SPINE CME

Received July 29. 2012; accepted

after revision June 19, 2013.
From the Department of Radiology
(R.J.Y., M.E.H., S.K., G.K., E.L.) and
Spinal Cord Lesions in Patients the Brain Tumor Center (R.J.Y., SK.,
G.K., E.L.), Memorial Sloan-
Kettering Cancer Center, New York,
with Cancer New York; and Department of
Radiology (E.P.), New York
Presbyterian Hospital/Columbia
University Medical Center, New
E. Pollack, M.E. Hartman, E. Lis, S. Karimi, G. Krol, and R.J. Young
York, New York.
Erica Pollack and May E. Hartman
contributed equally to this work.
Paper previously presented in part
at: Annual Meeting of the American
CME Credit Society of Spine Radiology,
The American Society of Neuroradiology (ASNR) is accredited by the Accreditation Council for Continuing Medical Education February 16 –19, 2012; Miami Beach,
(ACCME) to provide continuing medical education for physicians. The ASNR designates this enduring material for a maximum of Florida.
one AMA PRA Category one creditTM. Physicians should claim only the credit commensurate with the extent of their participation Please address correspondence to
in the activity. To obtain credit for this activity, an online quiz must be successfully completed and submitted. ASNR members Robert J. Young, MD, Memorial
may access this quiz at no charge by logging on to eCME at http://members.asnr.org. Nonmembers may pay a small fee to access Sloan-Kettering Cancer Center,
the quiz and obtain credit via http://members.asnr.org/ecme. Department of Radiology, 1275
York Avenue, MRI-1156, New York,
New York 10065; e-mail:
youngr@mskcc.org
http://dx.doi.org/10.3174/ng.4130064
ABSTRACT
Patients with cancer are prone to unique disease processes different from those that occur
in the general population. Spinal cord lesions in patients with cancer may reflect neoplastic,
infectious, ischemic, hemorrhagic, metabolic, and toxic etiologies. As treatments become
more efficient in different cancers, subsequent early and late cancer and treatment compli-
cations may also become more frequent. The purpose of this article is to review common
spinal cord lesions in patients with cancer with an emphasis on imaging and clinical clues
that can narrow the differential diagnosis.

Learning Objective: List 5 imaging findings that differentiate neoplastic and non-neoplastic
sources of spinal pathology in patients with known malignancies.

INTRODUCTION between 2005 and 2009.3 Proper recogni-

Spinal cord lesions are uncommonly en-
countered in clinical practice. The differen-
tial diagnosis is limited, and recall of com-
mon entities is facilitated by mnemonics
such as HEALSME (Hemangioblastoma,
Ependymoma, Astrocytoma, Arteriovenous
malformation, Lymphoma, Syringohydro-
myelia, Sarcoidosis, Metabolic, Metastasis,
Multiple sclerosis, and Edema).1 The distri-
bution of spinal cord lesions in a cancer pop-
ulation, however, is different from that in the
general population and is less well-described.
The incidence of new cancer diagnoses is es-
timated to increase by 45% to 2.3 million in
2030, with dramatic and disproportionate
increases of 67% in the elderly and 99% in
minorities.2 In 2013, the number of new pri-
mary central nervous system cancers in the
United States is estimated to be 69,720 or
12% higher than the mean annual number
tion, diagnosis, and treatment of spinal cord
lesions in patients with cancer are growing
challenges for health care providers. Al-
though the categories (tumor, infection, met-
abolic, vascular, and so forth) may appear
similar to those in patients without cancer,
different pathologies are often observed in
patients with cancer due to unique tumor
conditions, treatments, and vulnerabili-
ties. The purpose of this article is to sum-
marize spinal cord lesions that may occur
in patients with cancer, with an emphasis
on differential points to assist in making
the proper diagnosis.
Malignant
Spinal cord invasion by leptomeningeal meta-
stasis. Increased survival for patients with
cancer has been associated with an in-
creased detection of leptomeningeal metas-

