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278 Vascular Surgery
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Fig. 31.1.
MRI showing cerebellar and brainstem infarctions.
Question 2
The etiology of infarction in the posterior circulation territory is:
A. Distal embolization of atheromatous material from vertebral or basilar artery
lesions.
B. Arrhythmia.
C. Bilateral carotid disease in patients with absent vertebral arteries.
D. Traumatic or spontaneous dissection of the vertebral artery.
E. Transient drop in central aortic pressure in a patient with severe bilateral
stenoses of both vertebral arteries.
An arteriogram showed a 60 percent stenosis in the fourth portion of the right
vertebral artery, and a tenuous, incomplete (dissected) left vertebral artery, which,
at the level of C1, became a normal artery and, higher up, joined with the opposite
vertebral artery (Fig. 31.2). A diagnosis of embolizing dissection of the left vertebral
artery was made. Because the dissection was not responsive to medical therapy, the
patient underwent a bypass from the left internal carotid to the left (suboccipital)
vertebral artery using a saphenous vein [1]. The proximal vertebral site of the
embolizing dissection was ligated above C1, immediately below the distal anastomosis of the carotid-vertebral bypass (Fig. 31.3). The patient did well from this
operation and stopped having symptoms. His anticoagulation was discontinued. He
remains asymptomatic after 5 years of follow-up.
Vertebrobasilar Ischemia: Embolic and Low-flow Mechanisms 279
Fig. 31.2.
arrow), dissected and partially occluded from C4 to C1 (between arrows), and normal distal to C1.
Reprinted from J Vasc Surg, vol. 30, Berguer R, Suboccipital approach to the distal vertebral artery, pages 344–9,
© 1999, with permission from The Society for Vascular Surgery.
Arteriogram: dissection of the left vertebral artery, which is occluded from its origin to C4 (lower
Question 3
Once the objective diagnosis of vertebral artery dissection is made in a patient with
vertebrobasilar symptoms the next step is:
A. Anticoagulation with heparin, then Coumadin.
280 Vascular Surgery
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Fig. 31.3.
carotid to the vertebral artery beyond C1.
Reprinted from J Vasc Surg, vol. 30, Berguer R, Suboccipital approach to the distal vertebral artery, pages 344–9,
© 1999, with permission from The Society for Vascular Surgery.
Postoperative carotid arteriogram showing a saphenous vein bypass from the distal cervical internal
B. Stenting of the dissection followed by antiplatelet therapy.
C. Surgical bypass of the dissected segment with ligation of the proximal vertebral
artery.
Vertebrobasilar Ischemia: Embolic and Low-flow Mechanisms 281
Commentary
Dissection of the vertebral artery may occur spontaneously or result from trauma
[2–6]. The traumatic event is usually an exaggerated extension or rotation of the
neck as may occur during sports and deceleration injuries.
Clinical presentation of dissection of the vertebral artery starts with pain over the
posterolateral aspect of the neck irradiating to the nuchal area. There may be an
interval of several days between the initial pain, announcing the dissection, and the
development of clinical symptoms. The latter are ischemic manifestations of the
dissection and appear in 60–90 percent of patients after an interval of several days,
usually 1–2 weeks. A carotid-vertebral duplex would not provide a discriminating
datum to help in the decision on the management of our patient because: (i) it
would be only confirmatory for a possible concomitant carotid atheroma, which has
never been shown to be the source of infarction in the cerebellum or brain stem; (ii)
infarction in the posterior region can only be evaluated by means of an arteriogram.
The latter will provide in addition the information about the carotid arteries that
you would have derived from the carotid-vertebral duplex. [Q1: D, E] [Q2: A, D]
The treatment of symptomatic vertebral artery dissection is empirical with systemic anticoagulation. Patients with posterior fossa symptoms should undergo MRI
before starting anticoagulation to rule out a subarachnoid hemorrhage. The latter
may occur following dissection and rupture of the fourth (intracranial) segment of
the vertebral artery.
