Clinical Neurology and Neurosurgery 108 (2005) 93–96

Case report

Concurrent cerebral and axillary artery occlusion: a possible source
of cerebral embolization from peripheral artery thrombosis
Wei-Hsi Chen, Shun-Sheng Chen, Jia-Shou Liu∗
Stroke Biology Research Laboratory, Department of Neurology, Chang Gung Memorial Hospital, 123 Ta Pei Road,
Niao Sung Hsiang, Kaohsiung 833, Taiwan
Received 6 February 2004; received in revised form 2 November 2004; accepted 26 November 2004

Abstract
Intracranial embolization usually arises from heart, precerebral artery or aorta but rarely the peripheral artery as retrograde upstream
of embolus should be overcome. We encountered a woman who experienced a transient right acronumbness followed by a sudden onset
of left hemiplegia and conscious change concurrently. Cranial computerized tomography revealed a hemorrhagic infarct at right lentiform
nucleus. Angiography disclosed right axillary artery occlusion at the proximal portion without collateral circulation. Cardioaortic survey and
coagulation profile were normal. Thrombectomy was done and radial flow was corrected rapidly. Post-thrombectomic heparinization did not
bring complication. Therefore, a distant embolism from peripheral artery at the upper limb should be alerted for cerebral ischemia. A lower
density of embolus and no-flow condition in her occluded axillary artery may facilitate the upstreamed embolization. Heparinization, under
closed monitor, is not contraindicated for preventing restenosis after thrombectomy in case of hemorrhagic transformation in brain.
© 2004 Published by Elsevier B.V.
Keywords: Cerebral ischemia; Axillary artery; Embolization; Heparinization; Thrombectomy

1. Introduction
Intracranial embolization, in single or multiple, is not uncommon in cerebral ischemia. The sources usually come from
cardiac embolus [1,2], carotid plaque, aortic arch atherosclerosis [3] or vertebral artery disease. A vasculopathic occlusion of peripheral artery is barely mentioned to associate with
a concurrent intracranial embolization in literature. We encountered a woman who had concurrent right axillary artery
occlusion and homolateral cerebral ischemia. This patient reminds the peripheral artery being a probable embolic source
in the development of cerebral ischemia.
2. Case report
A 90-year-old woman had hypertension known for three
years. On the morning of January 8, 2003 when she was
∗ Corresponding author. Tel.: +886 7 731 7123x3399;
fax: +886 7 311 2516.
E-mail address: josefliu@ms15.hinet.net (J.-S. Liu).

0303-8467/$ – see front matter © 2004 Published by Elsevier B.V.
doi:10.1016/j.clineuro.2004.11.018

taking her breakfast, she experienced a numb and tingling
sensation on her right hand. While she attempted to stand up
from her chair, a few minutes later, she found left side weakness and then fell down on the ground from chair. Slurred
speech and no movement of left side limbs were noted. She
was sent to our hospital within 6 h. Preceding infection, recent
craniofacial trauma, migraine, focal reversible neurological
deficit, vigorous emotionism or illicit drug usage was denied
by her.
On admission, blood pressure and pulse rate were
180/110 mmHg and 77 beats/min of the left arm but were
hardly detected on the right side. Respiratory rate was
14 breaths/min and body temperature was 36.5 ◦ C. She was
oriented but lethargic. The right hand was cold and pale.
Abnormal neurological signs were conjugated eyes tonic
gazing to right side, dysarthria, dysphagia, and hemiplegia,
hyper-reflexia, Babinskis’ sign and hypesthesia to pain at
the left side. Middle cerebral artery syndrome was interpreted initially. Cranial computerized tomography revealed
an obscuration at right corona radiata, caudate nucleus and
putamen at 7 h after onset (Fig. 1A). Chest X-ray disclosed

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Fig. 1. An obscuration (arrow) was found at right caudate, putamen and corona radiata 7 h after onset (A), and it turned to hyperdense with perifocal edema
and anterior horn compression (arrow) at 48 h later after onset (B). Hyperperfusion was considered. The perifocal edema and hyperperfusion were less severe
seven days later (C). Three months after onset, infarct was resorbed (D), in association with brain degeneration and an enlargement of right anterior horn.

no active cardiopulmonary disease. Transthoracic cardiac
echogram showed a hypertrophy of left ventricle and septum, but the ejection fraction and valvular movement were
normal. Transesophageal cardiac echogram did not reveal
patent foramen ovale or aortic arch atherosclerosis. Renal echogram did not disclose vascular stenosis. The 24-h
holter analyzer showed sinus rhythm without dysrthymia.
Transfemoral arteriogram revealed a complete occlusion at
the proximal portion of right axillary artery without collateral circulation (Fig. 2). No occlusion was seen in intracranial arteries (Fig. 2B and C). The luminal wall of aorta,
extracranial carotid artery, subclavian and vertebral artery
were not narrow. Transcranial doppler did not find an increase of systolic velocity or pulsative index in intracranial
arteries.
Stroke risk factor survey [4,5] was performed, including biochemistry, hematology, serology, coagulation profile,
lupus study, immunology and infection index. They were
within reference range except a 2-fold increase of Venereal Disease Research Laboratory and 640-fold increase
of Treponema pallidum hemoagglutination test. The protein C, protein S, antithrombin III, lupus anticoagulant and
anti-beta2-glycoprotein I antibody were normal. Erythrocyte
sedimentation rate was 12 mm. Cancer markers, including

