Case Report
Nonpulsatile Cerebral Perfusion in Patient With Acute
Neurological Deficits
Yo Sik Kim, MD; Oleg Y. Chernyshev, MD, PhD; Andrei V. Alexandrov, MD
Background and Purpose—An extremely low pulsatile cerebral perfusion can result in a massive cerebral infarction and
poor outcome. We report a patient who had complete recovery from initial neurological deficits in spite of nonpulsatile
perfusion in the middle cerebral artery.
Methods—We used carotid duplex and transcranial Doppler to evaluate cerebral hemodynamics and the National Institutes
of Health Stroke Scale (NIHSS) to score the neurological deficits.
Results—A 62-year-old man had a sudden chest pain and right hemispheric symptoms with NIHSS score of 18 on arrival.
Carotid duplex showed no blood flow in the right common carotid artery. Transcranial Doppler showed a nonpulsatile
waveform with slow antegrade flow in right middle cerebral artery. Chest CT angiography revealed type A aortic
dissection. After surgical repair for the aortic dissection with brain retroperfusion, the patient had dramatic recovery
from the initial neurological deficit, and normal pulsatile cerebral perfusion in the right carotid territory.
Conclusions—Nonpulsatile cerebral perfusion points to a proximal source of arterial flow obstruction that may necessitate
interventional treatment or surgery in order to restore brain perfusion and potentially reverse impending stroke. (Stroke.
2006;37:1562-1564.)
Key Words: acute stroke 䡲 ischemia 䡲 nonpulsatile

C

erebral arterial blood flow has pulsatile pattern except
for during cardiopulmonary bypass when direct heart
contractions are replaced with continuous pump-induced
flow. The pulsatility of cerebral perfusion is decreased when
an arterial occlusion is present in a proximal segment and
compensatory dilatation is induced in the distal vascular bed.
Extremely low pulsatile cerebral perfusion was noted in
patients with acute proximal internal carotid artery occlusion
and impending infarctions1,2 because it can lead to profound
hypoperfusion, ischemia and poor clinical outcome.
We would like to present a patient who achieved complete
recovery from a severe initial neurological deficit after
surgical correction of the nonpulsatile cerebral perfusion in
the middle cerebral artery (MCA).

Case Reports
A 60-year-old man was admitted after acute onset of the
left-sided hemiparesis. He also had sudden chest pain and
shortness of breath. He collapsed in his bathroom, and then
was unable to move his left extremities. He had history of
hypertension, myocardial infarction and cocaine abuse. He
arrived at hospital within 1 hour after onset. His blood
pressure was 110/80 mm Hg in the left arm. Arterial pulsation
was good in the left radial artery, but it was not measured in
the right side.

On examination, he had left hemiparesis, left facial palsy,
dysarthria, gaze preference to the right side, and left homonymous hemianopsia. The initial National Institutes of Health
Stroke Scale (NIHSS) score was 18 points.
Transcranial Doppler (TCD; PMD 100 Spencer Technologies) revealed a nonpulsatile flow in the right MCA at depth
range 40 to 65 mm with the mean flow velocities of 25
cm/second. The right anterior cerebral artery (ACA) showed
retrograde flow direction indicating the left-to-right anterior
cross-filling (Figure 1). The left ACA showed a normal
antegrade flow direction. Posterior communicating arteries
were not identified on both sides. The right vertebral artery
showed alternating flow with retrograde systolic flow and
antegrade diastolic flow suggesting a severe occlusive disorder proximal to its origin (Figure 1). Carotid duplex
(Sonosite, Bothell) with power mode did not show any flow
in the right common carotid artery (CCA). B-mode showed
echogenicity in the right CCA suggesting thrombus within
the lumen (Figure 1). Spectral Doppler showed a mid-systolic
velocity deceleration in the left CCA and left MCA. Such
deceleration could be caused by a narrowing of the aortic
lumen attributable to dissection creating transient suction
(Ventury) effect at the origin of the left CCA, which in turn
produces mid-systolic retraction in Doppler waveform of left

Received February 15, 2006; accepted March 8, 2006.
From the Department of Neurology (Y.S.K.), Wonkwang University School of Medicine, Jeonbuk, Korea; the Department of Neurology (O.Y.C.),
University of Texas Medical School at Houston, Houston, Texas, USA; and the Neurosonology and Stroke Research Program (A.V.A.), Barrow
Neurological Institute, Phoenix, Arizona, USA.
Correspondence to Yo Sik Kim, MD, Department of Neurology, Wonkwang University Hospital, 344-2 Shinyong-Dong, Iksan, Jeonbuk, South Korea,
570-711. E-mail yosik@wonkwang.ac.kr
© 2006 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org

DOI: 10.1161/01.STR.0000222938.84036.40

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Nonpulsatile Cerebral Perfusion

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Figure 1. Carotid duplex and TCD findings. TCD shows nonpulsatile flow in right MCA from depth of 60 mm to 40 mm (A and B) and
retrograde flow in right ACA (arrow in B). Left ACA shows normal direction and pulsatility (C). Left MCA shows mid-systolic flow deceleration (D). Right vertebral artery shows alternating flow with retrograde systolic flow and antegrade diastolic flow (E). Proximal basilar
artery shows antegrade flow (F). Duplex sonography shows echogenicity without flow signal in right CCA in power mode (H) and Doppler sonography (G). Left CCA shows mid-systolic flow deceleration in Doppler sonography (I and J).

