Endovascular embolectomy of acute
basilar artery occlusion
W. Yu, MD, PhD; D. Binder, MD, PhD; A. Foster-Barber, MD, PhD; R. Malek, MD; W.S. Smith, MD, PhD;
and R.T. Higashida, MD

Abstract—Acute basilar artery occlusion has a mortality rate approaching 90%. The authors describe a case of acute
basilar artery occlusion managed successfully with endovascular embolectomy. A 31-year-old man sought treatment for
confusion, dysarthria, and right-sided weakness. He soon became unresponsive and was found to have a vertebral artery
dissection and an associated basilar artery embolism. The dissection was managed with endovascular stenting, and the
basilar artery embolus was removed with a clot retriever at 7 hours. The patient recovered without neurologic deficit.
NEUROLOGY 2003;61:1421–1423

Acute basilar artery occlusion is a life-threatening
event with mortality rates of 75 to 91%.1,2 Patients
who survive rarely regain functional independence
and are at risk for recurrent strokes.1,3 In a case
report, some patients were noted to have a benign
outcome if they had short segment basilar artery
occlusion of atherothrombotic origin and adequate
collateral supply.4 Although anticoagulation has
been used for decades as the therapy of the choice,
the mortality rate of acute basilar artery occlusion
was 88% with heparin therapy.3 Recently, a number
of thrombolytic agents have been investigated for the
management of acute basilar artery occlusion. Despite good recanalization rate with aggressive intraarterial (IA) thrombolysis, the mortality rate in most
case series has remained 65 to 75%.2,5,6 Therefore, it
is imperative to develop more effective therapy for
this devastating condition. In this report, we describe a case of vertebral artery dissection and associated acute basilar artery occlusion and the
successful endovascular therapy of both lesions.
Case report. The patient was a healthy 31-year-old Asian man
without previous illness. He was struck on his face with head
twisting sideways during a football game. He was dazed and had
brief episodes of confusion. His neurologic examination and CT of
the head at a local hospital were reported as normal. A few hours
later, he developed “seizure-like activity” and was sent to a
trauma center for further evaluation. On arrival, he was noted to
have dysarthria and right-sided weakness. A repeat CT showed a
hyperdense basilar artery on two consecutive 5-mm cut images,
indicative of acute basilar artery embolism. He soon became incoherent and unresponsive with marked vertical nystagmus. Neither systemic anticoagulation nor IV thrombolytic therapy was
initiated because of a preliminary report of possible subarachnoid
hemorrhage. After intubation for airway protection, he was emergently transferred to the University of California, San Francisco 4
hours after symptom onset. Family consent was obtained for endovascular therapy after full discussion of the benefit and risks of

such therapy under an approved Food and Drug Administration
(FDA) protocol for use of an experimental clot-retrieval device for
acute cerebrovascular emboli. After an IV bolus of 2,000 U heparin, diagnostic angiography of the right vertebral artery demonstrated complete occlusion with an abrupt cutoff at the
midcervical portion of the vertebral artery at C4-C5 (figure 1, A
and B). The obstruction was gently traversed with a UCSF-2
catheter over a Bentson guidewire (Cook Incorporated, Bloomington, IN), and an injection of contrast medium confirmed the patency of the distal right vertebral artery above the dissection site.
IV abciximab was initiated with a bolus injection of 0.25 mg/kg
followed by an infusion of 0.125 ␮g/kg/min for 12 hours. A 6- ⫻
40-mm Magic Wall Stent (Boston Scientific, Natick, MA) was then
placed across the area of the dissection site with excellent restoration of blood flow (figure 1, C and D) at approximately 6 hours
after symptom onset. Angiography of the now patent right vertebral artery demonstrated a large embolus in the distal basilar
artery occluding both superior cerebellar arteries (SCAs) and the
right posterior cerebral artery (PCA) (figure 2A). An initial attempt at embolectomy was made with the Neuronet (Guidant
Corporation, Santa Clara, CA) to capture the embolus in the distal
basilar artery but was unsuccessful. The Concentric Retriever
(Concentric Medical, Mountain View, CA) was then used for clot
removal. The device was advanced through a 7-French guide catheter in the right vertebral artery, and the tip was placed in the
right PCA across the embolus over an Agility 0.014-inch microguidewire (Cordis Neurovascular, Miami, Florida) (figure 2B). The
clot was captured with the helical coils of the device (figure 2C)
and pulled back into the 7-French guide catheter. It was then
removed in toto from the guide catheter through the femoral artery sheath at 7 hours after stroke onset. The embolus recovered
from embolectomy measured 5 ⫻ 25 mm (figure 2D). Follow-up
angiography demonstrated complete recanalization of the basilar
artery with full restoration of blood flow to both SCAs and the
right PCA (figure 2E). The patient regained complete consciousness after the stent and embolectomy and was extubated with
only mild residual nystagmus and left-sided dysmetria for a few
hours. A follow-up brain MRI showed only a small infarction in
the left cerebellum and no infarct in the brainstem (figure 3). The
patient was discharged home with aspirin and clopidogrel 2 days
after the procedure. Two months later, he complained of episodes
of lightheadedness and was found to have a high-grade stenosis at
the proximal segment within the stent in the right vertebral artery. The stenosis was managed with balloon angioplasty without