Anticoagulation is empirically used for the treatment of symptomatic dissection
because the ischemia that follows is the consequence of embolization from the
double channel, not a low-flow effect. The fear of distal extension of the dissection
with anticoagulants has prompted some leading experts to give antiplatelet therapy
to patients with local symptoms (pain) and evidence of dissection but without
central manifestations of ischemia (central nervous system deficits or MR evidence
of infarction). Patients with massive infarction are not anticoagulated to avoid
intraparenchymal bleeding. There is no indication for wire-catheter-stent manipulation of a dissected vertebral. In patients who are anticoagulated appropriately and
continue to have intermittent symptoms, the dissected vertebral artery is considered to be the source of emboli. [Q3: A] In these circumstances, and if technically feasible, the dissected segment is excluded and bypassed [7, 8].
Vertebrobasilar Ischemia: Low-flow Mechanism
A 62-year-old woman with a healthy lifestyle presented with a history of
dimming of the visual field and passing out when she turned her head to the
extreme right. Three months before, she had been evaluated elsewhere with a
history suggestive of amaurosis fugax and bouts of imbalance and vertigo when
she turned her head to the right. A carotid endarterectomy had been performed
at another institution.
She continued to have severe vertebrobasilar symptoms with head turning. She
had a myocardial revascularization 20 years ago, at which point she stopped
smoking.
On examination, the patient appeared healthy, with normal and equal
(124/80 mm Hg) blood pressure in both brachial arteries. Neurological examina-
282 Vascular Surgery
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tion under resting conditions was normal. Her neck was silent. When her head
was turned to the right, the patient developed dimming of vision, loss of balance,
and a sensation of passing out. The arteriogram available from the previous
operation carried out elsewhere showed a clearly dominant large left vertebral
artery, but we could not see clearly the distal segment of the vessel. The right vertebral artery was small and diseased severely to a preocclusive level throughout
its second segment. There was no evidence of posterior communicating arteries.
Because the symptoms were repetitive and induced posturally, the patient was
scheduled for a dynamic arteriogram. First, we obtained a view with a selective
subclavian injection of the dominant left vertebral in the neutral position, which
was normal. Following this, the patient’s head was turned to the right; when she
became symptomatic, the contrast injection was repeated (Fig. 31.4). This
revealed a severe compression of the vertebral artery at the level of the pars
atlantica of C1.
The patient underwent exploration of the suboccipital space with dissection
and exposure of the vertebral artery where it crossed the lamina of C1. The compression mechanism was between the sharp upper edge of the lamina and the
occipital bone. A laminectomy was carried out to provide space for the artery
to pass from the exit of the transverse foramen of C1 to the foramen magnum
without bony compression (Fig. 31.5). The artery was examined by palpation
and direct duplex interrogation; we could find no element of plaque or stenosis in the lumen once the artery was freed and the laminectomy completed.
The patient became asymptomatic. Full-range motion of the neck no longer
caused syncope or vertigo.
Question 1
Which of the following statements regarding posturally induced symptoms is true?
A. The mechanism for ischemia is the restriction of flow by external compression
of the artery.
B. The mechanism for ischemia is embolization from the damaged wall (dissection)
or thrombus overlying the endothelial lining of the artery at the site of trauma.
C. Both mechanisms may exist.
Question 2
Which of the following statements are correct?
A. When dynamic symptomatic compression of the vertebral artery is demon-
strated, angioplasty (with or without stent) is never indicated.
B. Angioplasty of a stenosed or dissected vertebral artery at the suboccipital
level is likely to result in rupture of the artery or formation of an arteriovenous fistula.
C. Angioplasty and stenting of the distal vertebral artery is successful in stenosing
lesions caused by external compression.
Vertebrobasilar Ischemia: Embolic and Low-flow Mechanisms 283
Fig. 31.4.
head turned to the right. The single, dominant vertebral artery is severely compressed above C1 in its pars
atlantica.
Selective injection of a left subclavian artery while the patient is experiencing symptoms with her
Commentary
In patients with low-flow ischemia secondary to extrinsic compression of the artery,
the clinical picture is repetitive and can be induced by manipulating the patient’s
head in the trigger position.
Patients with symptoms occurring with head rotation or extension should have a
dynamic arteriogram to show the anatomic lesion (extrinsic compression) at the
284 Vascular Surgery
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Fig. 31.5.
been removed.
Three-dimensional reconstruction of a CT scan of the craniocervical junction. The lamina of C1 has
same time as the patient experiences symptoms. Patients with low-flow symptoms
(repetitive) and no evidence of embolization (negative MRI) may show
deformity/compression of one vertebral artery but a normal contralateral vertebral
artery during head rotation or extension. If the contralateral, undisturbed artery is
of normal size and empties normally into the basilar artery, then the role of the
compression of one vertebral artery causing the symptoms must be doubted.
