178
fossa of the brain. This is generally explained
as being due to the proportionally higher
intracranial blood flow (15%), which is con-
sistent with hematogenous spread of embolic,
metastatic tumor cells [ 5 ]. Others have dis-
cussed that the retrograde dissemination via
the paravertebral venous plexus may best
explain posterior fossa metastasis from retro-
peritoneal organs, which are particularly
overrepresented in the frequency of posterior
fossa metastasis [ 6 ].
The genomic landscape of brain metastases
also differs from the parental tumor in many
instances. Recent reports highlight correlations
between particular KRAS and epidermal
growth factor receptor (EGFR) mutations and
organotropic metastasis [ 7 , 8 ]. Tumor exosome
data also point toward metastatic specificity
driven by expression patterns of key extracel-
lular matrix proteins, such as integrins, and
likely others [ 9 ]. Ultimately, the question of
organotropic metastasis remains open for inves-
tigation, and as new technologies become avail-
able for assessing the biological underpinnings
of metastasis, patterns and distributions of met-
astatic brain lesions will become increasingly
clear. Nevertheless, the prevalence of brain
metastasis demands that neurosurgeons under-
stand the individualized interventions suitable
for each patient, the surgical anatomy of the
posterior fossa, the nonsurgical options such as
stereotactic radiosurgery (SRS), and the impor-
tance of coordination with other neuro-onco-
logical team members.
Metastasis to the Base of Skull
Skull base metastasis (SBM) represents a distinct,
challenging, and relatively rare clinical entity.
These metastatic lesions may cause significant
morbidity when interfering with important neuro-
vascular structures. Most data regarding patients
with SBM comes from case reports, small case
series, and retrospective analyses comparing treat-
ment modalities. SBMs are estimated to occur in a
small percentage of the general population, with up
to 3% incidence of temporal bone metastatic
lesions [ 10 ]. However, SBM is most commonly
diagnosed in patients who have a known history of
metastatic cancer, especially when osseous metas-
tasis is already confirmed [ 11 ]. SBMs to the base of
the frontal, ethmoidal, sphenoidal, temporal, and
occipital bones are inherently more challenging to
detect than calvarial metastases because of their
variable clinical presentations and sequestered
anatomy. This difficulty likely leads to an underes-
timation of their true incidence [ 12 ].
The three most common cancers contributing to
skull base metastases are the breast, lung, and pros-
tate, whose rate of metastasis were estimated at
40%, 14%, and 12%, respectively, in a cohort of 43
patients [ 11 ]. Prostate carcinoma represents the
most frequent culprit in men, while carcinoma of
the breast is the most frequent skull base metastasis
found in women [ 13 ]; however, many other cancers,
such as colon, melanoma, and lymphoma, may
metastasize to the skull [ 14 – 16 ]. A large fraction of
the time—28% in one meta- analysis [ 17 ]—SBM
may incite the initial presentation of previously
undiagnosed cancer. Further, as patients harboring
widely metastatic lesions live longer because of
improved current therapies, the prevalence of SBM
is undoubtedly increasing, and modern neurosur-
geons should be aware of the presentation and chal-
lenges presented by patients harboring these lesions.
The pathophysiology of SBM is relatively
understudied, yet it is widely accepted that hema-
togenous spread directly (as from primary tumors
of the lung or other tumors) or retrograde venous
seeding through Batson’s plexus likely account
for the vast majority of SBM [ 17 , 18 ].Patient Presentation
Patients with metastasis to the cerebellum may
have varied and dramatic clinical presentations.
Metastases within the cerebellum may cause dys-
metria, dysdiadochokinesia, dysarthria, truncal
instability, and ataxia. Symptoms related to
brainstem or fourth ventricular compression are
also common in patients with infratentorial
metastasis, often producing nausea and vomiting,B.D. Weaver and R.L. Jensen