Magnetic resonance imaging (MRI) of the cervical spine is commonly performed for evaluation of cervical pain, radiculopathy, and myelopathy. Radiologists must recognize less common non-neoplastic disease processes to provide accurate diagnoses.
is a Neuroradiologist at Robert Wood Johnson University Hospital,
New Brunswick, NJ.
is an Instructor of Radiology at Harvard Medical School and a
Neuroradiologist at Brigham and Women's Hospital, Boston, MA.
is an Assistant Professor of Radiology at Harvard Medical School
and a Neuroradiologist at Brigham and Women's Hospital.
Magnetic resonance imaging (MRI) of the cervical spine is a
commonly performed study for evaluation of cervical pain,
radiculopathy, and myelopathy. Recognition of less common
non-neoplastic disease processes is essential in order to diagnose
and properly treat these entities.
Subacute combined degeneration of the cervical spinal
Cobalamin or vitamin B12 is an organometallic compound not
produced by the human body but is incorporated, instead, into the
diet via meat and dairy products. It is bound in the duodenum to
intrinsic factor (IF). This cobalamin-IF complex is resistant to
proteolysis and is absorbed into the blood stream as it makes its
journey to the distal small bowel.
This route of B12 intake is adequate for everyone except for strict
vegetarians and their breastfed children. Pernicious anemia is the
most common cause of cobalamin deficiency in temperate climates.
Other conditions leading to cobalamin deficiency include
malabsorption states, ileal resection, massive bacterial
colonization of the intestines, and tropical sprue.
Cobalamin deficiency affects not only the blood (megaloblastic
anemia) and gastrointestinal tract, but also the nervous system,
where it can result in subacute combined degeneration (SCD). The
peri-pheral nerves, spinal cord, and cerebrum may also be involved.
In the spinal cord, involvement of the dorsal columns, lateral
corticospinal tracts, and, occasionally, the lateral spinothalamic
tracts leads to signs and symptoms, such as hand and feet
paresthesia, numbness, sensory loss, gait ataxia, and mainly distal
lower extremity weakness. If untreated, ataxic paraplegia may
Histologically, multifocal demyelination and vacuolization may
be found in the posterior, lateral, and, occasionally, anterior
Axonal degeneration and, ultimately, axonal death is
The progression of demyelination is often from dorsal columns to
lateral columns, with subsequent Wallerian degeneration. Cervical
and thoracic cord lesions are typical, and the medulla may also be
MR imaging of SCD includes expansion of the affected cervical
and thoracic cord segments with T2 prolongation, mainly of the
dorsal columns and, occasionally, slight enhancement after
(Figure 1). Lateral column involvement on MR imaging is usually not
apparent, even though signs and symptoms may be attributable to
Within the brain, multiple confluent areas of white matter T2
prolongation are seen. The differential diagnoses of an
intramedullary lesion exhibiting non-
specific characteristics similar to SCD include infectious (herpes
virus, HIV vacuolar myelopathy), inflammatory (sarcoid),
demyelinating (multiple sclerosis), ischemic, and, to a lesser
degree, neoplastic processes (astrocytomas and ependymomas).
The main findings indicating the diagnosis of SCD are the clinical
picture and the dorsal signal abnormality.
Treatment for cobalamin deficiency is intramuscular
cyanocobalamin administration and management of any underlying
disorder. Although patients show excellent response to treatment
with regard to the hematologic manifestations, neurological
symptoms may remain refractory.
Early treatment initiation may lead to clinical improvement in
myelopathic symptoms with an accompanying decrease in dorsal spinal
cord T2 prolongation.
Early diagnosis is critical, as clinical improvement of SCD is
inversely proportional to its duration and severity.
Arteriovenous malformations/fistulas of the cervical
The nomenclature of spinal vascular lesions has evolved with
better understanding of lesional angioarchitecture.