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Fig 1. Leptomeningeal and spinal cord metastases from breast carcinoma. Sagittal T2-weighted (A) and contrast sagittal (B) and axial (C) T1-weighted
images reveal nodular leptomeningeal disease along the surface of the cervical cord with focal dorsal intramedullary invasion at the C3 level. A
sclerotic hypointense bone metastasis is also present in C6.
tases.4 This is probably due to 2 main factors: First, in the
past, many patients would have died of their primary can-
cers because the treatments were less effective; therefore,
many did not have the opportunity to develop leptomenin-
geal metastases.5 Second, continued technologic advances
have yielded high sensitivity to modern imaging methods
that was not previously available. Breast and lung cancer
account for the largest numbers of patients with leptomen-
ingeal metastases, which are usually seen in patients with
late stage cancer in the setting of widely disseminated
disease.4,6
Primary CNS cancers that also commonly metastasize to
the leptomeninges include medulloblastoma, ependymoma,
and glioblastoma.7 Lower extremity weakness and pares-
thesias are the most common presenting symptoms, with
simultaneous presentation of symptoms localized to sepa-
rate spinal levels being highly suggestive of leptomeningeal
metastasis.6 CSF analysis remains the criterion standard for
diagnosis, though multiple CSF samplings may be neces-
sary,4 with accuracy described as only 54% after 1 sam-
pling and 90% after 3 samplings.8 MR imaging remains
critical for disease management and has a growing role for
diagnosis, though it may be more sensitive for detecting
leptomeningeal metastases from solid tumors than from
hematopoietic malignancies.4,9
MR imaging in leptomeningeal disease reveals focal or dif-
fuse nodular and/or plaquelike enhancement along the sur-
face of the spinal cord and subarachnoid space on contrast
T1-weighted images. Tumor nodules may also be visualized
along the surface of the cauda equina or on nerve roots. On
T1-weighted images, the CSF demonstrates slightly hypoin-
tense signal intensity, which can blur the distinction be-
tween CSF and the cord. The leptomeningeal metastases
may cause T2 hyperintense reactive changes and vasogenic
edema in the spinal cord or may directly invade the spinal
cord (Fig 1).
Direct Spinal Cord Metastasis
Spinal cord metastases are rare. The most common presen-
tation is a solitary lesion in the cervical or thoracic cord.10
Lung and breast cancer again account for the most common
primaries to metastasize to the cord. Similar to leptomenin-
geal disease, the growing incidence of spinal cord metasta-
ses is probably associated with improvement in systemic
control of disease.11 The route of spread is often hematog-
enous via arterial supply or direct extension from the lep-
tomeninges. Radiation therapy and corticosteroids are the
mainstay of palliative care after diagnosis of intramedullary
metastasis, which carries a dismal prognosis of 65% mor-
tality in 6 months.10 Clinical findings are often nonspecific;
weakness is the most common presenting symptom.
MR imaging of a spinal cord metastasis usually shows a
well-circumscribed expansile lesion with avid homoge-
neous enhancement on contrast T1-weighted images and
extensive hyperintense edema on T2-weighted images
(Fig 2). Cystic features and hemorrhage are uncommon
(Fig 3) and help to distinguish metastases from primary
neoplasms such as ependymomas. The rim sign (more in-
tense peripheral enhancement) and flame sign (ill-defined
flame-shaped enhancing tail at the superior and/or infe-
rior margin) were also recently described as specific
for metastasis.12 Lymphoma and post-transplant lym-
phoproliferative disorders may also cause spinal cord
lesions (Figs 4 and 5).
Nonmalignant
Vascular: infarct. Cancer is widely considered a hypercoag-
ulable state, with prophylactic anticoagulation advocated
for some patients with cancer.13,14 Spinal cord infarction is
most commonly seen in the upper thoracic and thoracolum-
bar cord because the blood supply to these areas is less
redundant compared with other regions of the cord. Pa-
tients usually report the acute onset of severe pain, followed
within hours by motor and sensory impairment and incon-
tinence. By admission, most patients are paraplegic and
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Fig 2. Spinal cord metastasis from lung carcinoid. Sagittal and axial T2-
weighted (A and B) and contrast T1-weighted (C and D) images show an
expansile spinal cord metastasis at the T8 level. Isolated spinal cord me-
tastasis is less common than direct invasion from overlying leptomenin-
geal metastases.
functional outcomes remain poor.15 Suspicion based on
clinical presentation is often crucial to a prompt work-up;
diagnosis can be confirmed with MR imaging.
MR imaging typically demonstrates spinal cord enlarge-
ment with T2 hyperintense and T1 hypointense changes. T2
hyperintense changes may also be present within the adja-
cent vertebral body, indicative of vertebral infarction. Dif-
fusion restriction on diffusion-weighted imaging sequences
and a lack of contrast enhancement in the acute phase are
critical to the imaging diagnosis (Fig 6).
Hemorrhage
Hematomyelia or spinal cord hemorrhage is a rare cause of
myelopathy, but patients with cancer have unique risk
factors that may increase the incidence of spontaneous
spinal cord hemorrhage. Patients with cancer are often
maintained on anticoagulation for prophylaxis or for
long-term treatment of a previous thrombosis. Patients
on thrombotic prophylaxis may have up to a 22.5% in-
crease in absolute risk of bleeding complications com-
pared with untreated controls.16 Primary spinal cord tu-
mors, metastasis, and previous radiation therapy also
increase the risk of hemorrhage.17
MR imaging findings in hematomyelia depend on the
timing of imaging and the stage of the blood products. T1
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Fig 3. Hemorrhagic spinal cord metastasis. Sagittal and axial T2-
weighted (A and B) and contrast T1-weighted (C and D) images show a
large expansile intramedullary metastasis in the cervical and thoracic
cord. There is mild heterogeneous enhancement near the central T2 hy-
pointense acute blood products. This child had widely disseminated
stage IV high-risk metastatic neuroblastoma.
hyperintense signal intensity is highly suggestive of hemor-
rhage. Lesions are commonly expansile and contain mixed
blood products manifest by T2 hyperintense signal intensity
and central or peripheral hypointense signal intensity (Fig
7). Susceptibility artifacts with signal-intensity dropout
may be visible on gradient echo sequences, with blooming
due to the paramagnetic effect of blood products.18 Diffu-
sion-weighted images should be interpreted with caution,
because the blood products may appear hyperintense19 and
mimic acute infarction.
Infection
Spinal cord infection or myelitis is uncommon compared
with other spinal infections that may involve the vertebrae,
intervertebral disk, epidural space, meninges, or subarach-
noid space. Patients with cancer are often immunocompro-
mised or immunosuppressed by cancer treatments and are
prone to infection from unusual causes such as fungi, as
well as more common bacterial, viral, and parasitic etiolo-
gies.20 Spread is usually hematogenous, but contiguous ex-
tension from adjacent diskitis/osteomyelitis or meningitis
may also occur.
MR imaging usually demonstrates enlargement of the
spinal cord. While this finding is nonspecific and can
mimic tumor, skip areas between regions of spinal cord
Fig 4. Post-transplant lymphoproliferative disorder. Axial T2-weighted (A) and contrast axial (B) and sagittal (C) T1-weighted images demon-
strate a ring-enhancing spinal cord lesion in the conus at the T11 level. Mild leptomeningeal disease is also present over the surface of the distal
cord and cauda equina nerve roots. This child had high risk pre-B-cell acute lymphocytic leukemia and developed non-host-related Epstein-Barr
viremia.

