doi: 10.2169/internalmedicine.9774-22
Intern Med Advance Publication
http://internmed.jp

【 CASE REPORT 】

Intracranial Myeloid Sarcoma Mimicking Hypertensive
Intracerebral Hemorrhage
Shuhei Ikeda 1, Masaomi Tsutsumi 1, Mai Fujita 2, Sho Okamoto 2, Makoto Eriguchi 1 and
Hideo Hara 1

Abstract:
We herein report a case of intracranial myeloid sarcoma mimicking hypertensive intracerebral hemorrhage.
A 71-year-old man with a history of acute myeloid leukemia was admitted with acute-onset dysarthria. A
hematoma-like lesion was found on computed tomography in the left putamen. Magnetic resonance imaging
(MRI) and cerebrospinal fluid cytology confirmed the diagnosis of intracranial myeloid sarcoma. The patient
showed a favorable response to chemotherapy, and follow-up MRI revealed shrinkage of the tumor. Since the
computed tomography findings resemble those of intracerebral hemorrhage, it is important to suspect intracranial neoplasm, particularly in cases with a history of hematologic diseases.
Key words: Myeloid sarcoma, stroke mimic, extramedullary malignancy, magnetic resonance imaging,
cerebrospinal fluid examination
(Intern Med Advance Publication)
(DOI: 10.2169/internalmedicine.9774-22)

We herein report a case of intracerebral MS mimicking
spontaneous hypertensive intracerebral hemorrhage (ICH).
Making the distinction is crucial, since a timely diagnosis
and treatment are linked to a better survival (12, 13).

Introduction
Myeloid sarcoma (MS) is rarely seen as a solid extramedullary tumor derived from malignant primitive myeloid
cells. It is commonly caused by acute myeloid leukemia
(AML) or chronic myeloid leukemia (CML) and is mostly a
relapse of the primary disease (1, 2). AML relapses usually
occur in the bone marrow, whereas extramedullary relapses
occur as MS lesions in any part of the body or as leukemic
cell infiltration in the body cavity fluid or cerebrospinal
fluid (CSF) (3). Besides AML relapses, MS can manifest as
extramedullary lesions at the onset of AML or even as an
isolated MS (4). It frequently affects the skin (28.2%),
lymph nodes (16.3%), testes (6.5%), and intestines (6.5%),
and the central nervous system (CNS) (3.3%) only rarely
experiences it (1). Its clinical presentation is mostly determined by the mass size and position, as well as the mechanical compression of adjacent structures. Computed tomography (CT) findings demonstrate hyperdensity (5) but
are difficult to distinguish from other diseases, such as hematoma, abscess, and meningioma (6-11).

Case Report
A 70-year-old man presented with pancytopenia. His hemoglobin level was 9.6 g/dL, his platelet count was 43×103/
μL, and his white blood cell count was 2.0×103/μL. A bone
marrow biopsy was normocellular with increased numbers
of erythroblasts. Micromegakaryocytes, giant neutrophils,
and megaloblastic alterations were seen. A diagnosis of
myelodysplastic syndromes (MDS) with multi-lineage dysplasia was made based on the World Health Organization
2016 classification (14). His Revised International Prognostic Scoring System score was 5, which is considered to indicate a high risk due to his moderate anemia, severe thrombocytopenia, intermediate karyotype, and low bone marrow
blast count.
After receiving supportive therapy without red blood cell
infusions for six months following the diagnosis of MDS,

１

Division of Neurology, Department of Internal Medicine, Faculty of Medicine, Saga University, Japan and ２ Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Japan
Received: March 16, 2022; Accepted: December 7, 2022; Advance Publication by J-STAGE: February 1, 2023
Correspondence to Dr. Makoto Eriguchi, eriguchm@cc.saga-u.ac.jp

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DOI: 10.2169/internalmedicine.9774-22

