This work presents an overview of

the radiologic appearance in

bone window setting of different
primary and secondary skull
tumors, bone dysplasia, congen-
ital and inammatory diseases
affecting the skull, and extrinsic
lesions exhibiting secondary
effects on the skull. The differen-
tial diagnosis of lesions affecting
the inner and/or outer table, or
the diploic space also is pre-
sented. Recommendations for
routine use of bone window
setting in brain CT scanning
includes 1) abnormal skull lms;
2) suspected congenital anom-
alies; 3) presence of enhancing
lesions in close proximity to
skull bone; and 4) suspected
metastatic disease.
B
one window images that rou-
tinely are acquired in CT exami-
nations of the head for trauma or
paranasal sinus disease can be useful in
the characterization of different skull
lesions. These images are excellent for
demonstration of skull tables and the
diploic space. Bone algorithm and l-
ters also enhance the ability to visual-
ize ne bony detail. Bone window
images obtained in conjunction with
routine brain scans may lead to fortu-
itous discovery or superior characteri-
zation of skull pathology.
CT window widths of 600 to 2,000
Hounseld units (HU) and window lev-
els of 160 HU to 500 HU accurately
delineate tissues of a large difference in
CT attenuation, such as bone and air.
Narrower window widths (80 HU to 150
HU) and lower center levels (40 HU to
50 HU) are employed to show small dif-
ferences in attenuation of soft tissues
such as brain, but are not as accurate as
bone window settings in depicting con-
tour, edge interface, and size of bone
structures.
Features of the calvaria
The calvaria is well differentiated
into three layers: inner, middle, and
outer tables. The inner and the outer
tables are composed of compact bone;
the middle table is composed of cancel-
lous bone. The inner and outer tables
vary little in thickness, except in places
where they are eroded by vascular struc-
tures and gyral impressions. The diploic
space is composed of an irregular net-
work of bony trabeculae and vascular
spaces. Blood within this space may act
as a uid cushion to absorb traumatic
forces.
1
Normal variants
Common benign lesions may repre-
sent normal variants or developmental
abnormalities in the skull. Such lesions
usually have characteristic radiologic
ndings and should not be confused
with other pathological entities. Pac-
chionian granulations or venous lakes
(gure 1) are arachnoid extensions pro-
jecting into the lumen of the main
venous sinuses. The edges are further
apart at the inner table level than at the
outer table, indicating a benign process
originating inside the skull.
1
Another
benign nding is the presence of circular
lucent defects of the calvaria, known as
doughnut lesions. These usually
do not exceed 2 cm in diameter and may
represent smaller versions of abnormal
lesions such as brous dysplasia,
eosinophilic granuloma, epidermoid
inclusion cyst, or osteoid osteoma.
3
Some cases of doughnut lesions may be
familial in nature.
4
Parietal thinning (gure 2) is charac-
terized by the generally bilateral and
symmetrical thinning of the parietal
bones with partial or complete absence
of the diploe and the outer table of the
skull.
5
Parietal foramina are holes in the
Value of bone window images
in routine brain CT:
Examinations beyond trauma
Dr. Snow and Dr. Brogdon are in the
Department of Radiology at University
of South Alabama Medical Center in
Mobile, AL. Dr. Williams was in the
Department of Radiology at University
of South Alabama Medical Center in
Mobile, AL. Dr. Georgy is in the
Department of Radiology at the Univer-
sity of California in San Diego, CA.
Bassem A. Georgy, MD; Ruth D. Snow, MD; Byron G. Brogdon, MD; J. Powell Williams, MD
FIGURE 1. Well-defined defect in the left
frontal bone (arrow) compatible with venous
lake is observed in a 59-year-old woman
undergoing serial CT examinations for left
middle cerebral artery infarction.
skull that represent a benign variant of
incomplete ossication of the bones in
the region of the obelion on both sides
of the sagittal suture, and may be associ-
ated with severe pain and headache with
gentle pressure.
6
Parietal foramina also
may be familial and is possibly associ-
ated with faulty ossication of the clavi-
cles.
