Insights into Imaging

https://doi.org/10.1007/s13244-018-0643-0

PICTORIAL REVIEW

Radiological review of skull lesions

Carrie K. Gomez 1 & Scott R. Schiffman 1 & Alok A. Bhatt 1

Received: 10 April 2018 / Revised: 17 June 2018 / Accepted: 28 June 2018

# The Author(s) 2018

Abstract
Calvarial lesions are often asymptomatic and are usually discovered incidentally during computed tomography or magnetic
resonance imaging of the brain. Calvarial lesions can be benign or malignant. Although the majority of skull lesions are benign, it
is important to be familiar with their imaging characteristics and to recognise those with malignant features where more
aggressive management is needed. Clinical information such as the age of the patient, as well as the patient’s history is
fundamental in making the correct diagnosis. In this article, we will review the imaging features of both common and uncommon
calvarial lesions, as well as mimics of these lesions found in clinical practice.
Teaching Points
• Skull lesions are usually discovered incidentally; they can be benign or malignant.
• Metastases are the most frequent cause of skull lesions.
• Metastatic lesions are most commonly due to breast cancer in adults and neuroblastoma in children.
• Multiple myeloma presents as the classic Bpunched out^ lytic lesions on radiographs.
• Eosinophilic granuloma is an osteolytic lesion with bevelled edges.

Keywords Skull . Calvarial . Benign . Malignant . Lesions

Introduction inner and outer tables, and the diploe or marrow space
between them (Fig. 1) [1, 4]. Lesions of the calvarium
Calvarial lesions are often asymptomatic and are usually may originate from the bony structures or may be second-
discovered incidentally during computed tomography (CT) ary to invasion of scalp-based lesions or brain-based le-
or magnetic resonance imaging (MRI) of the brain or as sions into the skull vault [1, 4]. The skull base forms the
part of workup of local clinical symptoms or staging of floor of the cranial cavity and, therefore, similar lesions
other diseases [1–6]. Occasionally, they may present as a can occur in this region; however, there are lesions that
visible, palpable or symptomatic lump [1, 2, 4]. Clinical are also specific to this location such as chordoma and
parameters such as the age and clinical history are impor- chondrosarcoma.
tant factors to guide the radiological diagnosis. Calvarial Recognition of benign and malignant imaging features
lesions may be benign or malignant; fortunately, benign is important for the radiological diagnosis [1–6]. In gen-
tumours are the most commonly encountered lesions [1–6]. eral, benign tumours have well-defined borders with a
The skull vault is formed by the frontal, parietal, tem- narrow transition zone; sclerotic margins are frequently
poral and occipital bones and parts of the zygoma and present. On the other hand, malignant tumours have poor-
sphenoid bone. It is composed of two cortical tables; the ly defined margins, a wide transition zone, aggressive
periosteal reaction and often have a soft tissue compo-
nent; these lesions cause dramatic bony destruction with
* Carrie K. Gomez intracranial or extracranial extension (Table 1) [1, 4].
carrie_gomez@urmc.rochester.edu Skull lesions can be lytic or sclerotic, single or multiple
with varied composition; they may arise from osteogenic,
1
Department of Imaging Sciences, University of Rochester, 601 chondrogenic, fibrogenic, vascular and/or other elements
Elmwood Avenue, Rochester, NY 14602, USA of bone (Tables 2 and 3).
 Insights Imaging

Fig. 1 Image depicting the calvarium anatomy (a). The skull is composed is covered by periosteum. Underneath the calvarium are the meninges
of the marrow space (diploe), inner and outer tables. Covering the skull is comprised of the dura mater, arachnoid mater and pia mater. Diagram
the scalp which consists of the skin, subcutaneous dense connective of the skull depicts patterns of bone destruction in the skull (b)
tissue, galea aponeurotica and loose connective tissue. The outer table

Calvarial lesions are radiologically evaluated with CT mineralised tumour matrix [1–3, 6]. MRI is best to de-
and MRI. CT is the most accurate method for evaluating pict marrow involvement of the diploe and to evaluate
bone destruction of the inner and outer tables, the lytic the associated soft tissue component and invasion of
or sclerotic nature of the lesion and for the evaluation of adjacent tissues [1–3, 6]. Plain radiographs play a lesser
role, but are useful in the assessment and follow-up of
Table 1 Features of benign and malignant lesions
lytic lesions such as multiple myeloma; it may also be
the initial modality on which a lesion is found [2, 6].
Benign Malignant The differential diagnosis of calvarial lesions is im-
portant to decide whether biopsy, surgical intervention
Geographic/sharp margins Moth eaten or permeative
bone destruction
or conservative treatment is required for further manage-
Narrow zone of transition Wide zone of transition
ment [1, 2, 6]. In this article, we will review the imaging
Sclerotic margin Poorly defined margins
characteristics of benign and malignant skull lesions, as
well as systemic conditions affecting the skull. In addi-
Periosteal reaction: solid/uninterrupted Periosteal reaction: aggressive,
interrupted tion, normal variants which may be mistaken for pathol-
No soft tissue component Soft tissue component ogy, sometimes called Bpseudolesions^, will also be
reviewed.
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Table 2 Salient features of benign skull lesions on CT and MRI

Skull lesion CT MRI

Fibrous dysplasia Typically homogeneously sclerotic with Variable signal depending on amount of mineralised stroma and
Bground-glass appearance^. fibrous tissue. Most commonly hypointense on T1 and T2.
Osteoma Juxta-cortical sclerotic lesion. Hypointense T1, variable signal on T2 depending on amount of
cortical and trabecular bone.
Langerhans cell histiocytosis Lytic lesion with Bbevelled edges^. Variable signal, extensive marrow oedema is typically present.
BButton sequestrum^ may be present. Plus enhancement.
Osseous venous vascular Trabeculations, Bsunburst pattern^. BBunch of grapes^ appearance.
malformation (formerly Diffuse enhancement.
haemangioma)
Intraosseous meningioma Sclerotic lesion. Hypointense T1, variable signal on T2.
Hyperostosis.
Paget disease Lytic phase: Bosteoporosis circumscripta^. Lytic phase: hyperintense T2, hypointense T1 (with foci of
Mixed phase (lytic and sclerotic): skull vault interspersed T1 hyperintense yellow marrow).
enlargement; Bcotton-wool^ appearance. Mixed phase: yellow marrow maintained in all sequences.
Blastic phase: bone thickening and sclerosis. Blastic phase: Hypointense T1 and T2.
Calvarial sarcoidosis (usually Lytic. Variable signal, may enhance.
multiple) Well-demarcated margins. Can have periosseous soft tissue component.
Ossifying fibroma Expansile, lytic lesion or solid lesion with Solid component is isointense on T1 and iso/hypointense on T2.
areas of cystic changes. Heterogeneous enhancement of the solid component.
Epidermoid cyst Well-demarcated osteolytic lesion with Restricted Diffusion.
sclerotic margins. Do not enhance.
Remodelling and expansion of skull tables.
Dermoid cyst (typically midline Expansile osteolytic lesion. Fatty signal on T1, variable signal on T2.
near anterior fontanelle) Can have soft tissue component. May see peripheral enhancement.

