Brain Tumor Pathology
https://doi.org/10.1007/s10014-020-00367-x

CASE REPORT

Intravascular carcinomatosis of the brain: a report of two cases
Jackie Chan1 · Shino Magaki3 · Xinhai R. Zhang3,8 · Curtis Chin4 · Stanley Greenspan2 · Michael Linetsky5 ·
Mireille Kattar1 · Harry V. Vinters1,3,6,7
Received: 23 April 2020 / Accepted: 24 May 2020
© The Japan Society of Brain Tumor Pathology 2020

Abstract
Although central nervous system (CNS) metastases are common in advanced cancer, CNS involvement solely by intravascular tumor cells, known as intravascular carcinomatosis, is extremely rare. We report two cases of brain metastasis in
which tumor cells were restricted to the vascular lumina without parenchymal involvement, resulting in ischemic lesions.
The first patient is a previously healthy young woman who presented with symptoms of community-acquired pneumonia
and progressed to respiratory failure. Computed tomography of the brain showed infarcts of differing ages. At autopsy, she
was found to have widely metastatic cervical squamous cell carcinoma and cerebral tumor emboli with multifocal infarcts,
mainly microinfarcts. The second patient is an elderly man with cognitive impairment and mild Parkinsonism who presented
with symptoms of a urinary tract infection. Magnetic resonance imaging of the brain showed atrophy and changes suggestive
of chronic microvascular ischemic disease. Postmortem examination demonstrated prostatic adenocarcinoma and cerebral
tumor emboli with multifocal infarcts. These cases illustrate that this pattern of intracranial metastasis may rarely be a cause
of cerebral ischemic lesions and emphasize the importance of thorough pathologic examination of the brain.
Keywords Cerebral intravascular carcinomatosis · Infarct · Prostatic adenocarcinoma · Cervical squamous cell carcinoma ·
Autopsy

Introduction
Metastases are the most common central nervous system
(CNS) tumors, accounting for approximately half of all
intracranial neoplasms and increasing in incidence, usually
seen at advanced stages of the malignancy with associated
symptoms [1–3]. The reported 9–17% incidence of brain
Jackie Chan and Shino Magaki contributed equally to this work
* Shino Magaki
smagaki@mednet.ucla.edu
1

Department of Laboratory Medicine and Pathology,
University of Alberta, Edmonton, AB, Canada

2

Department of Radiology and Diagnostic Imaging,
University of Alberta, Edmonton, AB, Canada

3

Section of Neuropathology, Department of Pathology
and Laboratory Medicine, Ronald Reagan UCLA Medical
Center, David Geffen School of Medicine, 10833 Le Conte
Ave, Los Angeles 90095, CA, USA

4

Department of Pathology and Laboratory Medicine, Ronald
Reagan UCLA Medical Center, David Geffen School
of Medicine, Los Angeles, CA, USA

metastases in patients with cancer is likely an underestimate
as intracranial metastases have been found in up to a quarter of cancer patients in autopsy studies [1, 3, 4]. However,
many of these studies are older, recent studies being difficult with decreasing autopsy rates [3, 4]. The most common
malignancies to metastasize to the brain are carcinoma of the
lung (accounting for approximately half of brain metastases) followed by breast carcinoma (13–30%) and melanoma
(6–11%), which together account for the majority [3]. Brain
5

Department of Radiologic Sciences, Ronald Reagan
UCLA Medical Center, David Geffen School of Medicine,
Los Angeles, CA, USA

6

Department of Neurology, Ronald Reagan UCLA Medical
Center, David Geffen School of Medicine, Los Angeles, CA,
USA

7

Brain Research Institute, Ronald Reagan UCLA Medical
Center, David Geffen School of Medicine, Los Angeles, CA,
USA

8

Present Address: Department of Pathology, Rush University
Medical Center, Chicago, IL 60612, USA