From the Departments of Neurology (Drs. Yu, Foster-Barber, and Smith), Neurosurgery (Dr. Binder), and Neurointerventional Radiology (Drs. Malek and
Higashida), University of California, San Francisco, CA.
Supported as part of the MERCI Clinical Investigation by Concentric Medical, Mountain View, CA. W.S.S. had stock ownership of the company. None of the
other authors received financial support or compensation from the corporate sponsor.
Received September 3, 2003. Accepted in final form September 22, 2003.
Address correspondence and reprint requests to Dr. Wengui Yu, Neurovascular Service, University of California, San Francisco, 505 Parnassus Avenue, Box
0114, San Francisco, CA 94143; e-mail: wyu6228@itsa.ucsf.edu, or Dr. Randall T. Higashida, Division of Neurointerventional Radiology, University of
California, San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143; e-mail: Randall.Higashida@radiology.ucsf.edu
Copyright © 2003 by AAN Enterprises, Inc.

1421

Figure 1. Diagnostic angiography of right vertebral artery showed complete occlusion with an abrupt cutoff at
the midcervical portion of the vertebral artery at C4-C5
level (A, B). After mechanical recanalization and abciximab infusion, the right vertebral dissection was visualized (C) and stented (D).

complication. He has returned to work and remained neurologically intact 9 months after embolectomy.

Discussion. Until recently, anticoagulation with
IV heparin was the therapy of choice for acute basilar artery occlusion based on anecdotal reports. However, in a retrospective study of 25 patients who had
acute basilar artery occlusion requiring mechanical
ventilation, the mortality rate was 88% despite anticoagulant therapy.3 Three patients survived with a
locked-in syndrome without further neurologic improvement. Therefore, the therapy is of little benefit.
Recently, thrombolytic agents, including urokinase,
streptokinase, and tissue plasminogen activator
(tPA), have been administered either IV or IA for
acute basilar artery occlusion. Although recanalization rates have approached 44 to 83%, the mortality
rate has remained 65 to 75% because of rethrombosis, hemorrhagic complications, and irreversibility of
the stroke itself.2,5-7 Of note, patients with distal
basilar artery occlusion and adequate collateral circulation tended to have a lower mortality rate of
approximately 50% with IA thrombolysis.6 However,
the overall good outcome with no or mild deficit was
only 20 to 25%.6,7
Stenting of dissected extracranial arteries has been
reported. However, mechanical removal of emboli from
intracranial arteries has only been described in three
case reports. Microsnares have been used to retrieve
foreign bodies, such as detachable coils and catheter
fragments, in the circulation. Such a device was first
used successfully to retrieve an embolus from the mid1422

NEUROLOGY 61

November (2 of 2) 2003

Figure 2. Angiography of the stented right vertebral artery demonstrated a large embolus occluding both superior
cerebellar arteries (SCAs) and right posterior cerebral artery (PCA) (A). The clot was captured by the soft helical
coils of the Concentric Retriever and removed in toto from
the guide catheter through the femoral artery sheath (B,
C). The embolus recovered measured 5 ⫻ 25 mm (D). Repeat angiography demonstrated complete recanalization of
the distal basilar artery with full restoration of blood flow
to both SCAs and the right PCA (E).

dle cerebral artery in one patient with an acute stroke.8
Subsequently, there are two reports of successful retrieval of clots from the basilar artery using the snare
and Neuronet.9,10 In one of these reports, five patients
with basilar artery occlusion underwent mechanical removal of an embolus using the Neuronet.9 The device
failed to retrieve clots in the initial two patients but
succeeded in the subsequent three patients with flow
reversal by temporarily occluding the vertebral artery.
In this report, we initially attempted embolectomy
with the Neuronet but were unable to capture the embolus with this device. However, the embolus was suc-

Figure 3. Diffusion-weighted MRI at day 2 after embolectomy showed a small cerebellar infarction (A) and no infarct in the brainstem (B).

cessfully captured with the Concentric Retriever and
pulled back into the guide catheter without using flow
reversal as described.9 The patient recovered quickly
without neurologic deficit and remains healthy 9
months after the procedure.
Compared with thrombolytic therapy, endovascular embolectomy theoretically has a lower risk of
hemorrhagic complications and can be used in patients with contraindications for thrombolytic therapy. Per FDA-approved protocol, patients evaluated
within 8 hours of symptom onset are eligible for the
clinic trial of embolectomy. It must be noted that
experienced neurointerventional specialists may currently perform this procedure at 25 investigational
sites in the United States. Although large randomized controlled studies are required to evaluate the
safety and effectiveness of various clot-retrieval devices, our report corroborates previous reports9,10 and
indicates that endovascular embolectomy may be a
promising therapy for life-threatening basilar artery
occlusion and other types of strokes.