Benign calvarial lesions cases) with the skull being involved in both forms of
disease [1, 2, 4, 8, 9]. The monostotic form is the mildest
Fibrous dysplasia and most common form; it involves the ribs and cranio-
facial bones, and is typically diagnosed between 20 and
Fibrous dysplasia represents 2.5% of all osseous and 7% 30 years of age [1, 2, 8, 9]. The polyostotic form has an
of all benign osseous neoplasms [7]. Fibrous dysplasia earlier onset, typically in childhood and affected patients
results from abnormal differentiation and maturation of tend to have more severe skeletal and craniofacial in-
osteoblasts with progressive replacement of the normal volvement; it may also be associated with McCune-
bone by immature woven bone [1, 2, 5, 8, 9]. It is most Albright and Mazabraud syndromes [1, 2, 9]. Fibrous dys-
commonly seen in adolescents and young adults and can plasia preferentially affects the frontal and temporal bones
be monostotic (70% of cases) or polyostotic (30% of and may cross sutures [2]. The diagnosis is often

Table 3 Salient features of malignant skull lesions on CT and MRI

Skull Lesion CT MRI

Multiple myeloma (multiple) Osteolytic lesions without sclerotic rim, Bpunched-out Hypointense T1, hyperintense T2.
lesions^. BSalt and pepper marrow infiltration^ is the most
common pattern.
Typically enhance.
Osteosarcoma Lytic lesion, ill defined borders. Variable appearance.
Aggressive periosteal reaction.
Variable amount of osteold matrix.
Metastases (may be solitary or Lytic, sclerotic or mixed depending on the primary Hypo/isointense T1, hyperintense T2.
multiple) tumour. Typically enhance (unless sclerotic).
Chordoma (skull base, midline) Lytic destructive expansile lesion of the clivus. Hypointense T1, lobules of high signal on T2.
Heterogeneous enhancement.
Chondrosarcoma (skull base, Osteolvtic lesion. Hypo/isointense T1, hyperintense T2.
paramidline) Chondroid matrix with Brings and arcs^. BWhorls of enhancement^.
 Insights Imaging

incidental, but may present as an enlarging mass with signal on T1- and T2-weighted images given that the ho-
symptoms resulting from mass effect and narrowing of a mogeneously sclerotic form is most common (Fig. 2)
foramen transmitting one of the cranial nerves [1–4, 8, 9]. [1–9]. Lesions with highly mineralised stroma tend to
Malignant transformation is very rare and has been report- show lower signal intensities on T1- and T2-weighted
ed in 0.4–1% of cases [2]. An associated aneurysmal bone images, whereas lesions with high fibrous tissue tend to
cyst or pathological fracture may complicate this entity have intermediate signal intensity on T1-weighted images
[2]. and high signal on T2-weighted images [1, 2, 6, 8, 9]. It
CT demonstrates an intradiploic, expansile lesion with can be useful to get a CT if MRI findings are equivocal.
the characteristic Bground-glass matrix^ in all or part of Treatment is based on bisphosphonates. Surgical decom-
the lesion (Fig. 2) [1–9]. The outer table is more promi- pression is performed when there is severe mass effect [2].
nently affected compared to the inner table [1, 2, 4]. Three
patterns have been described: mixed lytic and sclerotic, Osteoma
homogeneously sclerotic and a predominantly cystic or
lytic pattern; but the homogeneously sclerotic (ground- Osteoma is the most frequent benign tumour in adults and
glass density) pattern is usually seen [1, 2, 4, 6]. Fibrous is most commonly seen in men between the fourth and
dysplasia can have varying signal and contrast enhance- fifth decades of life [1, 2]. It is a juxta-cortical tumour
ment on MRI depending on the ratio of fibrous tissue to made up of well-differentiated compact or cancellous
mineralised matrix [1–9]. The lesion is typically low bone [1, 2, 4–6]. Osteomas usually arise from the outer

Fig. 2 Fibrous dysplasia. Axial

(a) and coronal (b) head CT
images demonstrate an expansile
lesion with ground-glass matrix in
the right greater wing of the
sphenoid (arrows). Axial T1-
weighted (c), axial T2-weighted
(d) and axial post-contrast T1-
weighted (e) images show that the
lesion is hypointense with
homogeneous enhancement
(arrowheads)
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table and rarely from the inner table and can be sessile or Langerhans cell histiocytosis
pedunculated [1, 2, 4–6]. Inner table osteomas can be
misdiagnosed as ossified meningiomas; however, unlike Langerhans cell histiocytosis (LCH), formerly known as
meningioma, osteomas do not have a soft tissue compo- Bhistiocytosis X^ is due to an idiopathic proliferation of
nent and do not enhance [4, 6]. Langerhans cells in various tissues (bone marrow, central ner-
On CT, an osteoma is a juxta-cortical, well-defined, vous system, lung, liver, spleen, lymph nodes) causing focal
sclerotic, homogenous lesion [1, 2, 4–6]. On MRI, it or systemic disease [1, 2, 10, 11]. This disease is most com-
has homogenous low signal on T1-weighted images, mon in children between 6 and 10 years of age and can occa-
but variable appearance on T2-weighted imaging, de- sionally be seen in young adults [1, 2, 4, 6, 10]. Langerhans
pending on the amount of compact and cancellous/ cell histiocytosis comprises three clinical syndromes: (1) eo-
trabecular bone [1, 2, 4–6] (Fig. 3). When multiple os- sinophilic granuloma, which is limited to bone or lung; (2)
teomas are seen in the skull, Gardner syndrome should Hand-Schuller-Christian disease, which presents with
be considered, a disorder characterised by multiple os- calvarial lesions, exophthalmos and diabetes insipidus; (3)
teomas, colonic polyposis, sebaceous cysts and various Letterer-Siwe disease, the most aggressive form of LCH with
benign tumours such as lipomas and fibromas [1, 2] multi-visceral organ involvement [1, 2, 10, 11]. The most
(Fig. 4). frequent form of LCH is eosinophilic granuloma in which
Osteomas do not require treatment unless they cause mass the calvarium is frequently involved [1, 2, 6]. Lesions more
effect and disturb surrounding structures [1, 2]. frequently occur in the parietal or frontal regions [2, 6].

