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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6009_Библиотеки_им_академика_М_И_Перельмана.pdf
SECTION 8
Neoplasms, Cysts, and Other Masses
Extradural Neoplasms
Spread of Neoplasms 262
Blastic Osseous Metastases
Lytic Osseous Metastases
Hemangioma
Osteoid Osteoma
Osteoblastoma 270
Aneurysmal Bone Cyst
Giant Cell Tumor
Osteochondroma
Chondrosarcoma
Osteosarcoma 275
Chordoma
Ewing Sarcoma
Lymphoma
Leukemia
Plasmacytoma 280
Multiple Myeloma
Neuroblastic Tumor
266
267
268
269
271
272
273
274
276
277
278
279
281
282
Intradural Extramedullary
Schwannoma 283
Meningioma
Solitary Fibrous Tumor/Hemangiopericytoma
Neurobroma
Malignant Nerve Sheath Tumors
Metastases, CSF Disseminated 288
Paraganglioma
284
285
286
287
289
Intramedullary
Astrocytoma 290
Cellular Ependymoma
Myxopapillary Ependymoma
Hemangioblastoma
Spinal Cord Metastases
Primary Melanocytic Neoplasms/Melanocytoma 297
292
294
295
296
Nonneoplastic Cysts and Tumor Mimics
Cysts
CSF Flow Artifact 298
Meningeal Cyst
Perineural Root Sleeve Cyst
Syringomyelia
Tumor Mimics
Fibrous Dysplasia 303
Kümmell Disease
Hirayama Disease
Paget Disease
Bone Infarction
Extramedullary Hematopoiesis 310
Tumoral Calcinosis
300
301
302
304
306
308
309
311
Spread of Neoplasms
Anatomy-Based Imaging Issues
Neoplasms affecting the spine may spread by direct extension
via the lymphatic system, the hematogenous route, or along
the cerebrospinal fluid pathways. There can also be
combinations of these pathways involved with the most
typical being hematogenous metastatic dissemination to
vertebral bodies with subsequent direct extension into the
epidural space.
Primary tumors located in soft tissues may extend into the
vertebral column by direct extension. An example would
include lung carcinoma extending into the chest wall and
subsequently the paravertebral region and into the spinal
column and epidural space. Prostate, bladder, or bowel
Neoplasms, Cysts, and Other Masses
carcinoma may extend into the presacral space and
subsequently into the vertebral column and epidural space.
Nasopharyngeal carcinoma extends into the clivus and skull
base and may track along the cranial nerves. In rare cases,
there may be direct extension of a CNS tumor along the
biopsy or surgical tract. There are also rare cases of CNS
tumors extending through access via indwelling shunt tubing
to give systemic metastases. Findings of direct extension of a
neoplasm in the spine consist of a soft tissue mass with
adjacent bone destruction and variable neural compromise.
Direct extension of a neoplasm into the epidural space is more
likely from the vertebral body through the posterior
longitudinal ligament. The anterior longitudinal ligament and
disc are relatively resistant to tumor invasion. The anterior
longitudinal ligament is stronger than the posterior
longitudinal ligament and has fewer perforating vessels. Once
the tumor has access into the epidural space, it comes against
the tough dura, which is an effective barrier to tumor
penetration. These barriers result in the distinguishing
features between a disc space infection with adjacent
vertebral osteomyelitis (with the epicenter at the level of the
disc space) and neoplastic involvement (with the epicenter
involving the vertebral bodies with sparing of the disc space).
Direct extension of tumor may also be seen with a primary
cord tumor within the cervical spine, with extension into the
infratentorial space. Rarely, brainstem or cerebellar
neoplasms may extend into the upper cervical cord.
Lymphatic spread is of limited importance in spine imaging
relative to the more ubiquitous hematogenous spread. Local
spread of pelvic tumors within the lumbar spine without
pulmonary metastases would suggest a venous or lymphatic
route of extension.
