Bone Windows in Brain CT

This work presents an overview ofthe radiologic appearance inbone window setting of differentprimary and secondary skulltumors, bone dysplasia, congen-ital and inflammatory diseasesaffecting the skull, and extrinsiclesions exhibiting secondaryeffects on the skull. The differen-tial diagnosis of lesions affectingthe inner and/or outer table, orthe diploic space also is pre-sented. Recommendations forroutine use of bone window setting in brain CT scanningincludes 1) abnormal skull films;2) suspected congenital anom-alies; 3) presence of enhancinglesions in close proximity to skull bone; and 4) suspectedmetastatic disease.

B one window images that rou-tinely are acquired in CT exami-nations of the head for trauma orparanasal sinus disease can be useful inthe characterization of different skulllesions. These images are excellent fordemonstration of skull tables and thediploic space. Bone algorithm and fil-ters also enhance the ability to visual-ize fine bony detail. Bone window

images obtained in conjunction withroutine brain scans may lead to fortu-itous discovery or superior characteri-zation of skull pathology.

CT window widths of 600 to 2,000Hounsfield units (HU) and window lev-els of 160 HU to 500 HU accuratelydelineate tissues of a large difference inCT attenuation, such as bone and air.Narrower window widths (80 HU to 150HU) and lower center levels (40 HU to50 HU) are employed to show small dif-ferences in attenuation of soft tissuessuch as brain, but are not as accurate asbone window settings in depicting con-tour, edge interface, and size of bonestructures.

Features of the calvariaThe calvaria is well differentiated

into three layers: inner, middle, andouter tables. The inner and the outertables are composed of compact bone;the middle table is composed of cancel-lous bone. The inner and outer tablesvary little in thickness, except in placeswhere they are eroded by vascular struc-tures and gyral impressions. The diploicspace is composed of an irregular net-work of bony trabeculae and vascularspaces. Blood within this space may actas a fluid cushion to absorb traumaticforces.1

Normal variantsCommon benign lesions may repre-

sent normal variants or developmentalabnormalities in the skull. Such lesionsusually have characteristic radiologicfindings and should not be confusedwith other pathological entities. Pac-chionian granulations or venous lakes(figure 1) are arachnoid extensions pro-

jecting into the lumen of the mainvenous sinuses. The edges are furtherapart at the inner table level than at theouter table, indicating a benign processoriginating inside the skull.1 Anotherbenign finding is the presence of circularlucent defects of the calvaria, known asdoughnut lesions. These usually do not exceed 2 cm in diameter and mayrepresent smaller versions of abnormallesions such as fibrous dysplasia,eosinophilic granuloma, epidermoidinclusion cyst, or osteoid osteoma.3Some cases of doughnut lesions may befamilial in nature.4

Parietal thinning (figure 2) is charac-terized by the generally bilateral andsymmetrical thinning of the parietalbones with partial or complete absenceof the diploe and the outer table of theskull.5 Parietal foramina are holes in the

Value of bone window imagesin routine brain CT:

Examinations beyond trauma

Dr. Snow and Dr. Brogdon are in theDepartment of Radiology at Universityof South Alabama Medical Center inMobile, AL. Dr. Williams was in theDepartment of Radiology at Universityof South Alabama Medical Center inMobile, AL. Dr. Georgy is in theDepartment 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 leftfrontal bone (arrow) compatible with venouslake is observed in a 59-year-old womanundergoing serial CT examinations for leftmiddle cerebral artery infarction.

skull that represent a benign variant ofincomplete ossification of the bones inthe region of the obelion on both sidesof the sagittal suture, and may be associ-ated with severe pain and headache withgentle pressure.6 Parietal foramina alsomay be familial and is possibly associ-ated with faulty ossification of the clavi-cles.7 Another abnormality that may beseen is hyperostosis frontalis interna,8which is characterized by thickening ofthe inner table that may extend to thediploe of the frontal bone; this lesion iscommonly found in middle-agedwomen (figure 3). It is important to dif-ferentiate this normal variant fromhyperostosis that may occur secondaryto meningiomas.

Hereditary and developmentalabnormalities

A long list of developmental andhereditary diseases can affect the cal-varial bones. Hodges3 divided thehereditary abnormalities of the calvariainto five groups: suture abnormalities,abnormalities in shape and size,increased thickness and density, gener-alized thinning, and skull defects orholes. Table 1 summarizes the radio-logical findings of the common devel-opmental and hereditary diseases thatcan affect the skull calvaria (figures 4-6). Bone window setting also isextremely valuable in the evaluation ofnasal bone and temporal bone develop-mental anomalies (figure 7).

FIGURE 2. Parietal thinning in a 75-year-old woman shown in a lateral skull film (A). Bonewindow 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 normalbone window of matched age and sex is illustrated (B).