7
Another abnormality that may be
seen is hyperostosis frontalis interna,
8
which is characterized by thickening of
the inner table that may extend to the
diploe of the frontal bone; this lesion is
commonly found in middle-aged
women (gure 3). It is important to dif-
ferentiate this normal variant from
hyperostosis that may occur secondary
to meningiomas.
Hereditary and developmental
abnormalities
A long list of developmental and
hereditary diseases can affect the cal-
varial bones. Hodges
3
divided the
hereditary abnormalities of the calvaria
into ve groups: suture abnormalities,
abnormalities in shape and size,
increased thickness and density, gener-
alized thinning, and skull defects or
holes. Table 1 summarizes the radio-
logical ndings of the common devel-
opmental and hereditary diseases that
can affect the skull calvaria (gures 4-
6). Bone window setting also is
extremely valuable in the evaluation of
nasal bone and temporal bone develop-
mental anomalies (gure 7).
FIGURE 2. Parietal thinning in a 75-year-old woman shown in a lateral skull lm (A). Bone
window setting of brain CT (B) showed marked thinning of the inner and outer tables in pari-
etal regions (arrows).
A B
FIGURE 3. Incidentally noted hyperostosis frontalis in a 72-year-old woman (A). A normal
bone window of matched age and sex is illustrated (B).
A B
FIGURE 4: Neurobromatosis in a 3-year-
old girl. Dysplasia of the right sphenoid
wing is seen in a bone window image (A).
Soft-tissue density, likely representing a
plexiform neurofibroma, is seen filling the
defect in a corresponding T1-weighted
image (TR/TE= 650/16) (B).
A
B
FIGURE 5. Osteopetrosis in a 56-year-old
man showing a thick skull, increased bone
density, and obliteration of the diploic
space.
Inammatory lesions
Infections of the skull are rare
because of the relative resistance of the
calvarial bones to infection. When
infection does occur, it usually is by
direct extension from the paranasal
sinuses and mastoid air cells or from
trauma.
18
Subperiosteal abscess forma-
tion secondary to osteomyelitis exten-
sion from acute suppurative frontal
sinusitis results in the well known Potts
puffy tumor (gure 8).
19
Common pre-
disposing factors of Potts puffy tumor
are diabetes and immunosuppression.
If a Pseudomonas infection extends
through the cartilage of the external
auditory canal to the skull base in cases
of malignant otitis externa it may result
in osteomyelitis.
14
Additionally, asper-
gillosis and mucormycosis can invade
the calvaria (gure 9).
20
Osteitis is seen
as a focal or diffuse wavy thickening of
periosteum with sclerosis of bony mar-
gins; this periosteal thickening may
enhance following intravenous injection
of contrast material.
When an infection extends into the
bone marrow (osteomyelitis),
14
lytic
expansion and destruction are noted and
usually associated with a soft-tissue
mass. Granulomatous infection is seen
as a lytic area with or without sclerotic
CT appearance of common developmental and hereditary diseases of the calvaria on bone window setting.
Suture abnormalities
1. Craniosynostosis. Premature closure of a suture with decrease in the diameter of the skull perpendicular to the plane of the
affected suture.
2. Microcephaly. Failure of normal brain growth results in failure of the skull bones to grow.
3. Widening of sutures. Due to increased intracranial pressure or hypophosphatasia.
9
Asymmetry and abnormal shape
1. Arachnoid cyst. Temporal fossa, expansion and thinning of the inner table.
10
2. Neurobromatosis. Absent sphenoid wing
11
with focal calvarial defects adjacent to lambdoid suture (gure 4).
12
3. Dandy-Walker syndrome. Large posterior fossa with elevation of the torcula and attening and thinning of the occipital bone.
13
4. Arnold-Chiari syndrome. Widening of foramen magnum, concavity of the clivus, thinning of the occipital bone and small poste-
rior fossa.
14
5. Unilateral hypertrophy. Dyke-Davidoff-Massion syndrome
15
and Sturge-Weber-Dimitri syndrome.