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Brain Tumor Pathology

metastasis may present as the initial manifestation of malignancy in over 10% of cases, most subsequently found to have
a lung primary [2, 5]. The most frequent site of metastasis
is the brain parenchyma, often at border zones between vascular territories especially between the middle and posterior
cerebral arteries, and at the gray-white matter junction due
to the decrease in vessel diameter, with 80% occurring in
the cerebral hemispheres, 15% in the cerebellum and 5%
in the brainstem [1, 2, 6]. Dural metastases have been seen
in approximately 9% of patients with cancer, half showing
isolated dural involvement, in one autopsy series [1, 4, 7].
They result from hematogenous spread or direct extension
from the skull and are most often encountered in breast and
prostate carcinoma [1, 7]. There is a similar incidence of
leptomeningeal carcinomatosis in which diffuse infiltration
of the pia and arachnoid is seen [4, 7]. Miliary metastasis,
previously described as carcinomatous encephalitis, is an
uncommon pattern of metastasis, usually of lung origin,
that can mimic rapidly progressive dementia and demonstrates widespread tumor deposits in the Virchow–Robin
spaces that may extend into the subpial space [1, 8, 9]. A
very rare form of CNS involvement in which tumor cells are
seen exclusively in the vascular lumina without parenchymal extension has been termed intravascular carcinomatosis
[10–12].
Here we present two patients who showed multiple cerebral ischemic lesions on imaging with postmortem examination demonstrating CNS metastasis from cervical and
prostate carcinoma limited to the intravascular compartment, raising awareness that multifocal ischemic lesions may
rarely be a manifestation of metastatic disease and emphasizing the importance of careful brain pathologic examination.

Clinical summary and pathological findings
Case 1
A 37-year-old woman was transferred for a 2-week history
of progressive cough and dyspnea that did not resolve after
completing a course of antibiotics for presumed community-acquired pneumonia. She had no significant past medical history except for uterine fibroids and two episodes of
Methicillin-resistant Staphylococcus aureus skin abscess
due to injury at work. Chest computed tomography (CT)
showed multifocal airspace and ground-glass opacities in the
periphery of bilateral lungs and reactive lymphadenopathy
consistent with atypical pneumonia. She completed a course
of intravenous antibiotics and was discharged on home oxygen. However, the patient was admitted to the intensive care
unit at an outside hospital a few weeks later for progressive
respiratory failure. An extensive infectious disease workup
showed transient positivity for enterovirus/rhinovirus on

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bronchoalveolar lavage PCR and subsequent positivity for
Candida albicans in sputum, blood, and urine, and she
was placed on broad-spectrum antibiotics and antifungals.
Repeat chest CT showed extensive ground-glass opacities
and development of cystic bronchiectasis. She had also been
placed on steroids and undergone plasmapheresis for a possible autoimmune etiology, although evaluation for autoimmune disease, including serologic testing for anti-GBM,
ANCA, ANA, and anti-dsDNA, was negative. As urinalysis
showed hematuria and proteinuria, a renal biopsy was performed but was unremarkable with no evidence of vasculitis.
CT of the head showed cortical atrophic changes, an old left
cerebellar infarct (Fig. 1a, b), and more recent small right
thalamic perforator infarct (Fig. 1c, d). The patient eventually required intubation and extracorporeal membrane
oxygenation. She was placed on the waitlist for lung transplantation and started on cyclophosphamide, but developed
multiorgan failure and died after being transitioned to comfort care, one month after admission.
Complete autopsy revealed heavy lungs with diffuse
parenchymal hemorrhage, consolidation and necrotizing
cavitary lesions throughout. The uterus showed a 7 cm hemorrhagic and necrotic myometrial mass in the anterior wall
that was adherent to the bladder. On microscopic examination, the uterus (Fig. 2a), bladder wall, ovaries, lungs
(Fig. 2b), and hilar/mediastinal and peripancreatic lymph
nodes were involved by poorly differentiated squamous
cell carcinoma with extensive necrosis. The liver showed
intravascular and sinusoidal tumor cells with focal hemorrhage and necrosis. Immunohistochemistry was performed
with the following antibodies: CK AE1/AE3 (Dako, mouse
monoclonal, AE1/AE3, predilute), p63 (Dako, mouse monoclonal, DAK-p63, 1:100), p40 (Biocare, mouse monoclonal,
BC28, 1:100), p16 (Roche, mouse monoclonal, E6H4, 1:5),
CK7 (Dako, mouse monoclonal, OV-TL 12/30, 1:100), and
CK20 (Dako, mouse monoclonal, Ks20.8, predilute). On
immunohistochemistry, the tumor cells were positive for
pankeratin AE1/AE3, p63, p40 (Fig. 2c), and p16 (Fig. 2d),
patchy positive for CK7, and negative for CK20. The tumor
was positive for HPV 16 on genotyping. The lungs demonstrated multiple metastatic deposits and extensive angiolymphatic invasion in a background of diffuse alveolar damage.
There were also multifocal parenchymal infarcts with clusters of budding yeast and pseudohyphae morphologically
consistent with Candida species on Gomori methenamine
silver (GMS) stain (Fig. 2b, inset).
Gross examination of the brain showed no areas of
encephalomalacia in the cerebral hemispheres or deep
gray matter, and no lesions in the brainstem. There was an
approximately 1 cm linear region of encephalomalacia in
the left cerebellar hemisphere. No significant atherosclerosis
was identified. On histologic sections, multifocal subacute
to chronic infarcts (mainly microinfarcts) were seen in the