A B

FIGURE 4: Neurofibromatosis in a 3-year-old girl. Dysplasia of the right sphenoidwing is seen in a bone window image (A).Soft-tissue density, likely representing aplexiform neurofibroma, is seen filling thedefect in a corresponding T1-weightedimage (TR/TE= 650/16) (B).

A

B

FIGURE 5. Osteopetrosis in a 56-year-oldman showing a thick skull, increased bonedensity, and obliteration of the diploicspace.

Inflammatory lesionsInfections of the skull are rare

because of the relative resistance of thecalvarial bones to infection. Wheninfection does occur, it usually is bydirect extension from the paranasal

sinuses and mastoid air cells or fromtrauma.18 Subperiosteal abscess forma-tion secondary to osteomyelitis exten-sion from acute suppurative frontalsinusitis results in the well known Pottspuffy tumor (figure 8).19 Common pre-

disposing factors of Potts puffy tumorare diabetes and immunosuppression.

If a Pseudomonas infection extendsthrough the cartilage of the externalauditory canal to the skull base in casesof malignant otitis externa it may resultin osteomyelitis.14 Additionally, asper-gillosis and mucormycosis can invadethe calvaria (figure 9).20 Osteitis is seenas a focal or diffuse wavy thickening ofperiosteum with sclerosis of bony mar-gins; this periosteal thickening mayenhance following intravenous injectionof contrast material.

When an infection extends into thebone marrow (osteomyelitis),14 lyticexpansion and destruction are noted andusually associated with a soft-tissuemass. Granulomatous infection is seenas a lytic area with or without sclerotic

CT appearance of common developmental and hereditary diseases of the calvaria on bone window setting.Suture abnormalities1. 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 shape1. Arachnoid cyst. Temporal fossa, expansion and thinning of the inner table.102. Neurofibromatosis. Absent sphenoid wing11 with focal calvarial defects adjacent to lambdoid suture (figure 4).123. Dandy-Walker syndrome. Large posterior fossa with elevation of the torcula and flattening and thinning of the occipital bone.134. Arnold-Chiari syndrome. Widening of foramen magnum, concavity of the clivus, thinning of the occipital bone and small poste-

rior fossa.145. Unilateral hypertrophy. Dyke-Davidoff-Massion syndrome15 and Sturge-Weber-Dimitri syndrome.3

Increased thickness and/or density1. Osteopetrosis (Albers-Schonberg disease). Increased bone density of the entire skull with obliterated vascular grooves (figure

5) and encroachment on basal foramina.162. Childhood anemias. Hyperplastic erythroid elements result in marked thickening of the diploe with near obliteration of the outer

table (figure 6).14 Proliferation of the hyperplastic marrow beneath the periosteum and a perpendicular array of trabeculaeresult in hair-on-end appearance. Obliteration of the paranasal sinuses and mastoid air cells by overgrowth of marrow morein thalassemia and sickle cell anemia.

3. Sclerostosis. Hyperostosis and sclerosis, particularly the temporal bone.174. Other diseases. Van Buchems disease, Pyle disease, Engelmanns disease and Pyknodysosstosis.16

Generalized thinning of bone1. Osteogenesis imperfecta. Generalized thinning of the skull and persistent wormian bones.162. Chronic elevation of intracranial pressure. Accentuated digital markings due to imprint of the gyral surface of the brain, beaten

silver appearance.33. Regional thinning. Porencephaly, chronic subdural hygroma, arachnoid cyst.

Defects in the bones1. Encephalocele. Midline frontal or occipital defect with soft-tissue mass.142. 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 anddorsumn sellae (B) is seen.

A B

margins and localized soft-tissueswelling.18 Mucoceles of the paranasalsinuses often show smooth defects inrelation to the sinus walls and can beseen as extending into the orbit or theintracranial cavity.21

CT is not specific in differentiatingtumor from infection; however, it canhelp to define the extent of the lesionand is useful in following up the efficacyof treatment.14

Neoplastic diseasesThe most frequent neoplastic involve-

ment of the skull occurs by metastaticdisease or invasion from adjacent neo-plasms. Table 2 shows the radiologicfindings in bone window setting of themost 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 (figure 12). Bone destruction occurs with sarcomatous degeneration.10 En-plaque type maybe 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 eighthnerves tumors in the IAC are the most common. Erosion of the foraminal wall suggests malignancy.26

3. GliomasSuperficial tumors may cause focal expansion of the overlying skull vault.14 Optic nerve glioma causes enlargementof the optic foramina.

4. ChordomasWell-circumscribed destructive lesion containing bone debris and disproportionate large soft-tissue mass whichenhances heterogeneously.27 Common in the clivus.

5. Sellar tumorsAdenomas are rarely aggressive but may cause destruction of the skull base (figure 13).106. Glomus tumorsEnhancing mass with destruction of related bony structures (figure 14).