Hematogenous spread is the major pathway of extension of
malignant tumors to the axial skeleton. The Batson plexus is a
longitudinal network of valveless veins running parallel to the
spinal column. These veins lie outside of the
thoracoabdominal cavity and communicate with multiple
aspects of the venous system, including the vena cava, spinal,
portal, azygos, intercostal, pulmonary, and renal veins. Flow
direction in the Batson plexus is variable due to the variable
intrathoracic and intraabdominal pressures. Tumors in
multiple anatomic sites could cause metastatic lesions along
the course of the venous plexus without lung or liver
involvement. Prostate carcinoma cells could seed vertebral
bodies via the Batson plexus and not necessarily extend into
the vena cava. Breast carcinoma might also seed the vertebral
bodies via the azygos system into the Batson plexus. There is
only 5-10% of portal blood flow that might shunt to the
Batson plexus, explaining the relatively low frequency of
spinal metastatic lesions with GI and GU primaries. For the vast
262
majority of spinal metastases, there may be no clear answer to
the precise route to the end target. Homing properties of the
tumor cells and receptive properties of the implantation site
may be more important than any particular vascular route.
Spread along the CSF pathways is an important route for
primary intracranial tumors. Tumor emboli gain access to the
CSF via fragmentation, as well as being shed during surgical
manipulation. CNS tumor types showing subarachnoid spread
include medulloblastoma, ependymoma, pineal tumors,
astrocytoma, lymphoma and leukemia, choroid plexus
carcinoma, and retinoblastoma (poor prognosis with MYCN
gene amplification). Spread along the CSF pathways can also
occur following initial hematogenous dissemination of tumor.
For example, this pattern of spread would be present in cord
and leptomeningeal metastatic disease following the initial
hematogenous dissemination in lung and breast metastatic
disease.
Pathologic Issues
Forty percent of patients with cancer will develop visceral or
bony metastases during their illness. The spinal column is the
most common site of osseous metastases. Men are more
frequently affected with vertebral metastases, with a male to
female ratio of 3:2. Prostate, lung, and breast carcinomas
account for the vast majority of spinal metastases. Locations
are primarily thoracic (70%) > lumbar (20%) > cervical.
Primary tumors are generally composed of a variety of
biologically different cells in regard to ultimate metastatic
potential. Cells continually shed from the primary tumor and
gain access to the circulatory system. Less than 0.01-0.1% of
tumor cells survive to reach a distant site. Successful tumor
spread requires completion of a complex pathway, including
tumor separation from the primary source, access to blood,
CSF or lymphatic system, survival within the transport process,
attachment to the endothelium of a distant vessel as well as
exiting that vessel into the interstitial space, and finally
developing the vascular supply at a distant site. The distant
host environment site is a complex milieu. Multiple anatomic
pathways may be involved with varying flow patterns within
the veins and arteries.
Mechanisms of Tumorigenesis
Tumorigenesis in humans appears to be a multistep process.
These steps reflect genetic alterations that drive progressive
transformation of normal human cells into highly malignant
versions. Cancers in humans have been shown to have an agedependent incidence, which implicates 4-7 rate limiting,
stochastic events. Tumor development proceeds via a
succession of genetic changes, each conferring one or another
type of growth advantage, which leads to the progressive
conversion of normal human cells into cancer cells. By
definition, cancer cells will have defects in regulatory circuits
that govern cell proliferation and homeostasis. These defects
have been categorized into 6 types of alterations in cell
physiology: (1) Self-sufficiency in growth signals, (2)
insensitivity to growth inhibitory signals, (3) evasion of
programmed cell death (apoptosis), (4) limitless replicative
potential, (5) sustained angiogenesis, and (6) tissue invasion
and metastasis. Each of these 6 physiologic changes reflects
the successful breaching of an anticancer defense mechanism
that is hardwired into cells and tissues.
Normal cells require growth signals before they can move into
an active proliferative state. The signals are transmitted to the
cell via transmembrane receptors that bind a variety of
Spread of Neoplasms
signaling molecules, such as diffusible growth factors,
extracellular matrix components, and cell-to-cell adhesion
molecules (CAMs). Many cancer cells acquire the ability to
synthesize growth factors to which they are responsive, which
creates an abnormal positive feedback loop. Examples would
be the production of platelet-derived growth factor (PDGF) by
glioblastoma and tumor growth factor alpha (TGF) by
sarcomas. Epidermal growth factor receptor (EGF-R) is
upregulated in brain tumors.
Normal tissues have a variety of mechanisms that limit
proliferation. Signals include both growth inhibitors and
inhibitors within the extracellular matrix on the surface of
adjacent cells. Many antiproliferative signals are channeled
through the retinoblastoma tumor suppressor protein (pRb)
and its variations. Disruption of the retinoblastoma protein
pathway will allow cell proliferation by rendering the cells
insensitive to antigrowth factors by repressing the E2F
transcription factors.