3
Increased thickness and/or density
1. Osteopetrosis (Albers-Schonberg disease). Increased bone density of the entire skull with obliterated vascular grooves (gure
5) and encroachment on basal foramina.
16
2. Childhood anemias. Hyperplastic erythroid elements result in marked thickening of the diploe with near obliteration of the outer
table (gure 6).
14
Proliferation of the hyperplastic marrow beneath the periosteum and a perpendicular array of trabeculae
result in hair-on-end appearance. Obliteration of the paranasal sinuses and mastoid air cells by overgrowth of marrow more
in thalassemia and sickle cell anemia.
3. Sclerostosis. Hyperostosis and sclerosis, particularly the temporal bone.
17
4. Other diseases. Van Buchems disease, Pyle disease, Engelmanns disease and Pyknodysosstosis.
16
Generalized thinning of bone
1. Osteogenesis imperfecta. Generalized thinning of the skull and persistent wormian bones.
16
2. Chronic elevation of intracranial pressure. Accentuated digital markings due to imprint of the gyral surface of the brain, beaten
silver appearance.
3
3. Regional thinning. Porencephaly, chronic subdural hygroma, arachnoid cyst.
Defects in the bones
1. Encephalocele. Midline frontal or occipital defect with soft-tissue mass.
14
2. Epidermoid. Sharply demarcated defect with sclerotic edge and absent overlapping of the outer table due to ectopic epithelial
tissue included in bone during development.
TABLE 1
FIGURE 6: Polycythemia vera in a 27-year-old man who also has leukemia in remission. Dif-
fuse expansion of the diploic space (A) involving even the posterior clinoid processes and
dorsumn sellae (B) is seen.
A B
margins and localized soft-tissue
swelling.
18
Mucoceles of the paranasal
sinuses often show smooth defects in
relation to the sinus walls and can be
seen as extending into the orbit or the
intracranial cavity.
21
CT is not specic in differentiating
tumor from infection; however, it can
help to dene the extent of the lesion
and is useful in following up the efficacy
of treatment.
14
Neoplastic diseases
The most frequent neoplastic involve-
ment of the skull occurs by metastatic
disease or invasion from adjacent neo-
plasms. Table 2 shows the radiologic
ndings in bone window setting of the
most common primary osseous and car-
CT appearance of common extraosseus benign and malignant tumors
causing secondary effects on the skull on bone window setting
1. MeningiomaArises from the dural surfaces of the vault or near skull base. Hyperostosis and thickening of the calvaria adja-
cent to the tumor mass is present (gure 12). Bone destruction occurs with sarcomatous degeneration.
10
En-plaque type may
be difficult to distinguish the tumor itself from associated hyperostosis.
25
2. NeuromasCranial nerve sheath tumors cause uniform expansion of the affected canal or foramen.
10
Seventh and eighth
nerves tumors in the IAC are the most common. Erosion of the foraminal wall suggests malignancy.
26
3. GliomasSupercial tumors may cause focal expansion of the overlying skull vault.
14
Optic nerve glioma causes enlargement
of the optic foramina.
4. ChordomasWell-circumscribed destructive lesion containing bone debris and disproportionate large soft-tissue mass which
enhances heterogeneously.
27
Common in the clivus.
5. Sellar tumorsAdenomas are rarely aggressive but may cause destruction of the skull base (gure 13).
10
6. Glomus tumorsEnhancing mass with destruction of related bony structures (gure 14).
TABLE 3
CT appearance of common benign and malignant skull tumors in bone window setting
Benign tumors
1. OsteomaWell-dened dense, sessile lesion arises from external or internal tables and may extend intracranially (gure 10).
May be associated with Gardner syndrome.
3,14
2. HemangiomaHamartoma starts in the diploic space, characterized by lucent areas with prominent radiating or reticulated
trabeculae. May have sclerotic edge (gure 11).
3
3. ChondromaWell-dened lytic lesion with variable amount of calcication. Enhances on delayed scans due to minimal vas-
cularity.
