presenting with precocious puberty has been
cause of CPP of 45% (13/29) in our female population.
reported in patients with NF-1. In this review, of the 2
MRI of the brain was not routinely done in girls with
cases of brainstem glioma, one had histology of
CPP at this centre (Figure 1). Therefore, the true
glioblastoma multiforme which later recurred. Neither
incidence of a secondary cause of CPP could be higher.
case has NF-1.
It has been advocated that girls with CPP should have a Arachnoid cysts are relatively uncommon
cranial MRI as part of their assessment since clinical intracranial lesions, usually developmental in origin [13].
features, including age, are not helpful in predicting
The majority occur in the supratentorial compartment
those with underlying pathology [4]. This is the reverse
and, of these, roughly 9–15% occur in the suprasellar
for CPP in boys whereby most of the boys have a
region [11].
secondary cause of CPP with the main cause being a
It is known that tumours and other pathological
central nervous system tumour. Therefore, CNS disease processes involving the hypothalamus frequently modify
must first be ruled out before diagnosing a patient as sexual development. These lesions may destroy the
having idiopathic precocious puberty [5]. At this centre,
posterior hypothalamus, leaving the anterior
all males with precocious puberty were imaged. Imaging
hypothalamus intact, which leads to increased pituitary
was not routinely done in girls with CPP. This review
function and hence, causes CPP [14]. This also explains
showed that almost all (92%) males with CPP had how CPP occurs when suprasellar tumours such as
intracranial pathology. astrocytoma, arachnoid cyst or germ cell tumours
The most common underlying disorders include
compress upon the posterior hypothalamus due to the
tumours of the hypothalamic region, especially
close proximity of the hypothalamus.
hamartoma of the tuber cinereum, hydrocephalus and
Germ cell tumours most frequently arise in the
previous central nervous system (CNS) injury from any
pineal and suprasellar region and, in general, pineal
cause [1]. The prevalence of intracranial pathology in gland germ cell tumours outnumber suprasellar tumours
this review was 47% (25/53). This is similar to previous by a ratio of 2:1 [15]. The most common pineal tumours
reports, which demonstrated prevalence of intracranial
are germ cell tumours, besides pineal parenchymal
pathology of 15% to 49% [4, 6–8]. Several studies have
tumours or astrocytomas [16]. The authors observed 2
reported on the incidence of hypothalamic hamartomas
germ cell tumours originating from the pineal gland and
in patients with precocious puberty, varying from 14% to
1 suprasellar germ cell tumour with intracerebral
58% [4]. In a review of MRI findings and clinical
metastases.
features, 8 out of 9 patients with hypothalamic
A previous study had shown that CPP occurred in
hamartoma had precocious puberty [9]. In this review, it
3% of their entire population of children with NF-1,
was also found that hypothalamic hamartoma was the
which is markedly higher than its incidence in the
most common tumour causing CPP in the patients,
general population (0.06%) [17]. CPP was found
accounting for 10 out of 34 of the abnormal imaging
exclusively in those children with NF-1 who had optic
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pathway tumours (OPTs) involving the optic chiasm [17, still a place for clinical assessment. Imaging is
18]. Therefore, it is peculiar that our only patient with mandatory in all boys with CPP. Hypothalamic
NF-1 had myelin vacuolation without OPTs but still hamartoma was found to be the most common finding on
presented with CPP. Two NF-1 cases who presented with imaging in CPP while testicular adrenal rest tumour was
CPP but without OPTs have been reported. It was the most common finding on imaging in PPP.
theorised that the temporary neurologic manifestations of
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