Evasion of programmed cell death (apoptosis) commonly
occurs through mutations involving the p53 tumor suppressor
gene. The inactivation of this p53 protein is seen in over 50%
of human cancers.
The limitless replicative potential of cancer tumors is seen in
cultures of tumor cells that have become immortalized.
Normal human cell types in culture have a capacity for no
more than 60-70 doublings. The ends of the chromosomes
appear to be involved in this process, which are called the
telomeres. The erosion of the telomeres occurs through
successive cycles of normal cell replication causing them to
lose their ability to protect the ends of the chromosome DNA.
This leads to eventual cell crisis and cell death. In contrast,
telomere maintenance is evident in all types of malignant
cells. In cancer, telomeres are maintained at a length above
some critical threshold, which allows unlimited cell
multiplication.
Abnormal angiogenesis is perhaps one of the more
recognized aspects of abnormal cell physiology in cancer.
Angiogenesis promoting signals are classically seen with
vascular endothelial growth factor (VEGF) and fibroblast
growth factors (FGF). More than 2 dozen angiogenic-inducing
factors are known, with a similar number of inhibiting-type
proteins.
Metastatic Disease and Cell Motion
Tumor metastases are the cause of 90% of human cancer
deaths. Tumor invasion and tumor metastases are very
complex processes, with multiple genetic and biochemical
factors. These can be described as tumor invasion, tumor cell
dissemination through the blood stream or lymphatic system,
colonization of distant organs, and outgrowth of the
metastasis. Several classes of proteins are involved in
tethering cells to their surroundings and are altered in
invasion and metastases. CAMs and integrins are involved in
this cell-to-cell regulatory signaling. The basement membrane
is the 1st barrier tumor cells must breech. Receptors on the
surface of cells recognize the glycoprotein of the basement
membrane to which they attach. Attachment is followed by
proteolysis of type IV collagen of the basement membrane by
tumor-specific collagenase. Locomotion follows basement
membrane lysis, with cells crossing that defective basement
membrane with access to the interstitial space, lymphatics,
and blood vessels. Chemoattractants can activate cell
migration and invasion through activation of specific
Neoplasms, Cysts, and Other Masses
receptors and downstream intracellular signaling pathways.
This appears to ultimately reorganize the actin cytoskeleton.
Rho/Rac GTPases are well-known regulators of cytoskeletal
organization. Rac activation induces membrane ruffles,
adhesion complexes, and lamellipodia formation.
Tumor dissemination and cell motility occurs along 3 different
pathways, including epithelial-to-mesenchymal transition
(EMT), amoeboid transcription, and collective migration. In
EMT, the cell elongates and degrades the local matrix by
enzymes and migrates with pseudopodia-like projections. In
amoeboid transcription the cells become spherical and pass
through gaps in the extracellular matrix. In collective
migration, sheets or clusters of tumor cells migrate. EMT
includes the downregulation of epithelial markers in tight
junctions and cytokeratin filament network and upregulation
of mesenchymal markers, like N-cadherin, vimentin, integrins,
tenascin C, and fibronectin, fibroblast- specific protein 1. Ncadherin seems to be the most important of this group of
markers. EMT can be controlled by intrinsic oncogenic
activation like KRAS mutation or Her2 overexpression. In some
cancers, such as lung, the central role of EMT regulator
belongs to TGFβ. TGFβ ultimately promotes EMT by
regulating genes that control cell proliferation, apoptosis,
differentiation, motility and migration.
Clinical Implications
Spine metastatic involvement presents with unrelenting back
pain. Objective signs are uncommon, or occur late in the
disease (such as palpable mass and deformity). Back pain and
weakness is a sign of epidural tumor extension. Due to
spinothalamic tract crossing pattern, sensory levels may be 1-2
segments below the site of compression. Sensory
abnormalities are an uncommon presenting sign of metastatic
disease in the spine.