For our discussion, the classification system proposed by Anson and
will be used as follows: type I dural arteriovenous fistulas
(DAVFs), type II and IIIintramedullary arteriovenous
malformations (AVMs), and type IVintradural/extramedullary
(peri-medullary) spinal AVMs. Since a discussion of all four types
of vascular ab-normalities would be beyond the scope of this text,
only type I lesions will be discussed in the context of the
The most common lesions are type I lesions, which comprise up to
80% of all spinal AVMs, and are thought to be secondary and
acquired. They are 4 times more common in men, usually between 40
and 70 years of age, and are often found in the lower thoracic or
upper lumbar region. The angioarchitecture of these lesions is
composed of a radicular artery branch that communicates with an
intradural medullary vein via a fistula at the dural root sleeve.
This medullary vein then drains cephalad into serpiginous dilated
pial veins of the spinal cord. This results in chronic
arterialization of veins, leading to elevated pressures and venous
engorgement that produce changes in spinal cord parenchyma.
Ultimately, there is a decrease in tissue perfusion and a resultant
hypoxia due to transmission of these elevated venous pressures to
intrinsic spinal cord veins.
With time, this progressive spinal venous hypertension manifests
clinically as a distinctive chronic myelopathy with progressive
weakness and sensory deficits.
The most common symptom is progressive lower extremity weakness
without upper extremity involvement. Other manifestations also
include back pain, sensory deficits, and bowel and bladder
dysfunction. Delayed diagnosis is not uncommon, as there is usually
a slow progression of symptoms over a 2- to 3-year period.
The so-called Foix-Alajouanine syndrome or subacute necrotic
myelopathy, an eponym associated with type I lesions, is the result
of chronic venous ischemia that could potentially lead to cord
Radiographically, prone myelography demonstrates tortuous
vessels and cauda equina beading. It is a sensitive test, though
not as specific as MRI, which can show cord enlargement, central
cord T2 prolongation, dorsal serpentine flow voids (more specific),
and dilated vein enhancement
(Figure 2). Ill-defined and patchy enhancement of the affected
portion of the spinal cord is not uncommon. Nevertheless,
catheter-based spinal angiography remains the gold standard for the
diagnosis of spinal AVM.
For the cervical spine, type I lesions are rare,
and cervical DAVFs can manifest as a progressive myelopathy,
similar to those in the thoracolumbar spine. Interestingly, unlike
those in the thoracolumbar region, cervical DAVFs present more
often with hemorrhage, such as subarachnoid hemorrhage (SAH) at the
The angioarchitecture of cervical DAVF can take one of three forms.
First, as in the thoracolumbar spine, the feeding radicular artery
may drain into a medullary vein along the length of the cervical
spinal cord, usually dorsally, and present with myelopathy
(Figure 2). Interestingly, the signal abnormality from a cervical
DAVF tends not to involve the medulla.
Another pattern is that the DAVFs can decompress entirely into
the intracranial venous system and thus decrease venous
hypertension in the cervical cord. These patients may not present
with myelopathy but with SAH because of intracranial venous
enlargement. Alternatively, patients who drain caudally into a
medullary vein would be more likely to present with myelopathy than
The third scenario involves an intracranial DAVF that produces
cervical myelopathy. An intracranial DAVF can drain into spinal
veins and produce symptoms secondary to venous hypertension,
similar to DAVFs in the thoracolumbar spine.
These lesions can manifest as intracranial hemorrhage,
ischemia/infarction, mass effect from enlarged veins, increased
intracranial pressure, and cranial neuropathies. T2 prolongation
within the cervical cord and medulla, cord enlargement, and flow
voids dorsal and ventral to the cervical cord are typical MRI
The initial method of treatment of symptomatic type I DAVFs is
primarily endovascular with successful >80% of cases. Permanent
liquid agents, such as N-butylcyanoacrylate, are preferred as
particulate embolic material results in almost 100% recanalization.
If endovascular treatment is unsuccessful or contraindicated,
surgical removal of the nidus is usually a safe alternative.