TABLE 3

CT appearance of common benign and malignant skull tumors in bone window setting

Benign tumors1. OsteomaWell-defined dense, sessile lesion arises from external or internal tables and may extend intracranially (figure 10).

May be associated with Gardner syndrome.3,142. HemangiomaHamartoma starts in the diploic space, characterized by lucent areas with prominent radiating or reticulated

trabeculae. May have sclerotic edge (figure 11).33. ChondromaWell-defined lytic lesion with variable amount of calcification. Enhances on delayed scans due to minimal vas-

cularity.10,144. Ossifying fibromaLucent area with varying amount of calcification.14 Differentiated from fibrous dysplasia only histologically.5. Giant cell tumorLytic mass with possible flecks of calcification in the skull base; may have soft-tissue component.226. Aneurysmal bone cystLytic bubbly lesion showing contrast enhancement.14,23

Malignant tumors1. 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.242. ChondrosarcomaLytic and sclerotic areas with irregular calcifications. Common in skull base. Soft-tissue components are

present, and many have intracranial extension.10,143. FibrosarcomaLytic areas with soft-tissue mass.144. Fibrous histiocytomaLytic areas with occasional calcification 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 skullbase shows wide left jugular foramen (A). Collapsed image of 2D time-of-flight MRvenogram shows a prominent left-sided venous system (B).

A B

tilaginous tumors arising from the skullbones. Tumors of neuronal origin alsocan cause secondary effects on the skullbones (table 3).

Some tumors are particularly com-mon in the skull base; these includechordoma, chondroma, chondrosar-coma, giant cell tumors, dermoid andepidermoid tumors, sellar tumors,chemodectomas, and neuromas thatarise from cranial nerves traversing

skull base foramina. Coronal and sagit-tal images are very helpful in evaluationof the presence of such lesions. Scan-ning at a gantry angle of + 30 degrees tothe canthomeatal line is of particular usein evaluation of the jugular foramina.28

Metastatic disease, multiple mye-loma, and lymphomas are the mostcommon malignant tumors affecting thecalvaria, presenting chiefly as multiplelytic lesions.3 Kido et al29 found that CT

scans using bone window settings aremore sensitive than skull radiographs indetecting calvarial lesions.

Lytic metastases are more frequentthan blastic or mixed, and usuallyerode either the inner or the outer tableof the calvaria. Lesions of this typeusually are sharply circumscribed andconcave toward the eroded surface (fig-ures 15 and 16).29 Blastic metastasestypically are caused by carcinoma of

FIGURE 8. A 9-year-old boy with Pott's puffy tumor. Frontal skull tomogram shows a well-defined defect in thefrontal bones (A). Soft-tissue mass extending on both sides of the calvaria (B) is seen. A corresponding bonydefect 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 theinflammatory mass eroding into the sphenoid and ethmoid sinuses and extending into the cavernous sinus andmiddle temporal fossa. Corresponding bone window setting delineates the destructive process (B). Left carotidangiogram shows localized narrowing of the cavernous portion (arrow) (C).

A B C

FIGURE 10. A 62-year-old man with rightfrontal osteoma and intracranial extension.

FIGURE 12. Posterior fossa meningioma in a 74-year-old woman (A). Axial CT image withthe corresponding bone window setting (B).

A B

FIGURE 13. Pituitary macroadenoma in a 30-year-old man: (A) CT with bone window settingat 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 intothe clivus.

A B

FIGURE 14. A 21-year-old man with glomus jugulare tumor: (A) bone window setting of thebase of the skull shows expansion and destruction of the right jugular fossa and foramen; (B)external carotid angiogram shows an extensive vascular tumor.

A BFIGURE 11. A 14-year-old girl with heman-gioma of the right parieto-occipital region inlateral skull film (A) and bone window set-ting of the brain CT (B). (Image courtesy ofRafic Melhem, MD, Mobile, Alabama.)

A

B

the breast, prostate, colon, or bone.Medulloblastoma also has beenreported to cause calvarial blasticmetastasis.30 Metastasis to the endocra-

nial epidural space is prevalent inpatients with prostate cancer, and maybe associated with a soft-tissue massthat simulates meningioma.3

When a calvarial metastatic deposit isdetected, the presence of other skeletaldeposits 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 sueprficial 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 showsmultiple Iytic metastatic lesions scatteredthroughout 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 confined 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 carcinomametastasis. (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 showsan enhancing epidural metastatic lesion in the left parietal region. (B) Corresponding bonewindow setting shows multiple Iytic lesions with complete destruction of the calvaria at thesite of the epidural lesion.

A B

FIGURE 18. Different radiologic features of fibrous dysplasia: (A) and (B) Axial and coronal bone window settings of an8-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 hemorrhagiccyst with high signal fluid-fluid level in both T1-weighted (F) and T2-weighted (G) MR images.