Selected References
1. Balic M et al: Circulating tumor cells: from bench to bedside. Annu Rev Med.
64:31-44, 2013
2. Perlikos F et al: Key molecular mechanisms in lung cancer invasion and
metastasis: a comprehensive review. Crit Rev Oncol Hematol. 87(1):1-11,
2013
3. Ianari A et al: Cell death or survival: The complex choice of the
retinoblastoma tumor suppressor protein. Cell Cycle. 9(1):23-4, 2010
4. Chen HZ et al: Emerging roles of E2Fs in cancer: an exit from cell cycle
control. Nat Rev Cancer. 9(11):785-97, 2009
5. Fiorentino FP et al: Senescence and p130/Rbl2: a new beginning to the end.
Cell Res. 19(9):1044-51, 2009
6. Mazel C et al: Cervical and thoracic spine tumor management: surgical
indications, techniques, and outcomes. Orthop Clin North Am. 40(1):75-92,
vi-vii, 2009
7. Sciubba DM et al: Solitary vertebral metastasis. Orthop Clin North Am.
40(1):145-54, viii, 2009
8. Fokas E et al: Metastasis: the seed and soil theory gains identity. Cancer
Metastasis Rev. 26(3-4):705-15, 2007
9. Guillevin R et al: Spine metastasis imaging: review of the literature. J
Neuroradiol. 34(5):311-21, 2007
10. Christofori G: New signals from the invasive front. Nature. 441(7092):444-50,
2006
11. Demopoulos A: Leptomeningeal metastases. Curr Neurol Neurosci Rep.
4(3):196-204, 2004
12. Batson OV: The function of the vertebral veins and their role in the spread of
metastases. Ann Surg. 112(1):138-49, 1940
263
(Left) Axial graphic shows a
hematogenously disseminated
lytic metastatic lesion to the
thoracic vertebral body and
pedicle with subsequent direct
epidural tumor extension and
cord compression. (Right) Axial
T1WI C+ MR shows a large,
hematogenously disseminated
metastatic paravertebral mass
lesion involving thoracic body
with direct tumor extension to
the posterior elements, chest
wall, and epidural space with
Neoplasms, Cysts, and Other Masses
cord compression ſt.
(Left) AP bone scan in a case
of extensive blastic prostate
carcinoma shows multiple foci
of increased radiotracer
uptake that is consistent with
diffuse bone metastasis.
(Right) Sagittal T1WI C+ MR in
a patient with extensive
blastic prostate carcinoma
shows diffuse abnormal
decreased signal from all
vertebral bodies and posterior
elements with multiple foci of
Spread of Neoplasms
extension ſt causing mild
cord compression.
(Left) Sagittal T2WI MR in a
patient with multiple
myeloma shows 2 levels of
bony tumor involvement and
slight spinous process
expansion. There is severe cord
compression at both levels.
(Right) Sagittal T1 C+ FS MR of
multiple myeloma shows 2
levels of focal tumor
involvement with
enhancement and slight
spinous process expansion.
Cord compression is present at
both levels.
264
Spread of Neoplasms
Neoplasms, Cysts, and Other Masses
(Left) Axial NECT in a patient
with renal cell metastasis
shows a mass destroying the
right side of T7-T8 bodies,
extending into posterior
elements and crossing to
involve right ribs and
costovertebral joint. There is
bony expansion with a thin rim
soap bubble pattern ſt.
(Right) Coronal T2WI FS MR in
a patient with renal cell
metastasis shows a mass
involving the ribs and right
side of T7-T8 bodies with
epidural extension and cord
compression. Multiple flow
voids are present within the
mass.
(Left) Unenhanced T2WI MR in
a patient with a large cervical
cord metastatic lesion from
lung carcinoma shows diffuse
cord edema from the
cervicomedullary junction
inferiorly to C5. More focal
signal abnormality is present
at the C2-C3 level. (Right)
Sagittal T1WI C+ MR in a
patient with large cervical
cord metastatic lesion from
lung carcinoma via
hematogenous dissemination
shows enhancement of a large
intramedullary metastatic
lesion at the C2-C3 level.
(Left) Sagittal T1 C+ MR in a
patient with extensive nodular
leptomeningeal metastatic
disease from high-grade brain
oligodendroglioma shows a
massive nodular-enhancing
leptomeningeal tumor
following contrast
administration . This child
had rapid onset of flaccid
paraplegia suggesting cord
infarction from tumor
compression. (Right) Sagittal
T1 C+ MR shows a focal
epidural mass with cord
compression from metastatic
melanoma. The route of
dissemination is presumed
hematogenous.