CEA, ␣-fetoprotein, CA-125, CA-199 and tissue polypeptide antigen, did not increase. Cerebrospinal fluid analysis
showed total proteins to be 45 mg%, glucose 58 mg%, cytology 1 lymphocyte/ml, lactate 11.8 mg%, Link IgG index
0.23, and a negative Venereal Disease Research Laboratory
and Treponema pallidum hemoagglutination test. These laboratory tests indicated an inactive syphilis and did not support
coagulopathy.
Emergent thrombectomy was done immediately and heparin was given 1000 units/h intravenously for prophylaxis.
Clinical sign for bleeding and activated partial thromboplastin time were carefully monitored. Radial pulse was detected
at right hand rapidly after thrombectomy. The pathology of
the thrombus contained fibrin, blood clots and arterial tissue,
suggesting probably dissecting disease. The course of hospitalization was uneventful and she discharged with a residual
left hemiparesis. The obscuration in cranial computer tomography became hyperdense suggesting hyperperfusion at 48 h
(Fig. 1B). Perifocal edema was seen and the anterior horn
was compressed. An improvement of perifocal edema was
seen at seven days after onset (Fig. 1C). Three months later,
a resorption of the infarct was noted (Fig. 1D). A repeated
holter analyzer showed sinus rhythm and no atrial fibrillation
six months later.

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Fig. 2. Conventional angiography showed a complete occlusion of right axillary artery at thoracoacromial level (thick white arrow). A stump was seen at the
occlusive site (A). Pathology showed fibrin, blood clots and arterial tissues suggesting dissecting disease. The vertebral artery (thin white arrow) and internal
mammary artery were patent. There was no luminal occlusion at extracranial or intracranial carotid artery (B and C).

3. Discussion
Although cardiac holter has been done twice and shown
not to have significant dysrhythmia in this patient, some cardioelectric disorders, such as paroxysmal atrial fibrillation,
should be kept in mind due to a high unpredictability of time
onset in attack and frequency in multiple embolizations.
It is extremely unusual for a concurrent occlusion of cerebral and peripheral artery arising from an embolic source
other from heart, precerebral artery or aorta. We think that
this uncommon concurrence does not really represent a low
frequency of embolic source from the peripheral artery in
cerebral ischemia in that its etiology is still unknown in over
30% of patients. Paucisymptomatology or rapid recanalization of peripheral artery occlusion may hamper the alertness
in clinician or patient. In the light of an underestimation of
cerebral embolization from aortic plaque in prior [2,8], we
suggest that an investigation of embolic source from peripheral artery may aid for understanding the cause of cerebral
ischemia, especially in whom there is a high risk of dissecting
or atherogenic disease of peripheral artery.
Coagulopathy is another important cause for concurrent
multiple arterial thrombosis. A concomitant nephrotic syndrome, low antithrombin III level and concurrent cerebral and
femoral artery occlusion has been reported [6,7]. Indeed, a
broad spectrum of coagulation disorders is seen in nephrotic
syndrome and generally accepted for a tight relation with systemic thrombosis [9]. However, not all coagulation disorders

give rise to cerebral thrombosis, such as antithrombin III usually decreases in patients with nephrotic syndrome but is not
a potent risk factor for cerebral ischemia [10]. In our patient,
we are unable to identify any coagulopathy. One possibility is that the coagulation tests we perform are not enough
or her coagulopathy is transient and recovers already before
investigation.
Amar et al. [11] have reported three patients to have vertebrobasilar insufficiency rapidly after brachial or subclavian
artery intervention. They propose a vascular compromise
from propagative thrombosis, embolization, dissection,
inappropriate ligation, excessive head rotation, hypotension,
vasospasm or acute subclavian steal responsible for their ischemia. An embolization upstream has also been mentioned
in this circumstance [12]. A traumatic vascular injury may
potentiate procoagulation and elicit thrombosis, such as in
early rethrombosis of coronary artery after recanalization.
Thrombogenesis may result from: (1) a release of thromboplastin into the circulation; (2) an exposure of subintimal
collagen; or (3) an activation of inflammatory proteins or
platelets. Therefore, an injury of her axillary artery may
induce embolization or procoagulation and that subsequently
causes occlusion of her right brain. The proximity of upper
limb and neck promises an easy access of embolization from
axillary to carotid artery in our patient.
Obviously, one problem is how the thrombus upstreams
against the arterial pressure in our patient. There is no answer
in previous studies. We would like to introduce our thinking

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herein. Generally, the blood density is 1.04 m/cm3 and determined by the hematocrit, hemoglobin and iron content.
A thrombus rich in fibrin, platelet or lipid, such as our patient, may have a lower density and therefore, facilitates for
upstream embolization. The no-flow condition in occluded
artery further promotes the upstream expeditiously.
Thrombectomy rapidly corrects the radial blood flow in
our patient. Heparin is usually employed for preventing
restenosis after operation. Since our patient suffers hemorrhagic transformation, prophylactic heparinization is hestitated at that moment. Fortunately, there is no complication
under careful monitor. Accordingly, heparinization may not
be absolutely contraindicated for post-thrombectomic prophylaxis in case of hemorrhagic transformation in brain.
This patient reminds that: (1) an embolization upstream
or procoagulation from peripheral artery thrombosis possibly
contributes to cerebral artery occlusion and (2) heparinization is not absolutely contraindicated for post-thrombectomic
prophylaxis.

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