Case Report

Recurrent Transient Neurological Deficit Due to Intracerebral
Steal Phenomenon in Association with a Developmental Venous
Anomaly
Jean Hee Kim, MD,a Hyeyoung Jung, MD,a Woojun Kim, MD, PhD,a and
Jae Young An, MD, PhDb

We report a symptomatic developmental venous anomaly (DVA) not causing parenchymal abnormality to provide a pathophysiologic clue in patients with recurrent
transient neurologic deficit. A 32-year-old male presented with recurrent transient
motor aphasia and headache in the left fronto-temporal region for three years. The
symptoms usually lasted for one hour. Brain computed tomography (CT) angiography and magnetic resonance imaging using gradient recalled echo showed a prominent penetrating vein at the left frontal periventricular region. Brain CT perfusion
imaging performed during the symptoms revealed increased perfusion in the corresponding area with relatively decreased perfusion in the left fronto-temporal cortices.
Digital subtraction angiography revealed collecting venous blood from the left septal
and thalamostriate veins draining into the left cavernous sinus without early arteriovenous shunting. In this patient, an inciting incident might have led to imbalance of
the venous flow surrounding the DVA, causing venous hypertension and the intracerebral steal phenomenon in the surrounding area. The relatively hypoperfused cortical area adjacent to the DVA could be considered the cause of the transient motor
aphasia, while venous hypertension could be the cause of the headache.
Key Words: Developmental venous anomaly—Transient ischemic attack—
Intracerebral steal phenomenon—Asymptomatic vascular malformation
© 2021 Elsevier Inc. All rights reserved.

Introduction
Developmental venous anomaly (DVA) is a form of
intracranial vascular malformation with an incidence of
2.6% in a brain autopsy study.1,2 Usually presenting as a
benign form draining normal brain parenchyma, DVA

rarely requires surgical intervention, unless it is
symptomatic.1,2
We present a symptomatic DVA not causing parenchymal abnormality to provide a pathophysiologic clue for
patients with recurrent transient neurologic deficit.

Case report
From the aDepartment of Neurology, Seoul St. Mary's Hospital,
College of Medicine, The Catholic University of Korea, Republic of
Korea; and bDepartment of Neurology, St. Vincent’s Hospital, College
of Medicine, The Catholic University of Korea, 93, Jungbu-daero, Paldal-gu, Suwon-si, Gyeonggi-do, Republic of Korea.
Received June 15, 2021; revision received August 5, 2021; accepted
August 9, 2021.
Grant support: There is no grant supported for this case report.
Corresponding author. E-mail: nrjyan@gmail.com.
1052-3057/$ - see front matter
© 2021 Elsevier Inc. All rights reserved.
https://doi.org/10.1016/j.jstrokecerebrovasdis.2021.106058

A 32-year-old non-smoking male with no underlying medical history presented with recurrent transient motor aphasia
and throbbing headache in the left fronto-temporal region for
three years. The symptoms usually lasted for one hour. Upon
admission, no focal neurologic deficit was found.
Brain computed tomography (CT) angiography (Fig. 1A)
and magnetic resonance imaging using gradient recalled
echo (Fig. 1B) showed a prominent penetrating vein at the
left frontal periventricular region. Brain CT perfusion imaging
(Fig. 1C) performed in the presence of the symptoms revealed

Journal of Stroke and Cerebrovascular Diseases, Vol. 30, No. 11 (November), 2021: 106058

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J.H. KIM ET AL.

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Fig. 1. Computed tomography (CT) angiography (A) and magnetic resonance imaging using gradient recalled echo (B) show developmental venous anomaly
(arrows). CT perfusion images (C) reveal increased cerebral blood volume and cerebral blood flow in the left frontal area but relatively decreased flow in the left
fronto-temporal cortices, also observed as hypoperfusion in brain single-photon emission computed tomography (D). Digital subtraction angiography (E) presents
a venous anomaly draining from the left septal vein (hollow arrow) and thalamostriate vein (white arrow) to the cavernous sinus (arrow head).

increased perfusion in the corresponding area with relatively
decreased perfusion in the left fronto-temporal cortices, which
also was found on brain single-photon emission computed
tomography (Fig. 1D). Digital subtraction angiography
(Fig. 1E) revealed collecting venous blood from the left septal
and thalamostriate veins draining into the left cavernous
sinus without early arteriovenous shunting. Further treatment is being withheld as the patient has since remained
asymptomatic.

Discussion
The following possible pathomechanisms of symptomatic DVA have been proposed: (i) mechanical compression
of the cerebrospinal fluid from a dilated collecting vein;
(ii) increased/decreased outflow causing venous hypertension or thrombosis; and (iii) idiopathic.3
In the deep cerebral venous system, the thalamostriate,
septal, and choroid veins are the tributary veins draining
into the intracerebral vein.1,4 In the present case, the left
septal and thalamostriate veins drained into the left cavernous sinus instead of the intracerebral vein, and an
inciting incident might have led to imbalance of the
venous flow surrounding the DVA, causing venous
hypertension and the intracerebral steal phenomenon in
the surrounding area.1,5 The cortical area adjacent to the
DVA, which was relatively hypoperfused, could be considered as the cause of the transient motor aphasia. The

throbbing headache in the left fronto-temporal region
could have been brought from the venous hypertension
induced by the imbalance of the drain system. The headache has been differentiated from the complicated
migraine from his previous history without migraine
and relatively increased perfusion in the area of the
venous hypertension instead of hypoperfusion induced
by a vasoconstriction followed by downstream ischemia
in the complicated migraine.6
Symptomatic DVA, consisting 1% of patients of DVA
detected, is usually presented in different ways, such
as ischemic infarction, hemorrhage, headache, ataxia,
or seizure.7,9,10 Only two cases of transient neurologic
deficit without parenchymal involvement associated
with DVA have been reported, which is extremely
rare, even considering the rarity found in the symptomatic DVA itself presented as hemorrhage in studies
ranges from 0.22 to 0.68%.7 9 An intracerebral steal
phenomenon associated with an intracranial DVA
should be considered in patients with recurrent transient ischemic attacks.

CRediT authorship contribution statement
Hyeyoung Jung: Data curation, Formal analysis, Investigation. Jae Young An: Conceptualization, Project
administration, Investigation, Supervision, Validation,
Writing - review editing.

INTRACEREBRAL STEAL PHENOMENON

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