Figure 1. Brain computed tomography and magnetic resonance imaging of myeloid sarcoma. Computed tomography showed a hematoma-like lesion with a mean attenuation of 54 Hounsfield units in
the left putamen (a, arrow). The lesion showed hyperintensity on T2-weighted imaging (b). Diffusionweighted imaging showed a well-defined homogenous hyperintense lesion in the upper putamen (c).
Susceptibility-weighted imaging revealed no hemorrhagic changes in the lesion (d).

his condition developed into AML with myelodysplasiarelated changes. Approximately 30% of the blast forms in
the bone marrow were undifferentiated. Blastic cells were
positive for CD34, CD13, CD33, CD117, and myeloperoxidase with partial positivity for CD7 and CD64. A G-banding
analysis revealed a complex karyotype with additional del 7
q although chimeric fusion gene and FLT3-ITD analyses
were negative. Wilms’ tumor 1 (WT1) levels in the bone
marrow were 5.1×103 copies/μgRNA.
He was treated with an induction regimen consisting of
daunorubicin and a cytarabine-based induction regimen, but
induction therapy was a failure. He underwent allogeneic
hematopoietic stem cell transplantation (allo-HSCT) from a
human leucocyte antigen haploidentical donor after undergoing re-induction mitoxantrone, etoposide, and high-dose cytarabine chemotherapy. The conditioning regimen consisted
of fludarabine, busulfan, and melphalan without total body
irradiation. A total of 7.9×106/kg CD34+ cells were injected.
Graft-versus-host disease (GVHD) prophylaxes consisted of
PTCy (40 mg/kg on days +3 and +4), continuous infusion

of tacrolimus, and oral mycophenolate mofetil starting on
day +5. He had successful engraftment at day +15 and was
discharged at day +81 without acute GVHD. While he developed mild chronic GVHD of the skin at day +105, it was
resolved with topical steroids.
At day +233 after the stem cell transplant (SCT), he was
still in hematological full remission and had stopped immunosuppressive treatment. Magnetic resonance imaging
(MRI) screening 10 months after SCT showed no abnormalities. WT1 levels in peripheral blood were monitored
monthly and maintained below detection sensitivity.
At day +331, he presented to our hospital with acuteonset dysarthria that had started 3 days ago. On admission,
vital signs showed a blood pressure of 108/60 mmHg and a
pulse rate of 70 beats per minute. A neurological examination revealed mild dysarthria and a National Institutes of
Health Stroke Scale score of 1. No symptoms indicative of
brain tumor or meningitis, such as headache, nausea, and
meningeal irritation signs, were found. Laboratory data
showed a white blood cell count of 13.7×103/μL without
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DOI: 10.2169/internalmedicine.9774-22

Figure 2. Gadolinium-enhanced T1-weighted imaging before and after treatment. A ring-enhancing mass in the left putamen was visible on gadolinium-enhanced T1-weighted imaging performed
two weeks after admission (a, arrow). For four months after treatment, the putaminal mass decreased
in size (b).

Figure 3. Cytology of cerebrospinal fluid. Microscopy with Hematoxylin and Eosin staining of the
cerebrospinal fluid demonstrated infiltration of medium-to-large cells with a high nucleocytoplasmic
ratio. These immature cells had round-to-oval nuclei with blast-like chromatin and prominent nucleoli (a, ×200). Immunohistochemistry staining demonstrated that tumor cells were positive for myeloperoxidase, CD34 and terminal deoxymucleotidy1 transferase (b, c, d ×200).

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WT1 in PB
(copies/ʅgRNA)

