Five patients had limb weakness. Two patients had dysarthria. One patient had dysphagia. The nature of the clinical findings depended on whether the brainstem or cervical spinal cord was compressed. Brain MRI was performed in all 11 patients and 22 controls. The mean basilar diameter did not differ significantly between patients and controls 3.
In patients with VACS, vertebral artery dominance was observed in 10 of 11 Right vertebral artery hypoplasia was observed in 4 patients. Of the 11 patients with VACS, medullary compression was observed in 10 patients. One patient had cervical spinal cord compression. A year-old hypertensive woman suddenly lost her balance while walking out of an elevator. She felt that the ground and adjacent objects were moving and that she was swaying. There was no tinnitus, hearing loss, or a fullness in the ear.
The vertigo was not triggered by specific changes in the position of her head. Neurological examination revealed unsteady gait and was otherwise normal. MRI scan was performed and showed no acute infarcts on diffusion-weighted imaging scan. Severe indentation of the left medulla by a tortuous vertebral artery was observed on T2 weighted MR image Figure 1. Figure 1. Seventy-three-year-old woman presented with vertigo and imbalance.
Magnetic resonance imaging showed severe compression and indentation A of the left lower medulla. Note that the medulla was displaced to the right side B by the tortuous vertebral artery.
A year-old woman presented with progressive left leg weakness, spasticity and imbalance for 2 years. In the past, she was always healthy. On examination, she had spasticity in four limbs with exaggerated deep tendon reflexes and left lower extremity muscle strength was decreased.
MRI of the brain revealed anterolateral compression of the left base of the medulla oblongata by a tortuous vertebral artery. The patient received physiotherapy. The symptoms persisted. A year-old man had pain in the area of the neck and trapezius muscle and left leg weakness. He had a history of diabetes for 17 years. He was diagnosed with coronary artery disease 1 month before presentation. On neurological examination, the patient had decreased left leg muscle strength.
MRI scan showed a signal void region at the level of the atlas. Axial MR image revealed left anterolateral compression of the cervical spinal cord near the cranial-spinal junction by the left vertebral artery Figure 2. Figure 2. MR images in a patient with nape pain and left leg weakness.
A Sagittal T2 weighted MR image showing a signal void compressing the upper cervical spinal cord at the atlas level. B Axial T2 weighted MR image showing anterolateral compression of the spinal cord by left vertebral artery. In our study, we demonstrated that vascular compression of brainstem or cervical spinal cord can present with various signs and symptoms.
This syndrome, which we call VCAS, is distinct from basilar artery dolichoectasia. Dolichoectasia of the basilar artery has been associated with compression of the pons, cranial nerve palsies, and even ischemic events 2 , 4 , 9. The most widely used diagnostic criteria for vertebrobasilar dolichoectasia were proposed by smoker et al. Therefore, we did not use the term vertebrobasilar dolichoectasia to describe this condition.
In addition, vertebrobasilar dolichoectasia literally only describes the anatomical feature of a dilated arteriopathy. The current diagnostic criteria for vertebrobasilar dolichoectasia was based on imaging morphology but not clinical symptoms. In this report, we term this condition vertebral artery compression syndrome because all symptoms were caused by compression of medulla oblongata or cervical spinal cord with an offending vertebral artery.
The diagnosis of VACS is especially challenging for clinicians since this condition is not described as an entity in the literature. Sign in with Facebook. Sign in with Apple. Description The vertebral arteries arise from the subclavian arteries, one on each side of the body, then enter deep to the transverse process at the level of the 6th cervical vertebrae C6 , or occasionally in 7. The vertebral artery may be divided into four parts: The prevertebral part; V1 segment preforaminal runs upward and backward between the Longus colli and the Scalenus anterior.
In front of it are the internal jugular and vertebral veins, and it is crossed by the inferior thyroid artery; the left vertebral is crossed by the thoracic duct also. Behind it are the transverse process of the seventh cervical vertebra, the sympathetic trunk and its inferior cervical ganglion. It is situated in front of the trunks of the cervical nerves, and pursues an almost vertical course as far as the transverse process of the axis.
The atlantic part; V3 segment extradural or extraspinal issues from the C2 foramen transversarium on the medial side of the Rectus capitis lateralis. This part of the artery is covered by the Semispinalis capitis and is contained in the suboccipital triangle—a triangular space bounded by the Rectus capitis posterior major, the Obliquus superior, and the Obliquus inferior. The first cervical or suboccipital nerve lies between the artery and the posterior arch of the atlas.