265
Blastic Osseous Metastases
KEY FACTS
TERMINOLOGY
• Extension of primary tumor to spine where bone
production exceeds bone destruction
IMAGING
• Multiple osteoblastic lesions in spine
○ May coexist with areas of osteolytic tumor, soft tissue
mass
• MR signal typically diminished on T1, T2WI in areas of
osteoblastic metastases
• Sclerotic metastases usually tracer avid on bone scan
TOP DIFFERENTIAL DIAGNOSES
Neoplasms, Cysts, and Other Masses
• Treated metastases
• Discogenic sclerosis
• Hemangioma
• Paget disease
• Osteosarcoma
(Left) Anteroposterior plain
film shows diffuse extensive
bone sclerosis of the spine and
pelvis due to diffuse osseous
metastases from breast
carcinoma. (Right)
Anteroposterior bone scan
shows diffuse, patchy tracer
uptake in the thoracolumbar
spine, pelvis, sternum, and
multiple ribs due to diffuse
osseous metastases from
breast carcinoma.
PATHOLOGY
• Marrow infiltration, tumor stimulates osteoblastic response
○ New bone deposition on trabeculae, within
intertrabecular spaces
• Primary tumor, adults: Prostate, breast, carcinoid, lung, GI,
bladder, nasopharynx, pancreas
• Primary tumor, children: Medulloblastoma, neuroblastoma
CLINICAL ISSUES
• Pain: Progressive axial, referred, or radicular
• Epidural tumor, if present, may cause neurologic
dysfunction
• 90% of prostate metastases involve spine, with lumbar 3x
more often than cervical
DIAGNOSTIC CHECKLIST
• Defining response to therapy difficult since osteolytic
conversion (tumor progression) and fading (good response)
may look identical
266
(Left) Axial NECT through the
lower thoracic spine shows
patchy sclerosis of the
vertebral body due to blastic
metastases from prostate
carcinoma. (Right) Sagittal T1weighted MR shows low signal
involving the L3 body and
sacrum, reflecting diffuse
metastatic disease.
Extraosseous extension into
the epidural space is seen at
L3 st. There is no specific
signal change on the MR to
define the blastic nature of
these metastatic lesions.
Lytic Osseous Metastases
KEY FACTS
Neoplasms, Cysts, and Other Masses
TERMINOLOGY
• Spread of primary tumor to spine where bone destruction
exceeds bone production
IMAGING
• Multiple osteolytic lesions in spine
• Compression fracture with bowing of posterior cortex,
osteolysis extending into neural arch, extraosseous soft
tissue
• Lesion distribution proportional to red marrow (lumbar >
thoracic > cervical)
• Radiography requires 50-70% bone destruction and tumor
size > 1 cm for detection
• Bone scan can give false-negatives with aggressively lytic
tumor or with very small lesions
TOP DIFFERENTIAL DIAGNOSES
• Hematopoietic malignancy
• Benign (osteoporotic) compression fracture
• Schmorl node
• Normal heterogeneous marrow
• Spondylodiscitis
PATHOLOGY
• Spine is most common site of osseous metastases
• Common primaries causing osteolytic metastases
○ Renal, lung, breast, thyroid, GI tract, urothelial, ovarian,
melanoma, chordoma, paraganglioma
CLINICAL ISSUES
• Pain: Progressive axial, referred, or radicular
• Epidural tumor extension may cause neurologic
dysfunction
• Compression fracture
• Cord compression in 5% of adults with systemic cancers
(70% solitary, 30% multiple sites)
• Spine metastases found in 5-10% of cancer patients
(Left) Lateral radiograph
shows osteolysis of the C2
neural arch and superior
margin of the C3 arch ſt.
(Right) Sagittal T1WI MR in
the same patient shows a
large soft tissue mass
replacing the C2 arch .
There is also replacement of
marrow in the C2 body and
dens st. Subsequent work-up
disclosed non-small cell lung
carcinoma in the right upper
lobe.
(Left) Axial NECT shows large
thyroid carcinoma metastasis
to the vertebral body and left
facet/lamina of C3. There is a
thin rim of expanded bone
partially surrounding the
lesion. The extraosseous soft
tissue mass is not clearly seen
ſt. (Right) Axial contrastenhanced CT shows
enhancement of the mass ſt
that is typical of hypervascular
tumors like thyroid carcinoma.
The medial margin of the mass
is in the spinal canal, effacing
the thecal sac and contacting
the cervical cord. There is
extension into the foramen
.