DOI: 10.2169/internalmedicine.9774-22

Dysarthria

65
60
55
<50
Admission CSF cytology
Day 0

233

300

315

330

345

360

Discharge

PSL
375

390

405

420

435

450

Days aŌer SCT
TAC, MMF
AraC 40 mg, Dex 3.3 mg
RadiaƟon therapy

Figure 4. Clinical course of patient. The patient received allogeneic hematopoietic stem cell transplantation (day 0). On day 331, he was admitted with dysarthria, initially considered to be intracerebral hemorrhage. On day 353, the CSF cytology revealed atypical cells positive for a marker of myeloid origin cells. He was diagnosed with intracranial myeloid sarcoma relapse, and systemic
chemotherapy was started on day 359. After chemotherapy, he also received radiation therapy. On
day 444, he was discharged without any neurological deficits. AraC: cytarabine, CSF: cerebral spinal
fluid, Dex: dexamethasone, MMF: mycophenolate mofetil, PB: peripheral blood, SCT: stem cell
transplantation, TAC: tacrolimus

blast cells, hemoglobin level of 12.5 g/dL, platelet count of
229×103/μL, blood urea nitrogen level of 34.5 mg/dL, serum
creatinine level of 1.39 mg/dL, serum sodium level of 138
mEq/L, aspartate transaminase level of 28 U/L, alanine
transaminase level of 29 U/L, and lactic dehydrogenase level
of 260 U/L. The prothrombin time (PT) international normalized ratio was 1.15, and activated partial thromboplastine
time (APTT) was 26.5 s. WT1 levels in peripheral blood
were 61 copies/μgRNA. Brain non-contrast CT showed a
high-density area in the left putamen (Fig. 1a). He had multiple ICH risk factors, including hypertension requiring four
antihypertensive agents and use of direct oral anticoagulation for venous thromboembolism.
Under an initial diagnosis of spontaneous hypertensive
ICH, antihypertensive therapy was started, but the neurological deficit and follow-up CT showed unremarkable changes.
MRI performed after eight days of admission showed a lesion in the left putamen with isointensity on T1-weighted
imaging (WI), heterogeneous hyperintensity on T2WI
(Fig. 1b), and homogenous hyperintensity on diffusionweighted imaging with corresponding apparent diffusion coefficient hypointensity (Fig. 1c). Susceptibility-WI showed
slight hypointensity (Fig. 1d), which differed substantially
from the expected findings of a hemorrhagic lesion.
Gadolinium-enhanced MRI showed a mass with thick rim
enhancement (Fig. 2a).
We suspected that the lesion was most likely neoplastic,
e.g. post-transplant lymphoproliferative disorders or recurrence of AML, and performed a lumbar puncture. A CSF
examination revealed elevated protein (562 mg/dL) and cell
counts (2,249/μL). The CSF-to-serum glucose ratio de-

creased to 0.3. The CSF cytology was class V, and
hematoxylin-eosin staining showed infiltration of atypical
cells with a high nuclear-to-cytoplasmic ratio (Fig. 3a) that
were positive on immunohistochemical staining for myeloperoxidase and CD34, regarded as markers of myeloid origin
cells (Fig. 3b, c), as well as terminal deoxymucleotidy1
transferase (Fig. 3d). Morphologic findings were most consistent with undifferentiated blasts arising in the setting of
AML.
Based on the above findings, we diagnosed the patient
with CNS relapse of MS after allo-HSCT in AML. Wholebody CT was negative for de novo or recurrent tumors. A
bone marrow examination showed that complete hematological remission had been maintained. Other laboratory tests
were mostly normal. The patient was treated with systemic
cytarabine infusion and intrathecal injection of cytarabine
and dexamethasone. Four months after admission, he was
discharged without any neurological deficits and is currently
undergoing radiation therapy (Fig. 4). At day +444, followup MRI after treatment showed tumor shrinkage (Fig. 2b).

Discussion
Our case presented with acute neurological symptoms,
and CT showed a homogenous hyperdense lesion in the putamen one year after allo-HSCT for AML. We initially assumed acute ICH, which is frequently encountered in patients with hematological malignancies (15); however, MRI
revealed no hemorrhagic changes and instead indicated a
tumor-like lesion. CSF cytology ultimately led to a definite
diagnosis of intracranial MS.
4

5

Passarin
(Ref. 18)