Brain Tumor Pathology
Fig. 1  Axial CT demonstrating
an area of encephalomalacia
in the posteroinferior aspect
of the left side of the cerebellum (arrows) consistent with a
previous remote left posterior
inferior cerebellar artery infarct
(a, b). Axial CT showing some
decreased attenuation within the
right thalamus (arrows) in keeping with a more recent right
thalamic perforator infarct (c, d)

cortex, subcortical white matter (Fig. 2e) and cerebellum,
with scattered cortical and subcortical microvessels containing luminal plugs of epithelioid cells showing enlarged,
atypical nuclei (Fig. 2e, f) and immunopositivity for CK
AE1/AE3 (Fig. 2f, inset), compatible with tumor emboli
from squamous cell carcinoma.

Case 2
A 75-year-old man with a 7-year history of frontal predominant cognitive impairment and 4-year history of mild Parkinsonism with frequent falls, dysphagia and dysarthria, who
was being followed for possible progressive supranuclear
palsy, was admitted to an outside hospital for increasing
weakness and fever, concerning for a urinary tract infection

(UTI). The patient had been placed on antibiotics for a
possible UTI several weeks prior. He had a history of urinary frequency and nocturia attributed to benign prostatic
hyperplasia but with recent elevated prostate-specific antigen (PSA) levels concerning for prostate cancer. However,
he had declined further intervention. His past medical history also included recurrent venous thromboembolism with
pulmonary embolism on warfarin, hypertension, hyperlipidemia, and coronary artery disease with stent placement. At
the outside hospital, CT of the brain demonstrated no acute
intracranial process. Portable chest X-ray was unremarkable.
Laboratory testing showed creatinine of 0.80 mg/dL, hemoglobin of 9.5 g/dL, white blood cells of 5.8 × 103/mm3, and
platelets of 120 × 103/mm3. Urinalysis showed proteins and
ketones but was negative for leukocyte esterase and nitrites.

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Brain Tumor Pathology

Fig. 2  Squamous cell carcinoma invading myometrium (a, ×100).
Left lung with metastatic squamous cell carcinoma with necrosis (b,
×200) as well as fungal organisms morphologically consistent with
Candida species on GMS stain (b inset, ×400). Metastatic deposits
in the hilar lymph nodes demonstrating immunopositivity for p40
(c, ×40) and p16 (d, ×40). Subacute microinfarct (arrow) with histiocytic infiltrate, neuroaxonal spheroids and gliosis with an adjacent

small vessel containing a cluster of tumor cells (arrowhead) in the
subcortical white matter (e, 100x) and multiple emboli of squamous
cell carcinoma in the cortex (f, ×200), positive for CK AE1/AE3 on
immunohistochemistry (f inset, ×200), in the right middle cerebral
artery/anterior cerebral artery watershed region. Note immunoreactivity of cells within adjacent capillaries

He was discharged to a skilled nursing facility for hospice
care where he exhibited a rapid decline in mental status and
minimal food intake and died one week after admission to
the facility and one month after his hospital admission.
Magnetic resonance imaging (MRI) performed 2 months
prior to his last hospital admission demonstrated cerebral

volume loss, especially in the frontal lobes, mild midbrain
atrophy (Fig. 3a, b) on magnetization-prepared rapid gradient-echo (MP-RAGE) sequence, and patchy areas of fluidattenuated inversion recovery (FLAIR) hyperintensity in the
pons (Fig. 3c) and periventricular and subcortical white matter (Fig. 3d), suggestive of chronic microvascular ischemic

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Brain Tumor Pathology
Fig. 3  Sagittal (a) and axial (b)
MP-RAGE images demonstrating midbrain atrophy. On
the sagittal image, this classic
appearance of midbrain atrophy
is known as the “hummingbird
sign” (arrow). Axial FLAIR
images (c, d) showing patchy
areas of hyperintensity in the
pons (thick arrow) and periventricular and subcortical cerebral
white matter (thin arrows)