Cavernous malformations of the cervical spinal
The overall incidence of cavernous malformations (CMs) is
and the spinal cord harbors approximately 3% to 5% of CMs.
They are discrete masses consisting of endothelial-lined sinusoidal
vascular channels without intervening neuronal tissue. Cavernous
malformations are congenital lesions with a peak incidence in the
third and fifth decades. Interestingly, although intracranial
lesions show equal male and female predominance, spinal cord CMs
are more common in females
and are usually intra-medullary.
Clinically, CMs can present with a wide range of symptoms. Acute
symptoms are often secondary to hemorrhage, while a progressive
course may be due to microhemorrhages.
Treatment of CMs in the spinal cord depends on the symptoms and
age of the patient. Asymptomatic lesions are usually left alone
while symptomatic ones can be explored surgically because of the
threat of future hemorrhage and resultant neurologic decline.
One study proposes a hemorrhage rate for spinal CMs of 1.6% per
MRI is the study of choice for imaging for CMs, as arteriovenous
(AV) shunting is not characteristic and, thus, remains occult on
conventional arteriography. Intracranial and spinal-cord CMs have
similar MRI features that classically include central signal
heterogeneity (reflecting various stages of blood products)
surrounded by a peripheral dark hemosiderin ring without
significant edema, mass effect, vascular flow voids, or enhancement
(Figure 3). On gradient-recalled images, CMs bloom secondary to
blood products within the lesion. On CT, CMs often show focal high
attenuation with or without associated calcifications.
Cervical spine manifestations of intracranial
The clinical manifestations of decreased cerebrospinal fluid
(CSF) volume and CSF pressure were first described by Schaltenbrand
in 1938. The findings can be primary from idiopathic spontaneous
intracranial hypotension (IH) or secondary due to lumbar puncture
or perioperative or posttraumatic causes that allow CSF leakage via
The classic clinical presentation of IH is acute or subacute
postural headaches. These, however, may not always be postural,
particularly when associated with subdural hygromas or hematomas.
Other intracranial manifestations include cranial nerve palsies,
visual disturbances, photophobia, dysgeusia, auditory symptoms,
facial numbness and weakness, and, rarely, stupor.
The manifestations of IH are based on the Monroe-Kelly Rule,
which contends that CSF volume varies with intracranial blood
volume. This rule states that in the setting of an intact skull, a
decreased CSF volume will lead to brain and meningeal
vasodilatation. Since there is communication of the intracranial
and intraspinal venous systems, it is possible that dilatation of
brain meninges and intraspinal venous plexi will occur in concert.
It is important to note that CSF pressure is usually low in this
condition, but this is not always the case.
The intracranial MRI findings include diffuse dural enhancement,
prominent dural sinuses, enlarged epidural venous plexus, enlarged
pituitary gland, subdural collections (effusions or hematomas), and
downward displacement of the optic chiasm, pons, and cerebellar
Spinal manifestations of IH are similar to those described above,
such as dural enhancement (pachymeningeal), epidural venous plexus
dilatation, extradural fluid collections, and inferior cerebellar
and are best evaluated with MRI (Figure 4).
Cervical spinal epidural venous engorgement is most prominent at
C1-C2, with frequent extension to the clival plexus, and enhances
with contrast administration. Flow voids may also be present as
hypointense areas on T2-weighted imaging (T2WI).
Since there is no posterior epidural vein in the cervical spine,
the predominant epidural venous system is situated anterolaterally
within the spinal canal.
Care must be taken not to mistake an enlarged epidural venous
plexus for a meningioma or other dural mass.
Another important MRI finding of the spine is the presence of an
extradural fluid collection that is usually isointense to CSF on
T1-weighted imaging (T1WI) and T2WI. Mild enhancement of the fluid
collections or the adjacent dura has been reported when the
enhancement may be related to contrast leakage into the collection.
The location of these collections is not altogether clear and may
be either epidural or subdural.