Fig 5. Diffuse large B-cell lymphoma. Sagittal and axial T2-weighted (A and B) and contrast sagittal and axial T1-weighted (C and D) images reveal an
expansile T2 hyperintense spinal cord lesion in the cervical cord with mild ill-defined posterior enhancement, which is much smaller than the T2
abnormality. The patient had disseminated CNS lymphoma in the brain as well (not shown).

Fig 6. Spinal cord infarct. Axial (A) and sagittal (B) T2-weighted images reveal a central butterfly-shaped intramedullary hyperintensity of the central
gray matter in the distal spinal cord and conus. Sagittal diffusion-weighted image (C) shows corresponding diffusion restriction. Acute clinical signs
and symptoms are critical for making the correct diagnosis. This patient with metastatic non-small cell lung carcinoma developed sudden lower
extremity paralysis and anterior cord syndrome. Postmortem examination showed histiocyte infiltration of the anterior more than posterior horns with
neuronal pallor and loss of internal nuclear detail and axonal swelling. The cord infarct was related to severe calcific atherosclerosis of the abdominal
aorta.

enlargement should strongly suggest an infectious rather Autoimmune

than neoplastic etiology. Extensive T2 hyperintense
edema may be present. Nodular enhancement can also
mimic a neoplastic process, but enhancement is variable
because diffuse, peripheral, and heterogeneous patterns
may occur (Figs 8 and 9).
Paraneoplastic syndrome. A paraneoplastic syndrome is a
constellation of signs and symptoms that result from the
presence of cancer within the body but are not the direct
result of the tumor or a tumor metastasis. Several mecha-

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Fig 7. Treatment-related hemorrhage. Sagittal T2-weighted (A) and contrast T1-weighted (B) images illustrate an expansile nonenhancing spinal cord
lesion in the cervical and thoracic cord with T2 hypointense acute blood products. A sagittal image (C) from FDG PET/CT shows a striking decrease in
metabolic activity at the lesion levels (compare with normal avid activity in the cerebellum and upper cervical cord). Postmortem examination
revealed organizing necrosis and hemorrhage with underlying vacuolating and necrotic myelopathy in the anterior, lateral, and posterior columns.
There was no tumor or infection. The patient underwent multiple courses of chemotherapy and radiation therapy for desmoplastic small round cell
tumor of the parotid gland. Sclerotic hypointense bone metastases are present in C6 and T2.