disease. Lumbar spine X-ray performed over 1 year prior to
death showed moderate degenerative disc disease.
An autopsy limited to the brain and abdomen showed
a nodular prostate with invasive adenocarcinoma with a
Gleason score of at least 4 + 5 = 9 (Fig. 4a), with extensive
autolysis. The gastrointestinal tract, liver, pancreas, spleen,
adrenal glands, kidneys, and bladder showed no metastatic
tumor. Examination of the brain showed a smooth dura
with no masses or hemorrhage. There was mild cortical
atrophy in the frontal lobes and mild hydrocephalus ex
vacuo. No infarcts or masses were seen grossly. The substantia nigra and locus coeruleus were well-pigmented.
The basal vasculature demonstrated moderate to severe
atherosclerosis. Immunohistochemistry was performed
with the following antibodies: Aβ42 (EMD Millipore,

rabbit polyclonal, AB5078P, 1:150), Aβ40 (EMD Millipore, rabbit polyclonal, AB5074P, 1:400), phosphotau (Thermo Fisher, mouse monoclonal, AT8, 1:200),
and PSA (Dako, rabbit polyclonal, A0562, 1:10,000).
On microscopic examination, there were abundant tauimmunoreactive neurofibrillary tangles in the frontal
cortex, hippocampus, basal ganglia, midbrain, pons, and
dentate nucleus of the cerebellum, as well as tufted astrocytes and oligodendroglial coiled bodies, consistent with
progressive supranuclear palsy. There was no evidence
of significant amyloid plaques, as demonstrated by Aβ
immunohistochemistry, to suggest changes of Alzheimer
disease. Additionally, there were multifocal acute/subacute
(Fig. 4b) and chronic microinfarcts in the cerebral cortex
and subcortical white matter, basal ganglia, and brainstem

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Brain Tumor Pathology

Fig. 4  Prostate with extensive involvement by high-grade prostatic
adenocarcinoma (a, ×100). Multifocal acute/subacute microinfarcts
in the parietal cortex (arrows) (b, ×40). Metastatic prostatic adenocarcinoma in a small vessel (arrow), with surrounding rarefaction in
the subcortical white matter of the right frontal lobe (c, ×40), and

within the vasa vasorum (arrows) of the right middle cerebral artery
(d, ×100). Intravascular tumor cells (arrows) with enlarged nuclei and
prominent nucleoli (e, ×400) positive for PSA on immunohistochemistry (f, ×200)

with clusters of atypical epithelioid cells within multiple
small vessels in the cortex, subcortical white matter, some
with surrounding rarefaction (Fig. 4c), leptomeninges
overlying the cerebellum, and vasa vasorum of the right
middle cerebral artery (Fig. 4d). The cells demonstrated

enlarged nuclei with irregular nuclear contours, granular chromatin, prominent nucleoli, moderate amounts of
eosinophilic cytoplasm (Fig. 4e), and were positive for
PSA on immunohistochemistry (Fig. 4f), consistent with
metastatic prostatic adenocarcinoma.

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Brain Tumor Pathology

Discussion
The incidence of brain metastases is rising, likely due
to the aging population, more effective treatments that
prolong survival in patients with cancer, and improved
detection techniques [2, 3], and is a significant cause of
morbidity and mortality [13]. Two-thirds of metastatic
lesions result in symptoms including headache, focal
neurologic deficits, altered mental status, and seizures [2,
14]. Approximately 5–10% of patients may present with
sudden stroke-like symptoms from hemorrhage into the
tumor, especially in melanoma and renal cell carcinoma
[13]. The majority of metastases reach the CNS through
the hematogenous route; less frequently spread occurs in
a retrograde manner along the nerves, especially in squamous cell carcinoma and salivary gland neoplasms of the
head and neck [1, 2]. However, it is extremely rare to see
CNS tumor involvement limited to intravascular spaces
with only three cases reported in the literature [10–12].
The most recent report was in a 52-year-old female with
a history of inflammatory breast carcinoma treated with
right mastectomy and chemoradiation who presented with
altered mental status; autopsy demonstrated multifocal
areas of ischemic injury with tumor cells of breast origin occluding many capillaries throughout the brain [10].
This pattern has also been reported in a previously healthy
38-year-old female with acute onset of recurrent thrombotic disease including cerebral infarcts who was found on
postmortem examination to have thrombosis of the right
middle cerebral artery with luminal poorly differentiated
adenocarcinoma of undetermined primary [11]. The third
case is of an 84-year-old female who presented with acute
bilateral ballism and at autopsy was found to have gastric
adenocarcinoma with widespread intravascular dissemination involving lung, liver, pancreas, adrenal glands, and the
cerebrum, cerebellum, and meninges with multiple infarcts
in the cerebral hemispheres, cerebellum and brainstem
[12]. Interestingly, all cases have been in patients with no
known history of malignancy except for the patient with a
history of inflammatory breast carcinoma, and all were in
females except for our second patient in whom there was
a suspicion for, but no diagnosis of malignancy.
On MRI, intra-axial metastatic lesions usually present
as contrast-enhancing masses near the gray and white matter junction with the majority demonstrating T1 hypointensity, T2 hyperintensity and FLAIR hyperintensity,
although hemorrhagic metastases show T1 hyperintensity [15]. Leptomeningeal metastases can be seen as pial
enhancement along the sulci or basal cisterns, hydrocephalus or cranial nerve deposits while dural metastases may be
difficult to differentiate from meningiomas as both show
T1 hypointensity, homogeneous contrast enhancement and