Present
case

4

5

71/M

29/M

35/F

28/F

63/M

AML

Pineal
germinoma
and
testicular
cancer

AML

Renal
failure

AML

Primary
disease

AlloHSCT

Chemotherapy

Primary
MS

Extramedullary
relapse of
AML

Chemotherapy

Extramedullary
relapse of
AML

Extramed- Chemoullary
therapy
relapse of
AML
Primary
Renal
MS
transplantation

Onset

12

96

7

207

Dysarthria

Left
putamen

Drowsy,
Right basal
memory loss,
ganglia
paresthesia
and, ataxia
Drowsy, left Right basal
ganglia
hemiparesis,
left
homonymous
hemianopsia,
and right
conjugate eye
deviation
Headache
Right
frontal,
parietal
lobes, and
right
thalamus
Drowsy,
Right
headache
caudate
nucleus and
periventricular site

Site of
lesions

CT:
Hyperdensity
mass
MRI:
Gadolinium
enhancing mass

CT: No change
MRI:
Gadolinium
enhancing mass

Yes

No

CT:
Hyperdensity
mass
MRI: N/A

CT:
Hyperdensity
mass
MRI: N/A
CT:
Hyperdensity
mass
MRI: N/A

Imaging
findings

Yes

No

No

Multiple
lesions

N/A

Autopsy

Biopsy

Biopsy

N/A

N/A

Presence
of blast
cells (10/
μL)
N/A

CSF
findings

CD45+,
NASDCA+

MPO+

N/A

Negative

Death
(1)

NED (4)

CRT

Death
(12)

Death
(7)

NED
(86)

None

Radiation
therapy

None

CRT

Clinical
Pathological Treatment
outcome
findings
for MS
(weeks)

MPO+
Mildly
increased
proteins
and
absence of
atypical
cells
MPO+,
Positive Increased
proteins CD34, TdT
and
presence
of atypical
cells
(2,249/
μL).

N/A

N/A

Positive

HistologiCSF
cal
cytology
diagnosis

Diagnostic procedure

Allo-HSCT: allogeneic hematopoietic stem cell transplantation, AML: acute myeloid leukemia, CNS: central nervous system, CRT: chemoradiotherapy, MPO: myeloperoxidase, MS: myeloid sarcoma, NASDCA: naphtol AS-D
chloroacetate, NED: no evidence of disease, N/A: not available, TdT: terminal deoxymucleotidy1 transferase

Simpson
(Ref. 25)

Joselson
(Ref. 24)

2

3

Pippard
(Ref. 23)

1

Case
Age/
Reference
No
gender

Period
from
Treatdiagnosis
ment for
Clinical
of AML or
primary
presentations
other
disease
malignancy
(months)

Table. Clinical Features of the Thalamus and Basal Ganglia Myeloid Sarcoma Instances That have been Reported.