Likewise, the etiology of these extradural collections is
uncertain, but may represent the actual site of CSF leakage,
secondary to CSF hydrostatic changes,
or represent a transudate from spinal meningeal hyperemia.
An interesting cervical spinal finding in IH is the presence of
a paramedian fluid collection at the C1-C2 level in the posterior
soft tissues of the spine that follows CSF signal on both T1WI and
Three potential etiologies have been suggested. Yousry and
thought that the collection could represent the site of CSF leak,
or that it might represent transudate secondary to hydrostatic
pressure changes in adjacent rich venous plexi. Alternatively,
suggests communication of this cervical fluid collection with the
subarachnoid space, as CSF ascends in the epidural space from a
site of leakage in a more inferior location and ultimately
decompresses into the posterior cervical soft tissues at the C1-C2
Cervical spine sarcoidosis
Sarcoidosis is a multisystem disease that presents
histopathologically as noncaseating granulomas of unknown etiology
and clinically involves the central nervous system in approximately
5% of affected patients
and 16% of cases at autopsy.
This disease often mimics other central nervous system diseases,
such as multiple sclerosis, meningioma, tuberculous meningitis, and
vasculitis. Intracranial manifestations include dural thickening or
masses, enlarged pituitary stalk, leptomeningeal involvement,
enhancing and nonenhancing parenchymal lesions, and cranial
The cervical manifestations of sarcoidosis are similar to
intracranial findings and can have both intramedullary and
extramedullary involvement. Intramedullary findings, however, often
include an extramedullary component and can mimic spinal cord
neoplasms. Sarcoidosis of the cervical spine can be extensive,
infiltrative, and expansile, with significant associated
hyperintensity on T2-weighted images. The enhancement pattern may
be broad-based and peripheral (suggesting inflammatory changes
extending from the leptomeninges via perivascular spaces inward),
extending from adjacent to the spinal cord surface to the center of
(Figure 5). In the chronic stages of these intramedullary lesions,
cord atrophy without enhancement as well as gliosis may be present.
Spontaneous epidural hematoma of the cervical
Spontaneous spinal epidural hematomas are not common
However, with increasing use of MRI, this diagnosis may not be as
unusual as initially thought.
The most common location of hematomas is in the thoracic spine
though Sklar and colleagues
reported a predominance of cervical spine hematomas in their study.
They propose that this may be due to the fact that the majority of
their cases involved trauma that is more common in the cervical
Although spinal epidural hematomas are considered to be
spontaneous, they may be related to just minor trauma with a male
The epidural venous plexus is thought to be fragile and therefore
vulnerable to rupture.
Other etiologies include coagulopathies, rupture of vascular
malformations, vertebral body hemangiomas, hypertension, and
Acute pain is a common finding with concomitant neurologic deficit
based on the extent of cervical spinal cord compression.
MRI is the modality of choice for evaluation of hematoma, as it
gives the clinician information of anterior or posterior location,
extent, degree of cord compression, and acuity of the hematoma. It
also provides a basis for management and follow-up of potential
Signal characteristics can vary, but are isointense to adjacent
cord acutely, with conversion to hyperintensity in the subacute
stage on T1WI
(Figure 6). On T2WI, the majority of the signal abnormality is
though hyperintensity has also been described.
Gradient-echo images have been shown to be useful to demonstrate
of hemorrhage, while others report peripheral, linear enhancement
of acute spinal epidural hematoma.
Differential diagnoses from hematoma in the cervical spine
include epidural abscess, neoplasm, and lipoma.
One other diagnostic entity to consider is engorgement of the
anterior epidural venous plexus, as was described above in cases of
intracranial hypotension. The clincial scenario, with or without
contrast MR characteristics, however, should allow accurate
diagnosis in most cases.
Recognition of the less common non-neoplastic entities of the
cervical spine is important in order to diagnose and properly treat
these patients and avoid erroneous diagnoses.