10,14
4. Ossifying bromaLucent area with varying amount of calcication.
14
Differentiated from brous dysplasia only histologically.
5. Giant cell tumorLytic mass with possible ecks of calcication in the skull base; may have soft-tissue component.
22
6. Aneurysmal bone cystLytic bubbly lesion showing contrast enhancement.
14,23
Malignant tumors
1. Osteogenic sarcomaMalignant transformation of Pagets disease or post-radiation changes. Irregular destruction or blastic
expansion. May arise from the inner table and simulate intracranial mass.
24
2. ChondrosarcomaLytic and sclerotic areas with irregular calcications. Common in skull base. Soft-tissue components are
present, and many have intracranial extension.
10,14
3. FibrosarcomaLytic areas with soft-tissue mass.
14
4. Fibrous histiocytomaLytic areas with occasional calcication and destruction.
14
Usually seen after radiation therapy.
TABLE 2
FIGURE 7. A 35-year-old female with pulsatile tinnitus. Bone window setting of the skull
base shows wide left jugular foramen (A). Collapsed image of 2D time-of-flight MR
venogram shows a prominent left-sided venous system (B).
A B
tilaginous tumors arising from the skull
bones. Tumors of neuronal origin also
can cause secondary effects on the skull
bones (table 3).
Some tumors are particularly com-
mon in the skull base; these include
chordoma, chondroma, chondrosar-
coma, giant cell tumors, dermoid and
epidermoid tumors, sellar tumors,
chemodectomas, and neuromas that
arise from cranial nerves traversing
skull base foramina. Coronal and sagit-
tal images are very helpful in evaluation
of the presence of such lesions. Scan-
ning at a gantry angle of + 30 degrees to
the canthomeatal line is of particular use
in evaluation of the jugular foramina.
28
Metastatic disease, multiple mye-
loma, and lymphomas are the most
common malignant tumors affecting the
calvaria, presenting chiey as multiple
lytic lesions.
3
Kido et al
29
found that CT
scans using bone window settings are
more sensitive than skull radiographs in
detecting calvarial lesions.
Lytic metastases are more frequent
than blastic or mixed, and usually
erode either the inner or the outer table
of the calvaria. Lesions of this type
usually are sharply circumscribed and
concave toward the eroded surface (g-
ures 15 and 16).
29
Blastic metastases
typically are caused by carcinoma of
FIGURE 8. A 9-year-old boy with Pott's puffy tumor. Frontal skull tomogram shows a well-dened defect in the
frontal bones (A). Soft-tissue mass extending on both sides of the calvaria (B) is seen. A corresponding bony
defect is seen in bone window setting (C). Note also hypoplasia of the frontal sinuses.
A B C
FIGURE 9. A 58-year-old female with aspergillosis abscess in the orbital apex. Enhanced CT (A) shows the
inammatory mass eroding into the sphenoid and ethmoid sinuses and extending into the cavernous sinus and
middle temporal fossa. Corresponding bone window setting delineates the destructive process (B). Left carotid
angiogram shows localized narrowing of the cavernous portion (arrow) (C).
A B C
FIGURE 10. A 62-year-old man with right
frontal osteoma and intracranial extension.
FIGURE 12. Posterior fossa meningioma in a 74-year-old woman (A). Axial CT image with
the corresponding bone window setting (B).
A B
FIGURE 13. Pituitary macroadenoma in a 30-year-old man: (A) CT with bone window setting
at the skull base showing extensive bony destruction; (B) Sagittal T1-weighted (TR/TE=
600/20) image after gadolinium injection shows extension of the tumor intracranially and into
the clivus.
A B
FIGURE 14. A 21-year-old man with glomus jugulare tumor: (A) bone window setting of the
base of the skull shows expansion and destruction of the right jugular fossa and foramen; (B)
external carotid angiogram shows an extensive vascular tumor.
A B
FIGURE 11. A 14-year-old girl with heman-
gioma of the right parieto-occipital region in
lateral skull film (A) and bone window set-
ting of the brain CT (B). (Image courtesy of
Rac Melhem, MD, Mobile, Alabama.)