CCA and MCA.3 Based on ultrasound findings, CT angiography of the chest was performed. It showed type A aortic
dissection involving the ascending aorta, the origins of the
left CCA and right innominate arteries (Figure 2). The right

CCA and proximal subclavian artery were not visualized,
whereas the distal subclavian and right vertebral arteries were
present (Figure 2). His noncontrast brain CT scan was
normal.

Figure 2. Brain CT at 3 days after onset shows subcortical infarction in right frontal lobe (arrow in A). Chest CT angiography shows
type A aortic dissection involving ascending aorta (arrow in E) and the origins of right innominate artery and left CCA (arrow in C and
D). CT angiography shows distal segment of right subclavian artery, left subclavian artery (curved arrow in C and D), and right and left
vertebral artery (arrow in B), whereas the right CCA and proximal subclavian arteries were not visualized.

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Stroke

June 2006

The patient was transferred to cardiothoracic surgery, and
at 3 hours after symptom onset an urgent surgical repair for
the aortic dissection was initiated. Dissected ascending aorta
and aortic arch were replaced with an artificial graft. Left
CCA and right innominate artery were cleared of intimal
flaps. Surgery was performed with extracorporeal perfusion
pump, hypothermic isoelectric cardiac arrest, brain retroperfusion, and continuous TCD monitoring using previously
published methods.4
Follow-up brain CT scan showed subcortical infarctions
including right frontal lobe at 3 days after onset. It could be a
watershed infarction between right MCA and ACA (Figure 2).
The patient’s neurological deficit improved markedly within 2
days after surgery by ⬎12 NIHSS points, and he was subsequently sent home without any neurological deficit.

Discussion
The clinical significance of a nonpulsatile cerebral perfusion is
not well understood yet. Our case illustrates that a nonpulsatile
cerebral perfusion during acute cerebral dysfunction indicates a
proximal arterial occlusion, should prompt a thorough vascular
imaging, and may require an urgent intervention to open the
proximal occlusion. Timely repair may lead to good clinical
outcomes if cerebral perfusion is restored on time.
Pulsatility of cerebral perfusion is determined by the
pulsatile energy of blood column delivered during the cardiac
cycle to the cerebral vascular bed and by the degree of
compensatory dilatation of distal vessels.2 With an internal
carotid artery (ICA) occlusion, the MCA blood flow was
usually maintained through long narrow collateral channels
such as communicating arteries. These long narrow collateral
channels may prevent the transmission of pulsatile energy to
the MCA, leading to a delay in the systolic flow acceleration.
This may appear as a blunted signal on TCD.5
A proximal arterial occlusion causes compensatory dilatation of the distal vascular bed because it decreases vascular
resistance and creates a pressure gradient for collateral flow.
Patients with an ICA occlusion may show exhausted vasomotor reactivity, suggesting full dilatation of intracranial
vessels. If the collateral circulation is insufficient and takes a
long circuit to reach dilated MCA branches, the systolic
acceleration and velocity decrease further, and systolic velocity becomes nearly equal to the diastolic flow. These mech-

anisms contribute to the appearance of a nonpulsatile MCA
perfusion.
Nonpulsatile perfusion may be caused by several mechanisms, including prevention of transmission of pulsatile
energy, compensatory arterial dilatation distal to the occlusion, and insufficient collateral circulation. Therefore, nonpulsatile cerebral perfusion may be a sign of an exhausted
cerebral vascular reserve capacity.6
In a chronic ICA occlusion, nonpulsatile perfusion was not
associated with any cerebral dysfunction and returned to
normal pulsatile perfusion after removal of the proximal
occlusion.6 However, extremely low pulsatile perfusion in
acute ICA occlusion was associated with massive cerebral
infarction and poor outcomes.2 So, nonpulsatile cerebral
perfusion associated with acute cerebral dysfunction can be a
sign of impending irreversible cerebral ischemic injury unless
the offending lesion is corrected.
Our case illustrates that nonpulsatile cerebral perfusion
coupled with bilateral abnormal flow findings in an acute
stroke patient should make a clinician think about possible
aortic dissection. It also suggests poor collateral circulation
and may require an urgent intervention to repair the aortic
dissection.

Acknowledgments
Yosik Kim was supported by Wonkwang University in 2006.

References
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3. Kallman CE, Gosink BB, Gardner DJ. Carotid Duplex sonography: bisferious pulse contour in patients with aortic valvular disease. AJR. 1991;
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4. Estrera AL, Garami Z, Miller CC, Sheinbaum R, Huynh TTT, Porat EE,
Winnerkvist A, Safi HJ. Determination of cerebral blood flow dynamics
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Ann Thorrac Surg. 2003;76:704 –710.
5. Alexandrov AV, Neumyer M. Diagnostic criteria for cerebrovascular
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Prevention and Treatment. New York, NY: Futura: Blackwell. 2004;
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6. Lee YS, Yoon BW, Roh JK. Nonpulsatile cerebral perfusion in Takayasu’s
Arteritis. J Neuroimaging. 2003;13:169 –171.

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Nonpulsatile Cerebral Perfusion in Patient With Acute Neurological Deficits
Yo Sik Kim, Oleg Y. Chernyshev and Andrei V. Alexandrov
Stroke. 2006;37:1562-1564; originally published online May 4, 2006;
doi: 10.1161/01.STR.0000222938.84036.40
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2006 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628

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