Fig. 3 Osteoma. Axial (a) and

coronal (b) head CT images show
a juxta-cortical lesion along the
outer table of the left frontal bone
(arrows). Axial T1-weighted (c),
sagittal T1-weighted (d) and
coronal post-contrast T1-
weighted (e) images depict the
sclerotic/osteoblastic nature of
this lesion (arrowheads). Note the
well-defined margins and lack
of enhancement
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Fig. 4 Gardner Syndrome

(multiple osteomas). Axial head
CT images (a–c) show multiple
osteomas in the ethmoid air cells
(dashed arrows), left ramus of the
mandible (arrowhead) and right
anterior wall of the maxillary
sinus (thin arrow). This patient
was also found to have a
mesenteric desmoid tumour (thick
arrow, d)

Fig. 5 Langerhans cell

histiocytosis. Sagittal skull
radiograph (a) shows two lytic
lesions (arrowheads) in the
parietal skull, the largest one with
an associated soft tissue
component (thin arrow). Axial
head CT images (b, c) in the bone
and soft tissue windows in the
same patient demonstrate an
osseous destructive lesion in the
left frontal calvarium with
bevelled edges (dashed arrows)
and a soft tissue component (thick
arrows); pathology proven
eosinophilic granuloma in a 4-
year-old boy
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Fig. 6 Osseous venous vascular

malformation. Sagittal T1-
weighted imaging (a), axial T2-
weighted imaging (b) and sagittal
contrast-enhanced venogram (c)
show a hypointense T1,
hyperintense T2 and enhancing
lesion in the occipital bone
(arrows)

Clinically, the lesions can be asymptomatic or present as pal- Treatment varies depending on the severity and bony ex-
pable and/or tender masses [1, 2, 4, 6, 10]. tent. Single lesions can be treated with surveillance or system-
On radiographs, there may be one or multiple well-defined ic corticosteroids. In the more aggressive forms of disease,
punched-out osteolytic lesions [1, 2, 4, 6]. surgical excision, radiotherapy and chemotherapy are treat-
On CT, the early appearance of LCH is an osteolytic lesion ment options [2].
with bevelled edges due to unequal involvement of the inner and
outer tables (Fig. 5) [1, 2, 4–6, 10]. The centre of the lesion may Osseous venous vascular malformation
contain a Bbutton sequestrum^, a central residual intact bone [1,
2, 6, 10]. They lack a sclerotic rim or periosteal reaction [1, 2]. The International Society for the Study of Vascular Anomalies
Multiple lytic lesions may coalesce giving the appearance of a (ISSVA) classification system divides vascular anomalies into
geographic map [2]. They can also have a soft tissue component two primary biological categories: vascular neoplasms and
and may have extradural and extracranial extension [1, 2, 5, 6]. vascular malformations [13–15]. Vascular malformations in-
Later on, healing lesions, whether spontaneous or under treat- clude low-flow malformations (capillary, venous, and lym-
ment, become sclerotic with centripetal bone formation and dis- phatic), high-flow malformations (arterial malformation, arte-
appearance of the osteolytic lesions [2, 6]. riovenous malformation and arteriovenous fistula) and com-
MRI may aid in the depiction of bone marrow or soft tissue bined malformations (i.e. venolymphatic malformation). The
involvement, but the signal intensity of these lesions is non- previously called cavernous haemangiomas are actually ve-
specific; however, extensive bone marrow oedema is typically nous malformations [13–15]. Osseous venous malformations
present [10, 12]. Most frequently, LCH has low to intermedi- are benign slow-growing vascular bone tumours that account
ate signal on T1-weighted images and high signal on T2- for 2–10% of benign calvarial lesions and 0.2% of all bone
weighted images, except in the healing phase when the signal neoplasms [1, 2, 16–18]. They affect the frontal and parietal
is low on T2 imaging [6]. Eosinophilic granuloma enhances bones predominantly and are more common during the 4th
strongly with gadolinium and often has reactive dural or galeal and 5th decades of life [1, 2, 6, 16–18]. Fifteen percent of
enhancement [1, 2, 5, 6]. skull venous malformations are multiple [18]. These lesions
 Insights Imaging

are more frequent in women than men with a ratio of 3:2 [2, 6, trabeculae adjacent to the angiomatous channels [1, 2, 4,
16–18]. Calvarial venous malformations arise from vessels in 16–18]. CT shows a well-circumscribed intradiploic
the diploic space and are supplied by branches of the external osteolytic lesion with mild expansion of the outer table
carotid artery, with the middle meningeal and superficial tem- and relative sparing of the inner table. A sunburst pattern
poral arteries being the main sources [14]. Most of these vas- of trabecular thickening radiating from a common centre is
cular tumours in the skull contain dilated blood vessels sepa- the classic finding [2, 4, 16–18]. On MRI, the serpentine
rated by fibrous septa [2, 16, 17]. Usually they are small and vascular channels can be identified and the appearance
asymptomatic, but they can cause pain or present as a palpable depends on the fat content and vascularity of the lesions.
deformity [1, 2, 6]. Calvarial venous malformations affecting They are characteristically isointense to hyperintense on
the roof of the orbit can cause proptosis and even blindness; T1-weighted images and hyperintense on T2-weighted im-
and those located in the petrous bone may present with deaf- ages with a Bbunch of grapes^ appearance (Figs. 6 and 7).
ness or cranial nerve palsies [2, 13–15]. Growth of these neo- Low signal on T1 is due to decreased marrow fat or greater
plasms occurs by expansion of the outer table. Rarely, they vascular component and has been associated with a more
can have intracranial extension with few cases reported of aggressive behaviour. Punctate or reticular low T2 signal
erosion of the inner table and dura mater presenting as sub- may be present representing fibrous tissue or foci of calci-
dural haemorrhage [16, 17]. fication. These bony lesions enhance diffusely after con-
On plain radiographs, this vascular tumour presents as trast administration. Sometimes they can have an aggres-
an osteolytic lesion with the characteristic Bsunburst^ or sive pattern with a soft-tissue component and may simulate
Bhoneycomb^ trabecular pattern, which is due to thickened a malignant neoplasm [1, 2, 6, 16–18].

Fig. 7 Osseous venous vascular

malformation. Axial head CT (a)
shows osteolytic changes
(trabecular appearance) of the
clivus (dashed arrow) extending
into the left occipital condyle (thin
arrow). Sagittal T1-weighted (b),
axial T2-weighted (c) and post-
contrast sagittal T1-weighted
images (d, e) show abnormal
signal in the clivus (dashed
arrows) and left occipital condyle
(thin arrow) with enhancement
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Fig. 8 Intradural meningioma.