B

A

C

D

E

F

G

are detected as less well-defined multi-ple lesions that tend to coalesce andsometimes resemble a coarse version ofnormal diploic bone;3 a soft-tissue com-ponent may be associated.14 Multiplemyeloma (figure 17) usually presentswith multiple discrete, rounded holes ofvariable sizes, referred to as punched-out lesions.3 Dural based lymphoma andmetastatic disease can cause erosion anddestruction of the inner table and can beconfused with other non-neoplasticdural lesions, such as those found inchronic infections and sarcoidosis.

Endocrine, metabolic, and idiopathic lesions

In hyperparathyroidism, bone win-dow images on CT scans may show agranular or mottled appearance knownas the salt and pepper appear-ance.3,31,32 Brown tumors show a low CTdensity similar to that of epidermoidsand neurofibromatosis skull defects.14An accentuated temporal line due tosubligamentous bone resorption underthe temporalis muscle has beendescribed recently as a radiologic signof hyperparathyroidism.33

In acromegaly, hypertrophic thicken-ing of all the skull tables and expansionof the paranasal sinuses and sella turcicacan be noted. Diffuse osteoporosis maybe seen in Cushings syndrome.3,34 Inhypothyroidism (myxedema), retardationof cranial and facial development is man-ifested by an absence or underdevelop-

ment of paranasal sinuses and poorpneumatization of the mastoid air cells.Additionally, there is a delay in closure ofthe sutures, with poorly differentiatedinner and outer tables and poorly devel-oped diploic space.3,34 In hypervita-minosis A, generalized osteoporosis witha thin, poorly mineralized skull is usuallyseen, associated with relatively densesuture margins and hydrocephalus.35Generalized increased bone density andthickening with metastatic calcificationin the falx, tentorium, and dura are seenin cases of hypervitaminosis D.35 Sclero-sis and coarse trabeculation are associ-ated with fluorine ingestion.36

In fibrous dysplasia, the radiologicappearance will depend on the propor-tion of fibrous tissue to bone (figure18).31,37 Three categories of radiologicappearances of fibrous dysplasia havebeen described: pagetoid type, whichinvolves expansion of the bone withareas of sclerosis and luciences (mixedtype); sclerotic type; and cystic type,which may be complicated by sponta-neous hemorrhage.31,38,39 The outer tablehas a thin and delicate appearance, withdiffuse widening of the diploic space.Areas of poorly-defined dense nodules14or the characteristic homogeneousground-glass appearance also are com-monly seen.3 Extensive sclerosis mayaffect the base of the skull, sphenoidbones, or temporal bones.14 Arterialgrooves generally are enlarged, indicat-ing hypervascularity of the tumor.3 The

lesions may cause facial deformities, andmay encroach upon the cranial nerves.14

Bone window images of a patientwith Pagets disease can show a contin-uous spectrum of the disease, from theearly active lytic phase (osteoporosiscircumscripta) to the dense sclerosis ofthe healing phase (cotton-wool appear-ance) (figure 19). Sutures and vasculargrooves do not restrict the progress ofthis disease.14 Softening of the skull baseoccurs with basilar invagination andcompression on the basal foramina. Sar-comatous degeneration may occur andis characterized by bone destruction oradjacent bulky soft-tissue masses.40

Eosinophilic granuloma are usuallywell-defined lytic lesions that rarelyhave sclerotic margins. Two characteris-tic radiologic findings have beendescribed in relation to eosinophilicgranuloma:3 beveled edges due togreater involvement of the outer tablethan the inner table (figure 20) and but-ton sequestrum41 due to a bone island ordensity within the lesion. However,these findings, besides being rare, alsohave been described with otherlesions.3,42 Eosinophilic granuloma canheal spontaneously or with radiationtherapy, especially in children.43

ConclusionJudicious 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 topogramand bone window settings through skull base, respectively, showing diffuse thickening of thecalvaria with mixed sclerotic and Iytic changes. Bone softening causing basilar invagination isalso noted. (Image courtesy of John R. Hesselink, MD, San Diego, California.)

A B

FIGURE 20. Bone window setting on CT ofa 4-year-old-female with unusually largeeosinophilic granuloma with characteristicbeveled edges (arrow). (Image courtesy ofRafic Melhem, MD, Mobile, Alabama.)

CT scanning allows better characteriza-tion of associated bony lesions. Theability to define the origin of the lesionmay be helpful in reaching the finaldiagnosis (table 4). In a study of 333patients with calvarial translucencies,Thomas and Baker44 suggested someguidelines to reach a final diagnosisbased on plain film findings (table 5).The following indications are suggestedfor routine use of bone window settingsin brain CT examinations: 1) abnormalskull film; 2) suspected congenitalabnormalities; 3) presence of an enhan-cing lesion in relation to the skull bones;and 4) suspected metastatic disease. AR

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