The suboccipital approach permits access to the vertebral artery from the transverse process of C2 to the foramen magnum. The techniques used to relieve compression at the suboccipital level are laminectomy, laminectomy plus bypass, and
bypass alone.
Vertebrobasilar ischemia of postural origin is generally the consequence of
mechanical compression of the vertebral artery by osteophytes (and occasionally
ligaments) in its extracranial trajectory. The mechanism for symptoms is generally
low flow in a dominant vertebral artery that cannot be compensated for by flow
from a contralateral hypoplastic or absent vertebral artery. This compression is
seen very rarely in the first segment (origin–C6) caused by compression by the
tendon of the longus colli. It is usually observed in the second and third segments of
the artery. In the second segment (C6–C2), the artery is usually compressed by
osteophytes, and the symptoms generally appear with rotation of the neck. In the
third segment (C2–C0), the compression may occur at C1 or, more commonly, in
the pars atlantica of the artery between C1 and the foramen magnum. The artery is
Vertebrobasilar Ischemia: Embolic and Low-flow Mechanisms 285
compressed between the sharp upper edge of the lamina of C1 and the occipital
ridge. [Q1: C]
The ischemic symptoms are usually the consequences of low flow through a dominant vertebral artery because of complete or near-complete occlusion at the latter
by an osteophyte. Less frequently, the ischemic effects may be embolic from the
mural thrombi that develop at the site of repetitive trauma on the artery by the
offending osteophyte. In other cases, the artery may dissect at the point of repetitive
traumatic compression, which results in its occlusion and/or distal embolization.
Symptoms in patients with vertebrobasilar ischemia from the low-flow mechanism
are repetitive and can be reproduced every time the neck is brought to the trigger position. Patients with vertebrobasilar ischemia of embolic origin usually present with a
clinical stroke or TIA in different areas. MRI in the low-flow group is usually normal,
but in the embolic group it will show cerebellar, brainstem or occipital infarctions.
An arteriogram is needed to outline precisely the point of compression and to
discern the possibility of a dissection and/or tandem lesions. It is also important to
outline the entire course of the opposite vertebral artery to establish whether it is
complete, normal or hypoplastic, and whether at the time of the provocative
dynamic arteriogram the opposite vertebral artery fills the basilar artery normally
while the patient has symptoms. The latter suggests that the mechanism of symptoms is not low flow.
There is no role for angioplasty, with or without stent, in the treatment of extrinsic
compression of the vertebral artery. Balloon dilation of the thin-walled vertebral artery
against the hard bony prominence of an osteophyte is likely to result in the rupture of
the arterial wall and the formation of a false aneurysm or an arteriovenous fistula.
If the compression of the vertebral artery is limited to the V2 segment (C6–C2),
then the single or multiple elements of compression are bypassed by reconstructing
the artery to the level of C1. This is done through an anterior approach [8]. In
dynamic compression at the suboccipital level, the approach is posterior [1] and the
treatment consists of a laminectomy, a bypass or both. In the case of a bypass, the
inflow is obtained from the high cervical carotid. The latter is exposed by moving
aside the cranial nerves that block access to the internal carotid when approached
posteriorly. [Q2: A, B]
References
1. Berguer R. Suboccipital approach to the distal vertebral artery. J Vasc Surg 1999;30:344–9.
2. Mas JL, Bousse M-G, Harbourn D, Laplanc D. Extracranial vertebral artery dissection: a review of 13
cases. Stroke 1987;18:1037–47.
3. Mokri B, Houser OW, Sandok BA, Peipgzas DG. Spontaneous dissection of the vertebral arteries.
Neurology 1988;38:880–5.
4. Chiras J, Marciano S, Vega Molina J, Touboul J, Poirier B, Bories J. Spontaneous dissecting aneurysm
of the extracranial vertebral artery (20 cases). Neuroradiology 1985;27:327–33.
5. Ringel SP, Harrison SH, Noremberg MD, Austin JH. Fibromuscular dysplasia: multiple “spontaneous”
dissecting aneurysms of the major cervical arteries. Ann Neurol 1977;1:301–4.