Axial head CT images (a, b) show
hyperostosis of the left sphenoid
bone, clivus and petrous portion
of the left temporal bone
(arrowheads). Axial (c) and
coronal (d) post-contrast T1-
weighted images show a large
enhancing lesion along the left
sphenoid wing (thick arrows)
extending along the clivus and
sella (dashed arrows), as well as
left middle cranial fossa (short,
thick arrow); there is also
extension outside of the
calvarium (thin arrow)

Treatment of these lesions is mainly surgical; embolisation The meningiomas arising outside the dural compart-
may be performed before surgical intervention to reduce blood ment have been called ectopic, extradural or intraosseous
loss [2]. meningiomas. Lang et al. [19] has proposed the term
Bprimary extradural meningioma^ for such lesions; this
is to differentiate them from primary intradural meningi-
Intraosseous meningioma omas which may have secondary extracranial extension
and/or may have metastasised into the skull and adjacent
Meningiomas are the most common extra-axial dural based soft tissues.
tumours in middle-aged and elderly patients [1, 2, 6, 19]. The Intraosseous meningioma is a rare subtype of meningi-
characteristic finding of an intradural meningioma is reactive oma that account for <2% of all meningiomas [19–22].
hyperostosis of the adjacent calvarium (Fig. 8). Occasionally, The frontoparietal and orbital regions are the most com-
they can produce marked bone thickening with outward mon locations [2, 19, 20]. Although primary intradural
growth of the outer table of the skull [1, 4]. meningiomas occur twice as frequently in women

Fig. 9 Intraosseous meningioma.

Axial (a) and coronal (b) CT
images portray an intraosseous
meningioma in the right sphenoid
extending into the right lateral
orbital wall (arrows). Note the
expansion of bone and Bprickly^
border of the lesion
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Fig. 10 Paget disease. Axial head

CT (a, b) images demonstrate
increased cortical density and
trabecular thickening (arrows)

Fig. 11 Calvaria sarcoidosis.

Axial head CT (a, b) images show
three lytic lesions in the diploic
space of the frontal bones
(arrows) with involvement and
thinning of the cortex of the inner
tables (dashed arrows). Axial T1-
weighted imaging (c) depicts
hypointense lesions (arrows).
Post-contrast T1-weighted (d, e)
images demonstrate enhancement
of these lesions (arrowheads)
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Fig. 12 Ossifying fibroma. Water

view skull radiograph (a), axial
(b) and sagittal (c) head CT
images show a lytic lesion in the
frontal bone (arrowhead) with
barely perceptible anterior and
posterior cortical margins (dashed
arrows)

compared to men and predominantly in older adults, On CT, an intraosseous meningioma typically appears as a
intraosseous meningiomas occur with the same frequency sclerotic lesion with associated hyperostosis of the bone, and
in men and women and have a peak in the second decade irregular and spiculated borders (Fig. 9) [2, 4]. On MRI, the
of life [19]. It is thought that they are due to trapping of tumour has low signal on T1-weighted images and variable
embryonic arachnoid cap cells in the developing calvaria signal intensity on T2-weighted images [2, 4, 6]. Meningeal
in the cranial sutures (particularly the coronal suture) or enhancement is rare and is due to adjacent dural irritation or
due to trapping of arachnoid cells in a prior skull fracture invasion [1, 2, 4]. Intraosseous meningiomas can rarely be
or surgical osteotomy [2, 19, 20]. Calvarial intraosseous osteolytic and in those cases are more commonly malignant
meningiomas are more prone to develop malignant chang- [2, 4, 19].
es (11%) compared with primary intradural meningiomas In a symptomatic primary intraosseous meningioma, total
(2%) [19, 22]. tumour removal with a wide surgical resection followed by
Osteoblastic or mixed osteoblastic-osteolyic meningiomas cranial reconstruction is the treatment of choice. If only subtotal
compose most of intraosseous meningiomas, with the purely resection is possible due to involvement of critical structures
lytic form being the least common [1, 2, 4, 19]. Primary within the orbit, paranasal sinuses, or skull base, the residual
extradural meningiomas are classified as extracalvarial (type tumour should be followed radiologically. Adjuvant radiation
1), purely calvarial (type 2) or calvarial with extracalvarial therapy is recommended if the residual tumour is symptomatic
extension (type 3) [19]. or if there is evidence of disease progression [2, 19].
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Fig. 13 Epidermoid cyst. Axial

head CT portrays an expansile
lesion in the right frontal bone
(thick arrow) with thinning of the
inner and outer tables (dashed
arrows). Axial T1-weighted
imaging (b), axial T2-weighted
imaging (c), axial DWI (d) and
axial post contrast T1-weighted
imaging (e) show that the lesion is
hypointense on T1, hyperintense
on T2 with restricted diffusion
and absent internal enhancement
(arrowheads). Note that there
may be some enhancement along
the peripheral margins

Paget disease This anarchic bone behaviour produces disorganised new

bone in a mosaic pattern [2, 6, 23, 24]. Paget affects the skull
Paget disease (also known as osteitis deformans) is a chronic in 28–42% of cases, particularly the frontal and occipital
skeletal disorder characterised by abnormal and excessive bones. Other locations affected by Paget are the lumbar spine
bone remodelling. Paget disease is estimated to affect approx- (30–75%), pelvis (30–75% of cases), sacrum (30–60%) and
imately 3–4% of individuals older than 40 years [2, 5, 23–26]. femur (25–65%). Polyostotic disease is more common than
It is a progressive disorder that evolves through various stages monostotic disease [23, 24].
or phases of activity. Three major phases are recognised: the Skull involvement in Paget disease can lead to increase in
lytic phase (incipient active), in which osteoclastic resorption head size, hearing loss and entrapment of the cranial nerves in
predominates; the mixed phase (active), in which there is both their respective foramina. When the skull base is involved, there
osteoblastic and osteoclastic hyperplasia with predominantly is platybasia and basilar invagination in which the tip of the
osteoblastic activity; the sclerotic or blastic phase (late inac- odontoid projects more than 5 mm above the Chamberlain line
tive), in which the osteoblastic activity gradually declines. between the hard palate and basiocciput [23, 24].
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Fig. 14 Dermoid cysts. Patient 1:

Axial head CT (a) depicts a
midline fat-containing lesion in
the frontal region (thick arrow).
Patient 2: Axial bone window (b)
and coronal soft tissue window
head CT (c) show a dermoid cyst
in the left frontal bone involving
the outer table (dashed arrows).
Patient 3: Axial CT (d) and
coronal head CT portray a fat-
containing lesion in the left grater
wing of the sphenoid
(arrowheads)