Intern Med Advance Publication
DOI: 10.2169/internalmedicine.9774-22

Intern Med Advance Publication

DOI: 10.2169/internalmedicine.9774-22

MS, also called granulocytic sarcoma or chloroma, is a
rare solid extramedullary tumor made up of myeloblasts.
Clinical symptoms depend on its occurrence site, and nearly
half of MS patients are asymptomatic (16). Thus, a previous
cross-sectional imaging study reported that 24.5% of cases
were incidentally discovered (17).
MS on non-contrast intracranial CT typically presents as a
homogenously hyperdense mass (5) and can thus be mistaken for a subdural hematoma (7, 8), ICH (18), meningioma, or even an abscess (19). It can be challenging to
differentiate between MS and these diseases when patients
with hematologic diseases present with acute neurological
symptoms. MRI can provide useful information for distinguishing these disease lesions. For example, Intracranial MS
shows an isointense mass on T1WI and hyperintense mass
on T2WI with restricted diffusion and without susceptibility
artifacts on MRI (5). However, the time, cost, patient tolerance, clinical status, and MRI availability may preclude
emergent MRI (20) in the acute stroke setting, which is why
CT is recognized as the “gold standard”. We did not perform emergent MRI in the present case, but our patient had
an AML history and did not show any lesion expansion despite receiving anti-thrombotic therapy (21). We should have
considered a differential diagnosis including MS.
Spontaneous hypertensive ICH occurs most frequently in
the basal ganglia (caudate nucleus/putamen/globus pallidus/
subthalamic nucleus/substantia nigra) and thalamus (22). Although uncommon, certain cases of intracranial MS have
been described in these locations (Table) (17, 23-27). Three
cases, including our own, had an AML history, one received
a renal transplant, and another had received chemotherapy
for solid cancer. None of the cases presented with hematological relapse at the time of the initial evaluation. All cases
were evaluated by CT; four showed a homogeneously hyperdense mass, and one (Case No. 4) had no changes and was
undetectable on CT. MRI findings in that case included gadolinium enhancement, similar to our own patient. CSF cytology was performed in three patients, including our case, and
two had documented neoplastic cells. There have been few
reports on the association between intracranial MS and CSF
cytology, but in a small case series, four of five cases
showed blast presence (28). Since a brain biopsy is not possible for some lesion sites, CSF cytology may be an alternative evaluation in cases of suspected intracranial MS.
A young age, male gender, and certain biological statuses,
such as AML subtype, cytogenetic or chromosomal abnormalities, CD56, and/or T-cell markers, have previously been
described as risk factors for the development of extramedullary recurrence after allo-HSCT (29-32). Disease status such
as a history of extramedullary lesion, relapse or refractory
disease at the time of SCT, and hyperleukocytosis at diagnosis were also related to a high incidence of extramedullary
relapse (29-31, 33, 34). Several risk variables for extramedullary relapse, including male gender and refractory disease
status at the time of SCT, were present in this instance.
Our case presented with leukemic cells in the CSF, but a

bone marrow examination showed no leukemic involvement,
meaning that isolated CNS relapse of AML occurred following allo-HSCT. CNS relapse without bone marrow leukemia
is uncommon, with an incidence of about 2% after alloHSCT (35, 36). Isolated extramedullary MS after allo-HSCT
occurred in 9 of 19 (47.4%) cases in a previous MS case series study, while 5 (26.3%) had concurrent bone marrow relapse at the onset of MS, and 3 (15.8%) progressed to bone
marrow involvement within 2 years after the MS onset (37).
Even in rare cases, if left untreated, it is thought to proceed
quickly to systemic recurrence, with a terrible prognosis (38). Although there is no recognized surveillance technique, early identification and systemic treatment are related
to an improved survival (12, 13). Radiological studies are
not routinely done as a regular follow-up for patients after
SCT. Several studies on extramedullary relapse after alloHSCT have shown the utility of monitoring WT1 levels in
peripheral blood (39, 40); however, our patient had low WT
1 levels before and after the relapse. It should be emphasized that in cases where WT1 levels are relatively low from
the outset, WT1 levels may not be beneficial in checking for
relapses, both within and outside the marrow. Importantly,
for patients presenting with neurological impairments that
do not rule out intracranial MS, CSF cytology and MRI
should be conducted.
The pathophysiology of MS in the brain parenchyma is
unknown due to its rarity. Diapedesis across endothelium or
direct entry with petechial hemorrhaging can allow the migration of leukemic cells into the brain. The perivascular
clustering of leukemic blasts on biopsy samples lends
weight to this idea (25). In the present case, vascular risk
factors, including long-standing hypertension, caused endothelial damage in the deep area, which may have led to the
development of MS.
In conclusion, we report the case of a man with intracranial MS relapse following allo-HSCT whose findings closely
resembled those of ICH. Although deep cerebral MS is relatively rare, the rigorous distinction should be conducted,
even in elderly patients with hematologic disorders. MRI
and CSF studies may help diagnose MS.
The authors state that they have no Conflict of Interest (COI).
Acknowledgement
We wish to thank the patient and his family for their cooperation regarding this report. We obtained written informed consent
for this publication. We thank Enago (https://www.enago.jp/) for
the English language review of this manuscript.
Funding: This case report did not receive any specific grant
from funding agencies in the public, commercial, or not-forprofit sectors.

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