6. Noelle B, Clavier I, Berson G, Hommel M. Cervicocephalic arterial dissections related to skiing. Stroke
1994;24:526–7.
7. Caplan L. Posterior circulation disease. Cambridge, MA: Blackwell Science, 1996;257.
8. Berguer R, Morasch MD, Kline RA. A review of 100 consecutive reconstructions of the distal vertebral
artery for embolic and hemodynamic symptoms. J Vasc Surg 1998;27:852–9.
32. Neurogenic Thoracic Outlet Syndrome
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Richard J. Sanders
A 30-year-old woman presented with complaints of pain in her neck, right shoulder, right trapezius, right anterior chest wall, right arm, elbow, and forearm;
occipital headaches every other day; numbness and tingling in all fingers of the
right hand, worse in the fourth and fifth fingers; aggravation of her symptoms
when elevating her arms, especially to comb or blow dry her hair or drive a car;
weakness of her right hand and dropping coffee cups; and coldness and color
changes in her right hand. The symptoms had been present for one year and
began following a rear-end collision.
Her history began one year ago when her automobile was sitting still at a traffic
light and another vehicle hit her from the rear. She wore a seat belt and recalled
going forward and backward, but did not recall what happened to her neck at the
time of the accident. She had no immediate symptoms. On the next day she
awoke with a sore neck and pain above her shoulder blades. A few days later, she
began noticing headaches in the back of her head that radiated forward to behind
her eyes, and the neck soreness became progressively painful. Two or three
weeks later, pain developed in the right shoulder area and down the right arm.
Several weeks later, numbness and tingling developed in the fingers of the right
hand, more noticeable in the ring and baby fingers. Because of severe, persistent
right shoulder pain, arthroscopic repair of the right shoulder had been performed 6 months ago with partial improvement of her shoulder pain, but no
change in any of her other symptoms.
Her occupation was a legal secretary. Since the accident, although she had been
able to return to work, she was now able to work only 4 hours a day. She could
not type for more than 10 minutes because the pain and numbness in her right
hand was too uncomfortable. At home she could do light housework only. She
could not vacuum, wash windows or floors, or lift heavy laundry baskets.
Diagnostic studies to date included cervical spine X-rays, which were normal,
and an electromyography/nerve conduction velocity (EMG/NCV) study, which
revealed very mild nonspecific changes in the ulnar nerve distribution, but was
close to normal.
Treatment to date included 6 months of physical therapy with the following
modalities: heat, massage, ultrasound, neck stretching exercises, and posture
289
290 Vascular Surgery
correction. She was continuing neck stretching exercises at home on a daily basis
emphasizing doing each stretch slowly, holding each stretch for a minimum of
15 seconds, and performing no more than three repeats at each session. In spite
of this treatment, there was no improvement in her symptoms.
Question 1
What is the most common cause of neurogenic thoracic outlet syndrome (TOS)?
A. Neck trauma.
B. Cervical rib.
C. Anomalous bands.
D. Abnormal first rib.
E. All of the above.
On physical examination there was supraclavicular tenderness over the right
scalene muscles but no tenderness over the left scalenes; a positive Tinel’s sign over
the right brachial plexus and a negative sign over the left; and reproduction of arm
and hand symptoms with pressure over the right scalene muscles, but no such
symptoms with pressure over the left scalene muscles. Head rotation and head
tilting each caused pain in the contralateral hand and arm when turning and tilting
to the left side. This did not occur when rotating and tilting to the left side.
Abducting the arms to 90° in external rotation (AER position) reproduced the right
arm and hand symptoms within 15 seconds while no symptoms developed on the
left side.
Scalene muscle block, injecting 4 ml of 1% lidocaine into the right anterior
scalene muscle area, resulted in significant improvement in most of her physical
findings.
Question 2
The diagnostic criteria for neurogenic TOS include which of the following?
A. History of neck trauma.
B. Paresthesia in the hand involving all five fingers, more frequently in the fourth
and fifth.
C. Pain in the neck, shoulder, and upper extremity.
D. Occipital headaches.
E. Scalene muscle tenderness and duplication of symptoms in the 90° AER
position.
F. Cut-off of the radial pulse on Adson’s or 90° AER positioning.
G. Positive response to the scalene muscle block.
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