Early in the disease, osteolytic activity predominates. signal intensity can be seen on T2-weighted images, as
In this phase, advancing osteolysis presents as large areas well as strong enhancement. In this stage, on T1-
of radiolucency in the frontal and occipital bones, known weighted MR images, the marrow has decreased signal
as Bosteoporosis circumscripta^. The mixed phase is no- intensity, generally similar to that of muscle; however, it
table for four cardinal features, which comprise advanced typically contains small to extensive foci of intermixed,
osteolysis, coarsening and thickening of bone trabecula, normal and maintained yellow marrow. This feature is
cortical thickening and osseous widening. In this phase, important because it excludes malignant transformation.
there is homogeneous enlargement of the skull vault, In the mixed phase, the yellow marrow signal is main-
thickening of the tables and trabecula. The fluffy cotton- tained in all pulse sequences. In the late blastic inactive
wool appearance of the skull is characteristic in this phase phase, the marrow space has low signal intensity on both
with diploic dense lesions in previously sclerotic areas T1- and T2-weighted images representing sclerosis [2, 5,
(Fig. 10). Diploic widening is also seen in this phase [2, 6, 23, 24].
5, 6, 23, 24]. Sarcomatous degeneration of Paget has been described
As suspected, MRI features vary depending on the with varying frequency depending on the extent of disease.
stage of the disease. Initially, during bone resorption, high In patients with widespread skeletal involvement,
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Fig. 15 Cleidocranial dysostosis. Axial (a) and coronal (b, c) head CT radiograph (d) in the same patient depicts hypoplasia of the bilateral
images show islands of intra-sutural bones (dashed arrows) in the clavicles (arrows), confirming cleidocranial dysostosis
lambdoid and sagittal sutures representing wormian bones. Chest

sarcomatous degeneration may occur in 5–10% of cases, infiltration and associated periosseous soft tissue (Fig. 11).
whereas in patients with less skeletal involvement, neoplasm They have variable signal intensity and may enhance after
can occur in less than 1% of cases [23, 27]. administration of contrast [28–31]. Differential considerations
Treatment relies mainly on bisphosphonates [2]. include osseous venous malformation, eosinophilic granulo-
ma, metastasis, as well as chronic infection.
Calvarial sarcoidosis Partial or complete resolution of the sarcoid lesions can
occur spontaneously [30]. Treatment is usually indicated
Sarcoidosis is an inflammatory disorder of unknown when the symptoms include uncontrolled pain, stiffness or
cause characterised by the presence of non-caseating bony destruction. Therapy generally consists of oral cortico-
granulomas in tissues. Sarcoidosis involves multiple or- steroids; methotrexate and hydroxychloroquine can also be
gans, most commonly the lungs, skin and eyes but may used [32].
be seen in any organ system, including the musculoskel-
etal system [28]. Skeletal involvement is an uncommon Ossifying fibroma
manifestation of sarcoidosis. When it occurs, bone in-
volvement is usually limited to the vertebra and tubular Ossifying fibroma is a benign fibro-osseous tumour made
bones of the hand and feet with the classic lacy lytic of highly cellular fibro-osseous connective tissue. It is
appearance. Skull involvement in sarcoidosis is very rare more often seen in children and young adults and can
with few cases reported [28–31]. Clinically calvarial sar- affect the calvaria in approximately 12% of cases. It is a
coidosis may manifest with headaches and skull tender- benign slow-growing tumour, but a subset of these tu-
ness [28–30]. mours tends to be infiltrative and locally aggressive [33,
The lesions are osteolytic with well-demarcated margins 34]. Three forms of ossifying fibromas have now been
and usually multiple. In contrast to metastasis, the calvarial distinguished: classical ossifying fibroma, psammomatoid
tables are intact. They can also manifest as expansile lesions juvenile ossifying fibroma and trabecular juvenile ossify-
on CT imaging. MR can be used to assess bone marrow ing fibroma. The psammomatoid type of juvenile
Insights Imaging

Fig. 16 Multiple myeloma. Skull

radiograph (a), axial (b) and
sagittal (c) head CT show multiple
Bpunched out^ lytic lesions in the
calvarium (arrows), Bsalt and
pepper^ appearance

ossifying fibroma is reported more commonly than the Epidermoid and dermoid cysts
trabecular variety, is more aggressive and has a strong
tendency to recur [35]. Epidermoid and dermoid cysts are benign slow-growing le-
On radiographs, ossifying fibroma appears as a sions that may be congenital or acquired from post-surgical or
monostotic, round or ovoid, well-demarcated expansile post-traumatic implantation of epidermal or dermal inclusions
lesion. It may be predominantly cystic or sclerotic de- within the diploe. Clinically, they manifest as non-tender,
pending on the amount of non-calcified versus that of slowly expanding masses enlarging over years or decades
the mineralised regions. On CT, ossifying fibroma is a [1, 2, 4–6].
mass composed of enhancing soft tissue with varying Epidermoid cysts are lined with squamous epithelium and
amounts of internal punctate calcifications. Areas of low contain remnants of cholesterol and keratin. Intradiploic epi-
attenuation caused by cystic changes may be present, and dermoid cysts can occur in any part of the skull, but most
can have internal haemorrhage (Fig. 12) [33–35]. commonly occur laterally in the parietal and frontal bones.
On MRI, the solid component is usually isointense to mus- They are usually discovered in patients between 20 and
cle on T1-weighted images and isointense to hypointense to 50 years of age [1, 2, 6].
muscle on T2-weighted images. Post-contrast images show On CT, epidermoid cysts appear as well-demarcated
diffuse and heterogeneous enhancement of the solid compo- intradiploic osteolytic lesions with smooth sclerotic margins.
nent and thin peripheral enhancement of the cystic areas These lesions often cause remodelling and expansion of the inner
[33–35]. Differential considerations include fibrous dysplasia, and outer tables. Rarely, they may have increased attenuation on
aneurysmal bone cyst, osteoblastoma and cementum produc- CT, possibly due to haemorrhage, formation of calcium soaps or
ing lesions such as cemento-osseous dysplasia and high protein content (white epidermoids) [1, 2, 4–6, 36].
cementifying fibromas [34]. On MRI, epidermoids have fluid-signal intensity on T1-
Because of its locally aggressive nature and high recur- and T2-weighted images and have characteristic restricted dif-
rence rate, early detection and complete surgical removal are fusion on diffusion-weighted imaging (DWI). They do not
essential [34]. enhance after contrast administration (Fig. 13) [1, 2, 4–6, 36].
 Insights Imaging

Fig. 17 Parosteal osteosarcoma.