A
B
the breast, prostate, colon, or bone.
Medulloblastoma also has been
reported to cause calvarial blastic
metastasis.
30
Metastasis to the endocra-
nial epidural space is prevalent in
patients with prostate cancer, and may
be associated with a soft-tissue mass
that simulates meningioma.
3
When a calvarial metastatic deposit is
detected, the presence of other skeletal
deposits should be suspected.
29
Leu-
kemia and lymphoma deposits usually
Common calvarial lesions according to location.
Outer space Diploic space Inner table All tables
All scalp lesions Hematologic lesions Pacchionian granulation Acromegaly
Parietal thinning (anemias, leukemias) Chronic subdural hematoma Fibrous dysplasia
Osteoma Multiple myeloma Slow-growing sueprcial tumors Pagets disease
Periosteal osteosarcoma Metastasis Intracranial cysts Meningioma
Cushings disease Pagets disease Meningioma Metastasis
Chronic phenytoin therapy Hyperostosis frontalis Multiple myeloma
Bone islands Leptomeningial cysts Leukemia, lymphoma
Hyperparathyroidism Osteosarcomas Shunted hydrocephalus
Tuberous sclerosis Hyperparathyroidism
Advanced parietal thinning Parietal foramina
Advanced hyperostosis frontalis
Meningiomas
Cushings disease
TABLE 4
FIGURE 15. Bone window setting in a 71-
year-old woman with breast cancer shows
multiple Iytic metastatic lesions scattered
throughout the calvaria.
Guidelines in differentiating benign from malignant luciences of the skull.
Developmental benign lesions tend to be high in the skull and near the midline.
Half epidermoids are located paramedially.
Single, small lesions are likely to be benign.
Large single lesions may be benign; small, single malignant lesions are very rare.
Perilesional sclerosis strongly suggests a benign process.
Many benign lesions are conned to the diploic space.
Benign lesions have relatively smooth outlines compared to the irregular, invasive outline of malignant lesions.
(Adapted from Thomas JE, Baker HL, Jr: Assessment of roentgenographic lucencies of the skull: A systematic approach. Neurology 25:99-106, 1975.)
TABLE 5
FIGURE 16. A 61-year-old man with right frontal bone destruction from lung carcinoma
metastasis. (A) An irregular Iytic lesion affecting mainly the inner table. (B) Enhanced T1-
weighted (TR/TE=600/16) image shows an enhancing lesion in the same location.
A B
FIGURE 17. A 76-year-old male with multiple myeloma: (A) Enhanced axial CT scan shows
an enhancing epidural metastatic lesion in the left parietal region. (B) Corresponding bone
window setting shows multiple Iytic lesions with complete destruction of the calvaria at the
site of the epidural lesion.
A B
FIGURE 18. Different radiologic features of brous dysplasia: (A) and (B) Axial and coronal bone window settings of an
8-year-old boy who displays the typical ground-glass appearance; (C) Another patient showing coarse sclerotic nodules;
(D,E,F,G) A third patient shows the typical ground-glass appearance in bone window setting (D,E) and a hemorrhagic
cyst with high signal uid-uid level in both T1-weighted (F) and T2-weighted (G) MR images.
B
A
C
D
E
F
G
are detected as less well-dened multi-
ple lesions that tend to coalesce and
sometimes resemble a coarse version of
normal diploic bone;
3
a soft-tissue com-
ponent may be associated.
14
Multiple
myeloma (gure 17) usually presents
with multiple discrete, rounded holes of
variable sizes, referred to as punched-
out lesions.
3
Dural based lymphoma and
metastatic disease can cause erosion and
destruction of the inner table and can be
confused with other non-neoplastic
dural lesions, such as those found in
chronic infections and sarcoidosis.
Endocrine, metabolic, and
idiopathic lesions
In hyperparathyroidism, bone win-
dow images on CT scans may show a
granular or mottled appearance known
as the salt and pepper appear-
ance.