dural tail sign [15]. Miliary metastases are often observed
as numerous punctate lesions with contrast enhancement
and T2 hyperintensity, usually without ischemic changes,
mimicking infection such as tuberculosis, but may also be
undetectable [1, 8, 9]. Isolated tumor emboli have manifested as multifocal infarcts in the patients with a history
of breast carcinoma and adenocarcinoma of unknown
primary [10, 11]. In the patient with gastric adenocarcinoma, CT brain was normal although limited by movement
artifact [12]. Both of our patients also showed multifocal ischemic changes although they were subtle in our
second case. Graus et al. also describe cerebral infarcts
from tumor emboli, including metastases from breast and
osteosarcoma occluding the middle cerebral artery, and
tumor emboli and infarcts in two patients with squamous
cell carcinoma, one with esophageal primary and the other
with pharyngeal origin, but it is unclear if there were other
sites of involvement [16].
This pattern of CNS involvement in which tumor cells are
restricted to the intravascular compartment is reminiscent of
intravascular large cell lymphoma (IVLCL), a rare type of
lymphoma typically of B-cell lineage, in which malignant
lymphoid cells proliferate almost exclusively within capillaries and small arteries and veins [17, 18]. This entity was
previously referred to as neoplastic/malignant angioendotheliosis or angioendotheliomatosis proliferans systemisata,
thought to be due to widespread malignant transformation
of endothelial cells until the tumor cells were demonstrated
to be of lymphoid origin [17–19]. The lack of adhesion
molecules such as CD29 (integrin β1) and CD54 (ICAM1) has been suggested to underlie its predisposition for
intravascular growth [20]. Adhesion molecules including
VLA-4 (α4β1) and ICAM-1 also play a key role in carcinoma metastasis, with tumor cells metastatic to the brain
demonstrating elevated VLA-4 expression [21]. IVLCL has
a predilection for the brain and skin for unclear reasons and
also causes cerebral ischemic lesions in approximately half
of cases [17]. It is difficult to diagnose, previously often
only at autopsy, and important to keep in the differential of
multiple cerebral infarcts [17].
Brain metastases from cervical carcinoma are rare but
have been increasing, likely due to extended survival with
improved therapies [7, 22]. The majority have presented as
intraparenchymal masses, but they have rarely manifested as
dural or leptomeningeal metastases, and appear to spread via
the hematogenous route from the lungs, the most common
site of metastasis, as was likely in our first case [7, 23]. Prostate carcinoma also rarely metastasizes to the CNS, with a
predilection for the dura, possibly through retrograde spread
through the valveless Batson venous plexus [1]. The degree
of contribution of the tumor emboli and microinfarcts to the
rapid mental decline in the second patient is unclear as he
declined further workup or intervention. Although there was

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Brain Tumor Pathology

no evidence of metastatic tumor elsewhere, the evaluation
was limited as permission for postmortem examination was
restricted to the brain and abdomen.
Our cases increase awareness of tumor emboli as a pattern
of CNS metastasis. It often presents as multifocal ischemic
lesions and is especially important to consider in unusual
clinical presentations when extensive workup fails to reveal
an etiology. Our first patient and the reported patient with
unknown primary were both previously healthy young
females in their late 30s with multifocal ischemic lesions
in the brain [11]. The differential diagnosis may be broad in
this setting, including inflammatory and infectious etiologies, but undetected malignancy, among other prothombotic
processes, should be considered, particularly as affected
patients commonly do not have a history of a primary neoplasm. Ischemic lesions in cancer patients may be due to
intravascular carcinomatosis in addition to malignancyassociated coagulopathy [11].
Acknowledgements The authors would like to thank Dr. Gregory Fishbein (UCLA Medical Center) for his expertise on the autopsy findings
for patient 2.

Compliance with ethical standards
Conflict of interest The authors declare no conflict of interest.

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