Axial CT (a, b) images show a
lobulated exophytic mass
(arrowheads) with central dense
ossification in the left temporo-
occipital region. Axial T1-
weighted (c), axial T2-weighted
(d) and axial post-contrast T1-
weighted (e) images re-
demonstrate a juxta-cortical
enhancing lesion abutting the
outer table of the left temporo-
occipital bones (arrows) with a
small component extending into
the medullary cavity with
associated cortical disruption
(dashed arrows)

Dermoid cysts are lined by thick squamous epithelium Treatment of both epidermoid and dermoid cysts is surgical
and contain epidermal appendages such as sebaceous resection; recurrence is uncommon [2].
glands, sweat glands and hair follicles. They usually pres-
ent in the first 3 decades of life. These lesions typically Cleidocranial dysostosis
involve the midline of the skull near the anterior fonta-
nelle, but may also occur along the posterior and middle Cleidocranial dysostosis is a rare skeletal dysplasia with auto-
cranial fossae [1, 2, 4–6]. somal dominant inheritance due to mutation in the CBAF1
On CT, dermoids appear as expansile, osteolytic midline gene. It is a polyostotic disorder characterised by incomplete
lesions with a soft-tissue component extending into the adja- intramembranous ossification of midline bony structures. It
cent soft tissues and intracranially. They have attenuation of affects the skull, clavicles and eruption of teeth [38, 39]. In
lipid material because of their sebaceous secretions. the skull, multiple wormian bones due to islands of
Intralesional calcifications can be present. intrasutural bones in the sagittal and lambdoid sutures are
On MRI, they have a heterogeneous appearance with fatty characteristic. Premature fusion of the coronal suture or
signal intensity on T1-weighted images, variable signal on T2- brachycephaly, as well as frontal and parietal bossing has also
weighted images and thick peripheral enhancement after con- been described. Findings outside the skull comprise absent
trast administration (Fig. 14) [1, 2, 4–6, 37]. and/or hypoplasia of the lateral clavicle, supernumerary ribs,
Insights Imaging

Fig. 18 Skull metastasis. Patient

1: Axial (a) and sagittal (b) head
CT images show an expansile
destructive lesion in the frontal
skull (arrowheads), pathology
proven metastatic renal cell
carcinoma. Patient 2: Sagittal T1-
weighted (c) and sagittal post-
contrast T1-weighted (d) images
demonstrate an enhancing lesion
in the clivus (arrowheads) with
soft tissue component extending
into the sphenoid sinus (arrows)
and anterior to the midbrain
(dashed arrow). This lesion was
proven to be metastatic from
breast primary

hemivertebrae, hypoplasia of the iliac bones and short or ab- are usually disseminated through the axial skeleton, af-
sent limbs (Fig. 15) [38, 39]. fecting the vertebrae most commonly, as well as the ribs,
skull, pelvic girdle and proximal appendicular skeleton [2,
40–42].
Malignant calvarial lesions In the skull, radiographs show Bpunched-out^
osteolytic lesions with sharp non-sclerotic margins and
Multiple myeloma endosteal scalloping when lesions abut the cortex
(Fig. 16). These lesions may coalesce into larger
Multiple myeloma is a malignant bone marrow disorder osteolytic segments. The disseminated form with diffuse
characterised by monoclonal proliferation of plasma cells. It osteopenia is less frequently encountered in the skull.
is the most common primary skeletal neoplasm in adults Similarly, CT will show multiple lytic foci without a scle-
above 40 with a higher prevalence in men between the 5th rotic rim [2, 5, 6, 40, 42]. Plasmacytoma, which repre-
and 8th decades [1, 2, 5, 6, 40]. sents the focal solitary form of this neoplasm, is rare in
This disorder causes bone pain with laboratory abnormal- the skull [2, 40]. MRI is superior to detect bone marrow
ities consisting of anaemia, hypercalcaemia, high erythrocyte involvement. The lesions are hypointense on T1-weighted
sedimentation rate with normal C-reactive protein, and high images, hyperintense on T2-weighted images and enhance
total level of serum protein with a low albumin to globulin after contrast administration [2, 6, 40–42]. Five different
ratio due to overproduction of globulins (IgM, IgA). There is infiltration patterns have been described on MRI with the
also hyperuricaemia due to increased cell turnover and pro- Bsalt and pepper^ pattern of inhomogeneous bone marrow
teinuria with urinary excretion of Bence-Jones light chain im- infiltration being the most common. The other four pat-
munoglobulin, both of which are nephrotoxic, leading to renal terns include: normal bone marrow despite microscopic
failure [2, 40–42]. cell infiltration, focal involvement, homogeneous diffuse
Multiple myeloma has four main patterns: disseminated infiltration and combined diffuse and focal infiltration [5,
form with multiple round lytic lesions, disseminated form 40].
with diffuse osteopenia, solitary plasmacytoma and Treatment depends on the stage of the disease and is based
osteosclerosing fibroma [2, 42]. Multiple myeloma lesions on chemotherapy and grafting of haematopoietic cells [2].
 Insights Imaging

Fig. 19 Chordoma. Axial head

CT (a) shows an osteolytic
destructive lesion involving the
clivus (thick arrows) with
extension into the posterior
sphenoid sinus (arrowhead) and
impression on the pons (curved
arrow). Axial T1-weighted (b),
axial T2-weighted (c) and sagittal
post-contrast T1-weighted (d)
images demonstrate an expansile
mass centred at the clivus
extending into the sphenoid sinus
(arrowhead), left cavernous
region (short, thick arrows) and
partially encasing the left internal
carotid artery. This mass enhances
and displaces the pituitary gland
(thin, long arrow) and has mass
effect on the left aspect of the
pons (curved arrow)

Osteosarcoma should also be obtained. Treatment requires aggressive surgi-

cal therapy followed by chemotherapy [43].
Osteosarcoma is a malignant mesenchymal neoplasm in
which the tumour cells produce osteoid or immature bone. It Metastases
is the second most common primary skeletal tumour after
multiple myeloma [1, 43]. Metastases are the most common malignant bone tumours
Calvarial osteosarcomas may be primary arising de novo or in adults and are typically seen after the 5th decade of life.
secondary to malignant transformation of Paget disease and Metastases are usually secondary to breast, lung, prostate,
radiation therapy. Primary osteosarcoma occurs in the young kidney and thyroid cancer in adults and to neuroblastoma
population with peaks between the 1st and 2nd decades of life. or sarcomas in children. The most common calvarial me-
On the other hand, secondary osteosarcoma affects the elderly tastasis in adults is from breast cancer. In children, the
population [1, 43, 44]. most common calvarial metastases are from neuroblasto-
Unlike osteosarcomas of the extremities, calvarial osteosar- ma [1, 2, 4–6].
comas occur mainly in the 3rd and 4th decades of life [1]. Metastases may have an osteolytic, sclerotic or mixed
Multiple histological subtypes of osteosarcoma have been pattern depending on the primary tumour. Metastases
described which comprise the conventional or high-grade osteo- usually present as multiple osteolytic lesions with a
sarcoma, low-grade osteosarcoma, telangiectatic osteosarcoma, soft-tissue component extending into adjacent tissues
periosteal and parosteal osteosarcoma. Many lesions also contain [4–6]. When single and expanded osteolytic lesions are
other elements, such as fibroid or chondroid components [45]. encountered, metastasis from thyroid or renal neoplasm
The imaging appearance of osteosarcoma is variable de- should be suspected. Sclerotic metastases are seen in
pending on the histological type. In the skull, osteosarcoma p ro sta te ca nc e r. M et as ta t i c l es i o ns ar e u s u al l y
usually has a lytic appearance with variable amount of osteoid hypointense to isointense on T1-weighted images and
matrix. Also, it has ill-defined borders, aggressive periosteal enhance after contrast administration. The pattern of en-
reaction and an associated soft-tissue mass (Fig. 17) [1, 43, 44]. hancement is variable and may be homogeneous, hetero-
Approximately 5–10% of osteosarcomas have lung metas- geneous, peripheral ring or may lack enhancement in the
tasis at presentation and, therefore, imaging of the chest case of sclerotic lesions. Also, MRI is useful to assess
Insights Imaging