3,31,32
Brown tumors show a low CT
density similar to that of epidermoids
and neurobromatosis skull defects.
14
An accentuated temporal line due to
subligamentous bone resorption under
the temporalis muscle has been
described recently as a radiologic sign
of hyperparathyroidism.
33
In acromegaly, hypertrophic thicken-
ing of all the skull tables and expansion
of the paranasal sinuses and sella turcica
can be noted. Diffuse osteoporosis may
be seen in Cushings syndrome.
3,34
In
hypothyroidism (myxedema), retardation
of cranial and facial development is man-
ifested by an absence or underdevelop-
ment of paranasal sinuses and poor
pneumatization of the mastoid air cells.
Additionally, there is a delay in closure of
the sutures, with poorly differentiated
inner and outer tables and poorly devel-
oped diploic space.
3,34
In hypervita-
minosis A, generalized osteoporosis with
a thin, poorly mineralized skull is usually
seen, associated with relatively dense
suture margins and hydrocephalus.
35
Generalized increased bone density and
thickening with metastatic calcication
in the falx, tentorium, and dura are seen
in cases of hypervitaminosis D.
35
Sclero-
sis and coarse trabeculation are associ-
ated with uorine ingestion.
36
In brous dysplasia, the radiologic
appearance will depend on the propor-
tion of brous tissue to bone (gure
18).
31,37
Three categories of radiologic
appearances of brous dysplasia have
been described: pagetoid type, which
involves expansion of the bone with
areas of sclerosis and luciences (mixed
type); sclerotic type; and cystic type,
which may be complicated by sponta-
neous hemorrhage.
31,38,39
The outer table
has a thin and delicate appearance, with
diffuse widening of the diploic space.
Areas of poorly-dened dense nodules
14
or the characteristic homogeneous
ground-glass appearance also are com-
monly seen.
3
Extensive sclerosis may
affect the base of the skull, sphenoid
bones, or temporal bones.
14
Arterial
grooves generally are enlarged, indicat-
ing hypervascularity of the tumor.
3
The
lesions may cause facial deformities, and
may encroach upon the cranial nerves.
14
Bone window images of a patient
with Pagets disease can show a contin-
uous spectrum of the disease, from the
early active lytic phase (osteoporosis
circumscripta) to the dense sclerosis of
the healing phase (cotton-wool appear-
ance) (gure 19). Sutures and vascular
grooves do not restrict the progress of
this disease.
14
Softening of the skull base
occurs with basilar invagination and
compression on the basal foramina. Sar-
comatous degeneration may occur and
is characterized by bone destruction or
adjacent bulky soft-tissue masses.
40
Eosinophilic granuloma are usually
well-dened lytic lesions that rarely
have sclerotic margins. Two characteris-
tic radiologic ndings have been
described in relation to eosinophilic
granuloma:
3
beveled edges due to
greater involvement of the outer table
than the inner table (gure 20) and but-
ton sequestrum
41
due to a bone island or
density within the lesion. However,
these ndings, besides being rare, also
have been described with other
lesions.
3,42
Eosinophilic granuloma can
heal spontaneously or with radiation
therapy, especially in children.
43
Conclusion
Judicious use of bone window set-
tings in conjunction with routine brain
FIGURE 19. A 72-year-old man with advanced Pagets disease. (A) and (B) are CT topogram
and bone window settings through skull base, respectively, showing diffuse thickening of the
calvaria with mixed sclerotic and Iytic changes. Bone softening causing basilar invagination is
also noted. (Image courtesy of John R. Hesselink, MD, San Diego, California.)
A B
FIGURE 20. Bone window setting on CT of
a 4-year-old-female with unusually large
eosinophilic granuloma with characteristic
beveled edges (arrow). (Image courtesy of
Rac Melhem, MD, Mobile, Alabama.)
CT scanning allows better characteriza-
tion of associated bony lesions. The
ability to dene the origin of the lesion
may be helpful in reaching the nal
diagnosis (table 4). In a study of 333
patients with calvarial translucencies,
Thomas and Baker
44
suggested some
guidelines to reach a nal diagnosis
based on plain lm ndings (table 5).