Fig 8. Herpes simplex myelitis. Axial (A) and sagittal (B) T2-weighted images and contrast sagittal T1-weighted image (C) show a T2 hyperintense
enhancing spinal cord lesion in the dorsal right cord at the C1–C2 level. This patient had undergone chemotherapy for chronic lymphocytic leukemia
and developed leg weakness, paresthesias, and Lhermitte’s phenomenon. The patient was found to have disseminated herpes zoster infection, and
improved with acyclovir.

Fig 9. Fungal leptomeningitis. Axial T2-weighted (A) and contrast axial (B) and sagittal (C) T1-weighted images reveal nodular intradural extramed-
ullary nodular enhancing lesions. Mild T2 hyperintense spinal cord edema is present in A.

nisms of paraneoplastic syndrome have been well described these may have a diagnostic role, though failure to detect an
in the literature, but an immune-mediated response is most autoantibody does not exclude the diagnosis.22,23 The best
commonly implicated in paraneoplastic neurologic syn- studied antibodies include anti-Hu, anti-Yo, anti-Ri, and
dromes.21,22 Several autoantibodies have been identified; anti-Ma2, which precipitate a T-cell-mediated response

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Fig 10. Paraneoplastic syndrome. Axial (A) and sagittal (B) T2-weighted images and contrast sagittal T1-weighted image (C) demonstrate central T2
hyperintensity in the thoracic spinal cord, which extends from the medulla to the conus (not shown). This patient had testicular carcinoma with rapidly
progressive flaccid quadriparesis. Anti-Ma2 antibodies were found in the CSF, consistent with anti-Ma2-associated encephalomyelitis. Postmortem
examination revealed near-total neuronal depopulation of the entire spinal cord with lymphohistiocytic infiltrates and axonal degeneration of the
anterior and lateral columns, withering of the anterior roots, and sparing of the dorsal root ganglia.

that attacks the nervous system, neuromuscular junction,
and connective tissue.22,24 Clinical manifestations of para-
neoplastic neurologic syndromes, accordingly, include cer-
ebellar degeneration, brain stem encephalitis, myelopathy,
and peripheral nerve palsy.22
Paraneoplastic neurologic syndromes occur in ⬍1% of pa-
tients with cancer but account for approximately 10% of all
nonmetastatic neurologic complications.24,25 Paraneoplas-
tic syndromes are most commonly associated with small cell
lung cancer, breast cancer, lymphoma, plasmacytoma, and
gynecologic cancers. Symptoms may present before any
cancer diagnosis in more than half of patients.24 Diagnosis
of the primary neoplasm, however, is critical to appropriate
treatment. Stabilization or, rarely, improvement in symp-
toms requires a 2-pronged approach, with treatment of the
primary malignancy as well as immunosuppressive ther-
apy.22,24 Disabilities are usually permanent and severe.
pacity as a water-soluble vitamin, deficiency may lead to
subacute combined degeneration with myelopathy of the
cervical and upper thoracic cord. Demyelination and ax-
onal loss in the dorsal and lateral cord manifest with par-
esthesias of the hands and feet, loss of proprioception and
vibration sense, sensory ataxia, spasticity, and lower ex-
tremity weakness. A quarter of patients may present with
Lhermitte’s sign, transient and self-limited electric shock-
like sensations due to sensory axon damage in the dorsal
columns. Lhermitte’s sign may occur with spinal cord tu-
mors, bone marrow transplantation, chemotherapy, and
radiation therapy as well as noncancer conditions such as
multiple sclerosis.29
MR imaging demonstrates T2 hyperintensity throughout the
dorsal spinal cord that is symmetric and columnar, without
associated expansion or abnormal enhancement (Fig 11). MR
imaging findings often normalize with treatment.