Fig. 20 Chondrosarcoma. Axial

non-contrast CT (a) shows an
osteolytic destructive lesion
involving the right petro-occipital
junction and clivus (arrowhead).
Axial contrast-enhanced CT (b)
demonstrates this lesion to have a
soft-tissue component extending
anteriorly into the sphenoid sinus
(thick arrow) and posteriorly into
the prepontine cistern with mass
effect on the pons (dashed
arrow). Axial (c) and coronal (d)
CT angiogram images
demonstrate involvement of the
right petrous carotid canal
(arrowheads) with the lesion
surrounding the right internal
carotid artery (thin arrow). Note
the punctate calcifications
(chondroid matrix) within the
mass (curved arrow). Axial
T1-weighted (e) and axial
T2-weighted (f) images show a
lobulated lesion involving the
right petro-occipital junction and
clivus (arrowhead). Note the
extension of the lesion anteriorly
into the sphenoid sinus (thick
arrow) and posteriorly into the
prepontine cistern with mass
effect on the pons (dashed
arrow). Axial SWAN (g) shows
internal foci of low signal,
consistent with calcifications
(curved arrow). Post-contrast
axial T1-weighted imaging (h)
demonstrates heterogeneous
(“whorls” of) enhancement
(arrowhead)
 Insights Imaging

dural invasion and intracranial extension, in addition to or sarcomatous transformation occurs in 2–8% of
disease involving the brain parenchyma (Fig. 18) [1, 2, chordomas [49].
5, 6, 46]. The sacrococcygeal region is the most common location,
Treatment depends on the histological type of the neo- followed by the clivus, but can occur anywhere along the
plasm. Patients with signs of dura infiltration and related neu- primitive notochord, including the cervical, thoracic and
rological deficit should be offered neurosurgical therapy. lumbar spine [48–50]. Chordoma has been considered of
Radiation therapy is an alternative in cases of multiple or low metastatic potential; however, distant metastasis to
highly vascularised lesions [2, 47]. lung, bone, soft tissue, lymph node, liver and skin has been
reported [49].
Skull base chordomas can present with headaches and dip-
Chordoma lopia and affect men and women with an equal ratio [48].
Clival chordoma is a midline, lytic, destructive,
Chordoma is a malignant, locally aggressive tumour that orig- expansile lesion; intratumoral pieces of destroyed bone
inates from remnants of the notochord. It is seen in the adult may be present. When large, the mass can indent the pons
population between the 3rd and 7th decades of life [48]. with the characteristic Bthumb sign^ and may elevate the
Chordomas are divided into conventional, chondroid pituitary gland, and cause symptoms related to compres-
and dedifferentiated types. Conventional chordomas are sion. It can also invade or displace other structures includ-
the most common. They are characterised by the absence ing the cavernous sinus, jugular foramen and the sphenoid
of cartilaginous or additional mesenchymal components. and posterior ethmoid sinuses [48].
Chondroid chordomas contain both chordomatous and On MRI, chordomas have intermediate to low signal on
chondromatous features, and have a predilection for the T1-weighted images. Small foci of T1 hyperintensity can
spheno-occipital region of the skull base. Dedifferentiation sometimes be visualised in the tumour, a finding that

Fig. 21 Chronic anaemia. Sagittal

head CT (a) depicts widening of
the diploic space (thick arrows).
Axial T1-weighted (b), axial T2-
weighted (c) and sagittal T1-
weighted (d) images portray
widening of the diploic space
with generalised T1 and T2
marrow hypointensity
(arrowheads) consistent with red
marrow hyperplasia in this patient
with sickle-cell anaemia
Insights Imaging

Fig. 22 Renal osteodystrophy

and osteopenia. Patient 1: Axial
(a) and coronal (b) head CT
images depict granular de-
ossification with a Bpepper pot^
appearance (thick arrows) and
loss of distinction of the inner and
outer tables (dashed arrows) in
this patient with renal
osteodystrophy. Patient 2: Axial
(c) and coronal (d) head CT
images show demineralisation of
the skull (arrowheads) in this
patient with osteopenia. Note the
relative preservation of the
distinction of the inner and outer
tables in osteopenia

represents intratumoral haemorrhage or a mucus pool. They signal on T2-weighted images; there may be interspersed
have lobules of high signal on T2-weighted images with in- foci of low signal due to chondroid matrix calcification.
tervening septations that are low in signal. Other foci of low Post-contrast images show heterogeneous enhancement,
T2 signal may be due to calcifications or areas of old haem- classically with whorls of enhancing lines within the tu-
orrhage. On post-contrast images, they have heterogeneous, mour matrix (Fig. 20) [50–52].
avid enhancement; there may be a honeycomb pattern second- The prognosis depends on the extent of the tumour at diag-
ary to intratumoral areas of low signal intensity (Fig. 19) [48]. nosis and histological pattern. Conventional chondrosarcomas
Treatment includes surgical excision and radiotherapy have a slow growth pattern and a good prognosis. The mesen-
postoperatively in non-resectable tumours. Chordomas have chymal and dedifferentiated subtypes have an aggressive be-
a high rate of recurrence and, as a result, post-treatment fol- haviour. High-grade chondrosarcomas metastasises to lungs
low-up imaging is necessary [48, 50]. and bones more frequently [51]. Surgical resection has tradi-
tionally been the mainstay of treatment for intracranial
Chondrosarcoma chondrosarcoma. This has been combined with adjuvant radia-
tion and chemotherapy to improve recurrence rates and overall
Chondrosarcomas are slow growing malignant lesions account- survival [51, 52].
ing for 6% of the skull base neoplasms. They arise from remnants
of embryonal cartilage, endochondral bone or primitive mesen-
chymal cells. The typical location of this tumour is off-midline, Systemic conditions affecting the skull
centred at the petro-occipital fissure/synchondrosis [50–52].
On CT, an osteolytic soft tissue mass is seen at the The spectrum of systemic conditions that can affect the skull is
petro-occipital fissure with the characteristic chondroid broad and can be difficult to diagnose since each tend to have
matrix calcification (Brings and arcs^) and sharp non- diffuse involvement of the skull. Of these, three systemic con-
sclerotic transition zone. On MRI, this tumour has low ditions are often encountered in clinical practice and familiar-
to intermediate signal on T1-weighted images; it has high ity with their main features is key to diagnosis.
 Insights Imaging

Fig. 23 Arachnoid granulations.