The intracranial part; V4 segment intradural pierces the dura mater and inclines medialward to the front of the medulla oblongata; it is placed between the hypoglossal nerve and the anterior root of the first cervical nerve and beneath the first digitation of the ligamentum denticulatum. The vertebral artery arises from the supraposterior aspect of the first part of the subclavian artery. Unlike the internal carotid artery, which is an almost direct extension of its parent vessel the common carotid artery, the vertebral artery branches almost at right angles to its feeding vessel.
These differences in anatomy may well reflect in dissimilar flow dynamics between the origins of the carotid and vertebrobasilar cerebral circulations, with a consequent predilection to forming a different type of atherosclerotic plaque. Part one is from the origin to the point at which it enters the transverse foramina of either the fifth or sixth cervical vertebra. During the second part, it courses within the intervertebral foramina until exiting as the third part behind the atlas and heading towards the foramen magnum.
The final intracranial part begins as it pierces the dura and arachnoid mater at the base of the skull, and ends as it meets its opposite vertebral artery to form the midline basilar artery at the level of the medullopontine junction. In its extracranial portion the vertebral artery gives small spinal branches to the periosteum and vertebral bodies and muscular branches to the deep surrounding muscles of the region.
The short fourth intracranial part gives off major anterior and posterior spinal arteries to the medulla and spinal cord, minute penetrating vessels to the medulla and its largest branch—the posterior inferior cerebellar artery PICA , which supplies a small portion of the dorsal medulla and cerebellum. Occasionally this PICA branch is absent, and collateral vessels then feed the lateral medulla.
As it enters the skull, the vertebral artery wall shows marked change, with a reduction in the thickness of the adventitial and medial layers, and a reduction of elastic fibres in the media and external elastic lamina. Lesser degrees of asymmetry are also frequent.
These variations have little or no clinical significance, unless there is associated vertebral artery origin or proximal subclavian artery stenosis. The extracranial vertebral artery is affected by several pathological processes that cause stroke. Furthermore, atherosclerotic disease at the first part of the vertebral artery is commonly associated with similar disease in the internal carotid artery. Despite the possible differences in plaque appearance between extracranial vertebral and internal carotid artery disease, 10 it is generally considered that the two sites share a common pathogenesis, with stroke resulting from formation of emboli at the site of atherosclerotic plaque.
Also, in contrast to the ICA, the vertebral artery gives off numerous branches in the neck, therefore facilitating a considerable collateral blood supply, which often reconstitutes the distal artery after occlusion at the origin. Studies to date have been of small numbers in specialist cohorts. Posterior circulation stroke was defined by imaging studies and vertebrobasilar TIA was diagnosed by experienced stroke neurologists using Caplan's criteria. The risk factor profile for these patients was similar to that of anterior circulation stroke, and the mean age for the group was The distribution of ethnicity was similar to that of the registry as a whole, but there was a preponderance of men in the group with vertebral artery origin stenosis.
Unlike carotid disease, the prognosis of symptomatic vertebral artery stenosis is unknown. The only published prospective series of vertebral artery stenosis is from the Cleveland Clinic, 18 and included predominantly asymptomatic cases. Cases of occlusion or those who underwent operative procedures, presumably on symptomatic grounds, were excluded.
Perhaps unsurprisingly, the survival rate of the entire group was related to their carotid artery and concomitant cardiac disease. None of the isolated extracranial vertebral artery stenoses developed posterior circulation infarction.
Intracranial vertebral artery stenosis in the fourth segment of the vertebral artery often also involves the basilar artery, and is more strongly associated with brainstem infarction than extracranial vertebral artery stenosis. It has mainly been reported in symptomatic patients and is thought to be more common in Japanese, Chinese and Black Americans than in Caucasians.
The recurrent stroke rate in the territory of the stenotic vertebral artery was lower, at 7. The warfarin group had a lower recurrent stroke rate, but the numbers were small, and treatment was not randomized, making definite conclusions on the efficacy of warfarin difficult. The New England Medical Centre posterior circulation registry identified 75 cases of severe symptomatic intracranial vertebral artery occlusive disease, and suggested that the prime site of disease is distal to the origin of PICA.