267
Hemangioma
KEY FACTS
TERMINOLOGY
• Common benign venous malformation within vertebrae
• Usually intraosseous, may have epidural component
• Typically incidental lesion identified on imaging performed
for unrelated reasons
IMAGING
• CT: Well-circumscribed, hypodense lesion with coarse
vertical trabeculae (white polka dot appearance on axial CT)
• MR: Circumscribed lesion, hyperintense on both T1 and
T2WI with hypointense vertical striations
○ Atypical hemangiomas may have reduced T1 signal due
Neoplasms, Cysts, and Other Masses
to paucity of fat
• Often multiple (20-30%)
PATHOLOGY
• 11% of adult population
• Complications in < 1%
○ Pathologic compression fracture
(Left) Sagittal graphic of the
thoracolumbar junction shows
the typical striated pattern of
a hemangioma with thickened
bony trabeculae. There is
neither extraosseous
extension nor thecal sac
compromise. (Right) Lateral
radiograph shows vertical
striations within the L1
vertebral body , the socalled "corduroy vertebra,"
due to vertebral hemangioma.
○ Epidural hemangioma component with cord
compression
• Histology
○ Thin-walled sinusoidal channels lined by vascular
endothelium
○ Interspersed bony trabeculae with fat
• Majority confined to vertebral body proper
○ Uncommon in posterior elements/pedicles (10-15%)
CLINICAL ISSUES
• Bone CT may supplement MR evaluation in atypical
hemangioma to look for typical osseous findings
• No follow-up typically necessary with pathognomonic
imaging with small lesions and no extraosseous extension
• Aggressive hemangiomas
○ Vertebroplasty in conjunction with embolization may be
considered if concern for pathologic fracture
○ Surgical resection (corpectomy) or radiation therapy
268
(Left) Axial CECT shows fatty
attenuation within the lower
thoracic vertebral body with
multiple punctate thickened
trabeculae. (Right) Sagittal T1
C+ MR shows prominent
vertical striations within the
vertebral body consistent with
a hemangioma ſt. There is
extraosseous extension of the
tumor into the ventral
epidural space .
Osteoid Osteoma
KEY FACTS
Neoplasms, Cysts, and Other Masses
TERMINOLOGY
• Benign osteoid-producing tumor < 1.5 cm in size
• Tumor often called nidus to distinguish it from surrounding
reactive zone due to host response
IMAGING
• 10% occur in spine, in neural arch
• Focal scoliosis, concave on side of tumor
• Central nidus
○ Variable amount of ossification
• Reactive zone
○ Dense sclerosis, edema around nidus
○ Involves much larger area than tumor
○ Periosteal reaction variably present
○ Soft tissue mass or pleural thickening/effusion
○ Low signal on T1WI, high signal on T2WI, STIR
○ Enhances with gadolinium, iodinated contrast
TOP DIFFERENTIAL DIAGNOSES
• Osteoblastoma
• Stress fracture of pedicle or lamina
• Unilateral spondylolysis
• Unilateral absent pedicle or pars interarticularis
• Sclerotic metastasis
• Lymphoma
• Osteomyelitis
• Ewing sarcoma
CLINICAL ISSUES
• Night pain relieved by aspirin, NSAIDs
• 70% have scoliosis related to muscle spasm, concave on
side of tumor
DIAGNOSTIC CHECKLIST
• Thin-section CT most accurate in visualizing nidus
• Edema on MR mimics infection, malignancy
(Left) Axial graphic shows a
small, highly vascular tumor
nidus st of osteoid osteoma in
the left lamina, surrounded by
dense reactive bone .
(Right) Anteroposterior
radiograph shows focal, shortcurve levoscoliosis in a young
man with neck pain and no
trauma history. Painful
scoliosis raises concern for a
tumor or infection. Sclerosis
st at C6 on the right
suggested a possible diagnosis
of osteoid osteoma.
(Left) Axial bone CT in the
same patient shows a sclerotic
C6 osteoid osteoma nidus ſt.
Nidus may range from purely
radiolucent to completely
sclerotic. The lesion is sharply
demarcated and surrounded
by reactive sclerosis . The
lesion was missed on a prior
routine cervical spine MR.
(Right) Posteroanterior bone
scan (3-hour image) shows
scoliosis and intense, focal
uptake on the right at a T11
osteoid osteoma . Scoliosis
due to osteoid osteoma is
always concave on the side of
the tumor.
269