180
describe this as a dull ache behind the ear or in
the occipital region. The clinical picture of these
patients often reveals dysphagia and weakness of
the palate, hoarseness, and weakness of the ipsi-
lateral sternocleidomastoid and trapezius mus-
cles. Horner’s syndrome has been reported [ 20 ],
as has Collet-Sicard syndrome [ 11 , 21 , 22 ].
Jugular venous or transverse sinus compression
may result in increased intracranial pressure and
papilledema [ 11 , 21 , 22 ].
The occipital condyle syndrome is defined by
unilateral, often superficial, pain in the occipital
region. If the pain initially occurs in the absence
of neurological deficits, it often progresses within
a short period of time to dysphagia and dysar-
thria. Unilateral cranial nerve XII palsy is also
often present, and patients often complain of a
stiff neck [ 22 – 24 ] and pain exacerbated upon
flexion or contralateral rotation. The extent of
cranial nerve involvement and occipital and neck
pain is undoubtedly a function of size and loca-
tion of the offending tumor.
Diagnosis and Selection for Surgical
Intervention
Increased surveillance imaging using computed
tomography (CT) and magnetic resonance imag-
ing (MRI) of patients with known cancer has
allowed an increase in the detection of asymp-
tomatic intracranial lesions [ 25 , 26 ]. However, a
large number (~30%) of patients who are ulti-
mately found to have brain metastases have had
no previous diagnosis of cancer [ 27 ]. In these
patients, a thorough workup is mandatory during
treatment planning and should include extensive
imaging, using CT or MRI of the chest, abdo-
men, pelvis, and even radionucleotide bone scans
and positron emission tomography scans. For the
neurosurgeon, MRI with and without contrast is
the modality of choice and is mandatory before
surgical planning, unless it cannot be obtained
because of an MRI contraindication. Metastases
to the brain are typically found at the “gray-
white” junction and have abnormal vascular per-
meability. Therefore, extensive vasogenic edema
is common, and administration of contrast agent
typically produces enhancement of the metasta-
ses of interest, as nearly all metastases disrupt the
blood–brain tumor barrier. Patterns of MRI sig-
nal intensity are currently not robust enough to
use for diagnosis of specific metastatic tumors,
yet many important distinctions can be made.
Most brain metastases will show high T2 signal
intensity [ 28 ]. Necrotic and cystic lesions may
demonstrate sharp lesional demarcation but can
have variable T1 and T2 signals. T1 rim enhance-
ment is often noted [ 29 ]. Hemorrhagic metasta-
ses may have heterogeneous enhancement
patterns and incomplete rim enhancement and
can cause difficulty in diagnostic imaging.
Identification of the tumor body is usually suffi-
cient to diagnose a hemorrhaging metastasis ver-
sus an arteriovenous malformation or
parenchymal hematoma [ 30 ]. Notably, MRI
offers superior sensitivity to contrast-enhanced
CT for detection of metastases in the posterior
fossa as well as other small metastases through-
out the brain [ 31 ].
Imaging studies obtained for a patient with
suspected SBM include standard T1- and
T2-weighted MRI with and without contrast. It
may be helpful to rely on fat-suppressed images
in the context of gadolinium administration to
pick out enhancing lesions near bone and soft tis-
sue junctions [ 17 ]. Skull base CT scan bone win-
dows may provide confirmatory imaging or may
substitute for MRI only when absolutely neces-
sary. Radionuclide bone scans or positron emis-
sion tomography may be helpful in diagnosis of
bony SBM (Fig. 13.2). Laboratory tests should
include cerebrospinal fluid cytology to exclude
meningeal carcinomatosis [ 32 ].
The number and location of metastases, as
well as the overall clinical picture of each patient,
must be used to guide the decision to intervene
surgically. Single or solitary lesions, >3 cm in
diameter, and close to the surface of the brain are
most accessible to the neurosurgeon. This is
especially true in patients with a large posterior
fossa lesion causing mass effect, fourth ventricu-
lar compromise, and neurological symptoms
(Fig. 13.4). In patients with stable, or relatively
stable, metastatic disease, removal of these
lesions surgically has been shown to provide sub-B.D. Weaver and R.L. Jensen