References
1. Archer CR, Horenstein S. Basilar artery occlusion: clinical and radiographic correlation. Stroke 1977;8:383–391.
2. Hacke W, Zeumer H, Ferbert A, Bruckmann H, del Zoppo GJ. Intraarterial thrombolytic therapy improves outcome in patients with acute
vertebrobasilar disease. Stroke 1988;19:1216 –1222.
3. Wijdicks EFM, Scott JP. Outcome in patients with acute basilar artery
occlusion requiring mechanical ventilation. Stroke 1996;27:1301–1303.
4. Caplan LR. Occlusion of the vertebral or basilar artery: follow-up analysis of some patients with benign outcome. Stroke 1979;10:277–282.
5. Becker KJ, Monsein LH, Ulatowski J, Mirski M, Williams M, Hanley
DF. Intraarterial thrombolysis in vertebrobasilar occlusion. AJNR Am J
Neuroradiol 1996;17:255–262.
6. Brandt T, von Kummer R, Muller-Kuppers M, Hacke W. Thrombolytic
therapy of acute basilar artery occlusion. Stroke 1996;27:875– 881.
7. Cross DT, Moran CJ, Akins PT, Angtuaco EE, Derdeyn CP, Diringer
MN. Collateral circulation and outcome after basilar artery thrombolysis. AJNR Am J Neuroradiol 1998;19:1557–1563.
8. Chopko BK, Kerber C, Wong W, Georgy B. Transcatheter snare removal
of acute middle cerebral artery thromboembolism: technical case report.
Neurosurgery 2000;46:1529 –1531.
9. Mayer TE, Hamann GF, Brueckmann H. Treatment of basilar artery
embolism with mechanical extraction device: necessity of flow reversal.
Stroke 2002;33:2232–2235.
10. Wikholm G. Transarterial embolectomy in acute stroke. AJNR Am J
Neuroradiol 2003;24:892– 894.

Compound heterozygous PANK2
mutations confirm HARP and
Hallervorden-Spatz syndromes are allelic
H. Houlden, MD, MRCP; S. Lincoln, BSc; M. Farrer, PhD; P.G. Cleland, FRCP; J. Hardy, PhD; and
R.W. Orrell, MD, FRCP

Abstract—The authors describe a patient with hypoprebetalipoproteinemia, acanthocytosis, retinitis pigmentosa, and
pallidal degeneration (HARP) who has two compound heterozygote mutations of the PANK2 gene. IVS4 –1 G⬎T segregates with the lipid and erythrocyte changes in the mother and sister. No other family members have the lipid,
erythrocyte, or clinical abnormalities. The father and two brothers are heterozygous for Met327Thr. One other mutation
has been found in this PANK2 region associated with the HARP phenotype, suggesting a local genotype effect.
NEUROLOGY 2003;61:1423–1426

Hypoprebetalipoproteinemia, acanthocytosis, retinitis pigmentosa, and pallidal degeneration (HARP;
OMIM 200150) syndrome1,2 is a rare disorder that
shares many common clinical features with
Hallervorden-Spatz syndrome (HSS), also termed
neurodegeneration with brain iron accumulation 1
(NBIA1). HSS is characterized by early onset dystonia, spasticity, and dementia. Rare clinical features
include pigmentary retinopathy, choreoathetosis, ri-

gidity, seizures, and optic atrophy.3,4 Neuropathologically, HSS is characterized by bilateral degeneration
of the globus pallidus and substantia nigra pars reticulata with deposition of iron in the affected regions and more widely distributed neuronal axonal
spheroids.5,6 Lewy bodies and alpha-synuclein immunoreactivity have also been identified in HSS, suggesting a link with other neurodegenerative
disorders such as Parkinson disease and multiple

From the Department of Neurology (Drs. Houlden and Orrell), Royal Free Hospital, London; Department of Neuroscience (S. Lincoln and Dr. Farrer), Mayo
Clinic Jacksonville, FL; Department of Neurology (Dr. Cleland), Newcastle General Hospital, Newcastle-upon-Tyne, UK; Department of Neuroscience (Dr.
Hardy), NIH, Bethesda, MD; and University Department of Clinical Neurosciences (Dr. Orrell), Royal Free and University College Medical School,
University College London, UK.
Supported by the Wellcome Trust. H.H. was recipient of a Bogue Research fellowship.
Received March 27, 2003. Accepted in final form June 13, 2003.
Address correspondence and reprint requests to Dr. Richard W. Orrell, University Department of Clinical Neurosciences, Royal Free and University College
Medical School (Royal Free Campus), Rowland Hill Street, London NW3 2PF, England; e-mail: r.orrell@rfc.ucl.ac.uk
Copyright © 2003 by AAN Enterprises, Inc.

1423

Endovascular embolectomy of acute basilar artery occlusion
W. Yu, D. Binder, A. Foster-Barber, et al.
Neurology 2003;61;1421-1423
DOI 10.1212/WNL.61.10.1421
This information is current as of November 24, 2003
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