Axial head CT (a) shows well-
defined structures along the
inner table in the region of the
transverse sinus (arrowheads).
Axial T1-weighted (b) and axial
T2-weighted (c) images
demonstrate fluid signal
of these structures following
CSF along the transverse
sinus extending into the
occipital bone (arrowheads)

Chronic anaemia In patients with chronic renal insufficiency, imaging

shows diffuse increase in bone density, a finding that is
The skull changes of patients with chronic anaemia are due to seen more often in the axial skeleton, which has more
red marrow hyperplasia and consist of widening of the diploic trabecular bone than cortical bone. It is thought that this
space, and thinning and obliteration of the outer table. Before diffuse osteosclerosis may be due to the anabolic effect of
diploic widening, a coarse granular or stippled pattern can be parathyroid hormone [57].
seen in the upper parietal region. When the hyperplastic marrow In the skull, there is diffuse bone thickening with
perforates or destroys the outer table, fine bony spicules per- loss of distinction between the inner and outer tables,
pendicular to the outer table are seen, giving the typical Bhair- and granular de-ossification of the skull due to lytic foci
on-end^ appearance. This can be seen with thalassaemia, sickle interspersed within normal bone, giving the appearance
cell disease and iron-deficiency anaemia (Fig. 21) [5, 53, 54]. of Bsalt and pepper^ or Bpepper pot^ skull (Fig. 22)
[55–57].
Renal osteodystrophy

Renal osteodystrophy refers to the complex findings seen in Osteopenia

the setting of chronic renal insufficiency. Chronic renal failure
alters bone metabolism by multiple mechanisms. Phosphate Osteopenia is a condition characterised by decreased bone
retention and decreased vitamin D conversion leads to mineralisation. It may arise when bone formation is inade-
hypocalcaemia, which in turn, stimulates the production of quate or when bone resorption exceeds bone formation. It
parathyroid hormone, causing bone resorption [55–57]. has multiple causes including congenital, toxic, metabolic
The various skeletal features of renal osteodystrophy have been and idiopathic. In osteopenia, there is loss of both cortical
well documented including generalised demineralisation, thinning and trabecular bone, giving rise to a heterogeneous appearance
of the cortical bone, coarsening of the trabeculae, subperiosteal on imaging. In contrast to renal osteodystrophy, the distinction
resorption, bone cysts and pathological fractures [55]. between the inner and outer tables is preserved (Fig. 22) [57].
Insights Imaging

Fig. 24 Venous channels and

lakes. Axial (a), coronal (b) and
sagittal (c) head CT images depict
serpiginous structures in the
frontal and parietal bones
(arrowheads) representing
prominent venous channels.
Axial head CT (d) and axial post-
contrast T1-weighted (e) images
show a lucent focus along the left
parietal bone with enhancement
consistent with a venous lake
(dashed arrows). There are also
mildly prominent serpiginous
venous channels in the frontal
bones (thick arrows)

Fig. 25 Hyperostosis frontalis.

Axial (a) and coronal (b) head CT
images portray irregular
thickening of the inner table
of the frontal bone consistent
with hyperostosis frontalis
(arrowheads)
 Insights Imaging

Fig. 26 Parietal thinning. Axial

(a) and coronal (b) head CT
images shows thinning of the
parietal bones (thick arrows)

Normal variants mimicking pathology Venous channels and venous lakes

(Bpseudolesions^)
Venous channels consist of apertures in the skull through
Skull Bpseudolesions^ include arachnoid granulations, which emissary veins pass, connecting the venous sinuses of
prominent venous lakes, hyperostosis frontalis, thinning the dura mater with veins external to the skull. They look like
of the parietal bones and surgical burr holes. It is important serpiginous or linear lucencies with sclerotic borders through
to recognise these entities, so as to not mistake them for true the skull, and are, therefore, occasionally mistaken for sutures
pathology. or fractures [59].
Enlarged veins within the diploic space are known as
Arachnoid granulation venous lakes, corresponding to round or oval lucent foci,
frequently along the inner table of the skull (Fig. 24).
Arachnoid granulations, also known as pacchionian gran- These normal venous structures show intense enhance-
ulations are projections of enlarged arachnoid villi into ment after intravenous contrast administration on both
the calvaria or dural venous sinuses. They are involved CT and MR [59].
in the filtration of cerebrospinal fluid (CSF) from the sub-
arachnoid space to the venous system. Histologically, they Hyperostosis frontalis
are composed of dense collagenous connective tissue
admixed with clusters of arachnoid cells and a network Hyperostosis frontalis interna is a benign condition which
of delicate vascular space filled with CSF from the con- presents as irregular thickening of the inner table of the frontal
tiguous subarachnoid space [5, 58]. bone (Fig. 25). Although the aetiology is not clearly known,
The prevalence of arachnoid granulations increases oestrogen signalling is thought to be involved and, therefore,
with age. They normally measure a few millimetres, but most commonly seen in females [5].
can grow to fill and dilate the dural sinuses with expan-
sion of the inner table of the skull and are then called
Bgiant arachnoid granulations^. They can occur along Bilateral parietal thinning
any dural venous sinus, but are most commonly along
the transverse sinuses, particularly within the middle and Bilateral parietal thinning is an uncommon condition,
lateral portions. The second most common location is with prevalence of 0.25–0.8%. This condition is thought
along the superior sagittal sinus [5, 58]. to be due to non-progressive congenital dysplasia of the
On CT, they present as sharply marginated, hypoattenuating diploe. Parietal thinning is more common in women than
structures in close association with a dural venous sinus. On in men. The characteristic site of bilateral parietal thin-
MRI, they generally appear hypointense or isointense to the ning is the area between the sagittal suture and parietal
brain parenchyma on T1-weighted images and hyperintense prominence. Imaging features in the skull include sym-
on T2-weighted images (Fig. 23). They appear as filling defects metric thinning of the bilateral parietal bones involving
in the dural sinuses and can mimic a dural venous sinus throm- the outer table and diploe, giving a scalloped appearance
bosis, but are usually easily differentiated given their round (Fig. 26). In cases of progressive bone thinning,
well-defined shape and classic location [5, 58]. cranioplasty may be required [60].
Insights Imaging

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