Spinal cord lesions from paraneoplastic neurologic syn- Treatment-Related

dromes often show nonspecific features. Symmetric elon-
gated T2 hyperintensity with or without associated en-
hancement after contrast administration is usually found
along white matter tracts or central gray matter (Fig
10).23,25 The MR imaging findings may occasionally appear
normal, or the abnormal imaging findings may lag behind
clinical manifestations.
Metabolic
Vitamin B12 deficiency. Vitamin B12 is an important com-
ponent of blood cell biology, along with folic acid and fer-
ritin. Active vitamin B12 or holotranscobalamin only com-
prises 20% of the total serum vitamin B12, with the
remainder comprising inactive holohaptocorrin. Vitamin
B12 levels are affected by many different medications and
chemotherapy agents26,27 and may decrease with different
tumors such as acute leukemia.28 With limited storage ca-
Radiation-induced damage and necrosis. An increased in-
cidence in radiation-induced damage of the spinal cord is
anticipated due to the growing use of radiation therapy,
despite advances in image-guided radiation therapy tech-
niques. Radiation-induced changes may be classified as
acute complications, early delayed complications, or late
complications according to the interval between radia-
tion therapy and the onset of injury.30 While the first 2
categories are reversible, the latter that usually develops
ⱖ3 months after treatment is often progressive and
irreversible.31
Radiation-induced complications are poorly understood,
and there is no consensus threshold dose above which radi-
ation damage becomes much more likely.32,33 It is generally
accepted, however, that radiation dose per fraction, in-
terfraction interval, and total radiation dose are impor-

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Fig 11. Chemotherapy-related myelitis mimicking subacute combined degeneration in breast cancer. Sagittal (A) and axial (B) T2-weighted images
show small symmetric T2 hyperintense lesions in the dorsal columns of the mid- to distal thoracic cord. There is loss of the normal hypointense margin
of the dorsal cord on the sagittal image, without expansion or enhancement. The patient had undergone multiple chemotherapy regimens (including
ABI-007, bevacizumab, and capecitabine). Although the dorsal column distribution is typical for subacute combined degeneration from vitamin B12
deficiency, she had normal vitamin B12 and folic acid levels and no evidence of human immunodeficiency virus to suggest human immunodeficiency
virus–associated vacuolar myelopathy.

Fig 12. Radiation therapy–induced changes. Axial T2-weighted (A) and contrast axial (B) and sagittal (C) T1-weighted images reveal a punctate
enhancing lesion in the ventral right spinal cord at the C3 level 6 months after undergoing image-guided radiation therapy for a C3 chordoma. Note T1
hyperintense marrow changes in C2–C4 and a residual T2 hypointense enhancing chordoma in the right C2–3 neural foramen on the axial images. The
patient remained asymptomatic from this new cord lesion, which spontaneously resolved in 7 months.

Fig 13. Radiation therapy–induced changes. Axial (A) and sagittal (B) T2-weighted and contrast sagittal (C) T1-weighted images show numerous T2
hyperintense nonenhancing lesions throughout the spinal cord. This child had undergone craniospinal radiation (2340 cGy, posterior fossa boost to
5580 cGy) for standard risk medulloblastoma 7 years ago. He had only mild symptoms of imbalance. The spinal cord lesions remained stable for >6
months, although the medulloblastoma progressed with diffuse leptomeningeal metastases.

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tant factors.34 Clinical manifestations of radiation dam-
age to the spinal cord (eg, acute weakness and sphincter
dysfunction) can mimic those of spinal cord compres-
sion; a thorough understanding of a patient’s malignancy
and radiation therapy histories and a high index of sus-
picion are important for guiding appropriate work-up
and treatment.18
MR imaging findings in acute spinal cord necrosis include
an expansile ring-enhancing mass with edema and mass
effect, which can be easily mistaken for tumor recurrence.30
T1 and T2 hyperintense postradiation therapy changes in
the marrow of the adjacent vertebral bodies and posterior
elements can be a clue to diagnosis (Figs 12 and 13). Up to
half of patients who undergo spinal radiation therapy may
develop chronic spinal cord atrophy within the radiation
field.30
CONCLUSIONS
Although rare, spinal cord lesions in patients with cancer
may become more common with increasing cancer diagno-
ses and increasingly effective cancer treatments. The spec-
trum of spinal cord lesions in patients with cancer is broad
and may differ in frequency compared with patients with-
out cancer. Proper recognition of characteristic imaging
features and key clinical signs and symptoms is necessary
for determining the proper diagnosis and directing man-
agement and subsequent laboratory and/or pathologic
investigations.
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