The following indications are suggested
for routine use of bone window settings
in brain CT examinations: 1) abnormal
skull lm; 2) suspected congenital
abnormalities; 3) presence of an enhan-
cing lesion in relation to the skull bones;
and 4) suspected metastatic disease. AR
References
1. Ethier R: Thickness and texture. In: Newton TH
and Potts DG (eds), Radiology of the skull and
brain, pp 154-213. St. Louis, C.V. Mosby, 1971.
2. Keats TE, Holt JF: The calvarial doughnut
lesion: A previously undescribed entity. AJR
105:314-318, 1969.
3. Hodges FJ III: Pathology of the Skull. In:
Taveras JM, Ferrucci JT (eds), Radiology
DiagnosisImaging Interventional Vol lll, pp 1-21.
Philadelphia, J.B. Lippincott, 1994.
4. Bartiett JE, Kishore PRS: Familial doughnut
lesions of the skull. A benign, hereditary dysplasia.
Radiology 119:385-387, 1976.
5. Camp JD, Nash LA: Developmental thinnest of
the parietal bones. Radiology 42:42-47, 1944.
6. Pang D, Lin A: Symptomatic large parietal
foramina. Neurosurgery 11:33-37, 1982.
7. Eckstein HB, Chir M, Hoare RD: Congenital
parietal foramina associated with faulty ossication
of the clavicle. BJR 36:220-221, 1963.
8. Salmi A, Voutilainen A, Holsti LR, Unnerus C-E:
Hyperostosis crania in a normal population. AJR
87:1032-1040, 1962.
9. Taybi H, Kane PE: Hypophosphatasia and
hyperphosphatasia. In: Newton TH and Potts DG,
(eds), Radiology of the skull and brain, pp 674-677.
St. Louis, C.V. Mosby, 1971.
10. Whelan MA, Reede DL, Meisler W, Bergeron
RT: CT of the base of the skull. Radiol Clin North
Am 22:177-217, 1984.
11. Burrows EH: Bone changes in orbital neuro-
bromatosis. BJR 36:549-561, 1963.
12. Klatte EC, Franken EA, Smith JA: The radio-
graphic spectrum in neurobromatosis. Semin
Roentgenol 1:17-33, 1976.
13. Gooding CA: Size and shape. In: Newton TH
and Potts DG (eds), Radiology of the skull and
brain, pp 148-149. St. Louis, C.V. Mosby,1971.
14. Hasso AN, Vignaud J, LaMasters L: Pathology
of the skull base and vault. In: Newton TH, Hasso
AN, Dillon PW (eds), Modern Neuroradiology, vol-
ume 3, Computed tomography of the head and
neck, pp 3.1-3.26. New York, Raven Press, 1988.
15. Dyke CG, Davidoff LM, Masson CB: Cerebral
hemiatrophy with homolateral hypertrophy of the
skull and sinuses. SGO 57:588, 1933.
16. Winchester PH, Grossman H: Congenital
skull dysplasia. In: Newton TH and Potts DG (eds),
Radiology of the skull and brain, pp 653-661.
St. Louis, C.V. Mosby,1971.
17. Nager GT, Stein SA, Dorst JP et al: Sclero-
stosis involving the temporal bone: Clinical and
radiologic aspects. A J Otolaryngol 4:1-17, 1983.
18. Rumbaugh CL, Bergeron RT: Infections
involving the skull. In: Newton TH and Potts DG
(eds), Radiology of the skull and brain, pp 716-742.
St. Louis, C.V. Mosby,1971.
19. Procino ND: Potts Puffy tumor in a seven-
year-old boy. Ear Nose Throat J 57:84-88, 1978.
20. Centeno RS, Bentson JR, Mancuso AA: CT
scanning of rhinocerebral mucormycosis and
asperiglosis. Radiology 140:383-389, 1981.
21. Hesselink JR, Weber AL, New PFJ, et al: Evalu-
ation of mucoceles of the paranasal sinuses with com-
puted tomography. Radiology 133:397-400, 1979.
22. Epstein N, Whelan M, Reed D, Aleksie S:
Giant cell tumor of the skull: A report of two cases.
Neurosurgery 11:263-267, 1982.
23. Paige ML, Chiu YT Jr., Christ M: Aneurysmal
bone cyst of the temporal bone. Neuroradiol 18:
161-164, 1979.
24. Lee YY, Tassel PV, Nauert C, et al: Craniofa-
cial osteosarcomas: Plain lm, CT, and MR nd-
ings in 46 cases. AJR 9:379-385, 1988.
25. Buetow MP, Buetow PC, Smirniotopoulos
JG: From the Archives of the AFIP, Typical,
atypical, and misleading features in meningioma.
Radiographics 11:1087-1106, 1991.
26. Hedeman LS, Lewinsky BS, Lochridge GK,
Trevor R: Primary malignant schwannoma of the
gasserian ganglion. Report of two cases. J Neuro-
surg 48:279-283, 1978.
27. Krol G, Sundaresan N, Deck M: Computed
tomography of axial chordomas. J Comp Asst
Tomogr 7:286-289, 1983.
28. Daniels DL, Williams AL, Haughton VM: Jag-
ular foramen: Anatomic and computed tomo-
graphic study. AJR 142: 153-158, 1983.
29. Kido DK, Gould R, Taati F, et al: Comparative
sensetivity of CT scan, radiographs and radionu-
clide bone scans in detecting metastatic calvarial
lesions. Radiology 128:371-375, 1978.
30. Palacios E, Shannon M, Fine M: Unusual
metastasis from a medulloblastoma: Case report.
Neuroradiol 17:219-222, 1979.
31. Olmsted WW: Some skeletogenic lesions with
common calvarial manifestations. Radiol Clin
North Am 19:703-713, 1981.
32. Ellis K, Hochstim RJ: The skull in hyper-
parathyroid bone disease. AJR 83:732-742, 1960.
33. lto K, Aoki J, Kobayashi S, et al: Accentuated
temporal line on the frontal skull radiograph: A sign of
hyperparathyroidism. Radiology 192:497-502, 1994.
34. Minagi H: Skull changes in endocrine dis-
eases. In: Newton TH and Potts DG (eds), Radiol-
ogy of the skull and brain, pp 665-673. St. Louis,
C.V. Mosby,1971.
35. Taybi H: Vitamin deciency and intoxication.
In: Newton TH and Potts DG (eds), Radiology of
the skull and brain, pp 678-684. St. Louis, C.V.
Mosby,1971.
36. Calenoff L: Osteosclerosis from intentional
ingestion of hydrouoric acid. AJR 87:1112-1115,
1962.
37. Leeds N, Seaman WMB: Fibrous dysplasia of
the skull and its differential diagnosis. A clinical and
roentgenographic study of 46 cases. Radiology
78:570-582, 1962.
38. Rries JW: The roentgen features of brous
dysplasia of the skull and facial bones. A critical
analysis of 39 pathologically proven cases. AJR
77:71-88, 1957.
39. Graf CJ, Perret GE: Spontaneous recurrent
hemorrhage as an unusual complication of brous
dysplasia, case report. J Neurosurg 52:570-573,
1980.
40. Smith J, Botet JF, Yeh SDJ: Bone sarcomas
in Paget disease: A study of 85 patients. Radiology
152:583-590, 1984.
41. Wells PO: The button sequestrum of
eosinophylic granuloma. Radiology 67:746-747,
1956.
42. Sholkoff SD, Mainzer F: Button sequestrum
revisited. Radiology 100:649-652, 1971.
43. Sartoris DJ, Paker BR: Histocytosis X:
Rate and pattern of resolution of osseous lesions.
Radiology 152:679-684, 1984.
44. Thomas JE, Baker HL, Jr: Assessment of
roentgenographic lucencies of the skull: A system-
atic approach. Neurology 25:99-106, 1975.