The gold standard for diagnosing vertebral artery stenosis remains Digital Subtraction Angiography DSA , although this has a small morbidity and associated mortality. Another potential use of TCD is the detection of emboli from a stenosis, 37 and many studies have detected asymptomatic embolization in patients with symptomatic carotid stenosis. Helical or spiral computerized tomography angiography CTA is able to image the extracranial vertebral artery without the risks associated with catheter angiography, but its use has not been fully validated against DSA.
In one promising study of 24 patients with symptoms of vertebrobasilar ischaemia, CTA visualized the vertebral origin in all cases, and was able to detect all the extracranial vertebral artery stenotic lesions found by DSA. Magnetic resonance imaging MRI used alone can detect intracranial vertebral artery disease, 41, 42 but it is best used in combination with magnetic resonance angiography MRA to assess both extra and intracranial vertebral arteries.
In the 62 patients with extracranial vertebral stenosis, the origin of the vertebral artery was not always well demonstrated, resulting in lower sensitivity results. Intracranial vertebral artery stenosis sensitivity was the least impressive, and lesions were missed, particularly at the junction between the intracranial and extracranial vertebral artery portions.
Reports to date have concentrated on carotid artery disease, but there is also a suggested improvement over conventional MRA in detecting lesions at the origin of the extracranial vertebral artery.
This lack of signal could exacerbate the problems with differentiating low flow due to high grade stenosis and occlusion, and is not necessarily helped by the use of contrast. Medical treatment alone has been the standard treatment for posterior circulation stroke, although other than for cardioembolic causes, this has tended to ignore the specific pathophysiological process underlying the event.
To date, there have been no randomized trials of the use of different antiplatelet therapies or anticoagulation against antiplatelet therapy, in known cases of extracranial vertebral artery atherosclerotic stenosis.
This compared anticoagulation with warfarin to an INR of 1. Surgery for vertebral artery stenosis can be performed either by endarterectomy or reconstruction. Endarterectomy for atherosclerotic stenosis at the origin and proximal extracranial vertebral artery has been performed via a supraclavicular incision since the early s, with variable success rates. Complications including lymphoceles, fistulas, vocal cord paralysis and pneumothorax are all well recognized.
Similar problems with access exist for endarterectomy of intracranial vertebral artery stenosis, which usually involves a limited suboccipital craniotomy.
Although a technically feasible operation, success rates are poor, and revascularization is the preferred surgical treatment in suitable cases. Reconstruction for extracranial vertebral artery stenosis involves transposition of the vertebral artery, usually to the common or internal carotid artery, 46, 49 but has also been reported with transposition to the subclavian and thyrocervical trunk arteries.
Endarterectomy of the carotid or vertebral artery is often performed at the time of the transposition procedure. Other series have described vocal cord paralysis and phrenic nerve injury as other notable complications.
Surgery has been performed less frequently in recent years for cases refractory to medical treatment. This is because there is now a growing literature of case series suggesting that endovascular intervention, with percutaneous transluminal angioplasty PTA and stenting, is a safe and effective treatment for extracranial vertebral artery atherosclerotic stenosis, especially at the vertebral artery origin.
Some early reports where PTA alone was performed for VA origin stenosis were associated with a marked incidence of restenosis, comparable to that seen in PTA of ostial renal artery stenosis, partly due to vessel wall recoil.
From the coronary literature, there is some suggestion of improved rates of patency and restenosis in stented vessels, and also diminished rates of thromboembolism when stents are used.
A further advantage of primary stenting is a reduced rate of intimal dissection at the time of the procedure. However, these results are from series of selected cases, and data from randomized controlled trials are required. Until then, the use of such intervention is likely to remain largely experimental.
The same can be said of endovascular intervention for intracranial vertebral artery stenosis. The condition itself, which is frequently associated with concomitant basilar artery stenosis, carries a greater stroke risk than extracranial vertebral artery stenosis—some 17 times the expected stroke rate of a normal population matched for age and sex. Intracranial stenting as reported seems to be a more technically difficult procedure than endovascular extracranial intervention, and the balance of benefit and risk is more uncertain.
Vertebral artery stenosis is an important aetiology of posterior circulation stroke. This should allow an improved understanding of the natural history of this disease process in terms of its liability to cause disabling stroke and death.
Until the natural history is clearer, it is difficult to evaluate specific medical treatments and interventions fully, although endovascular intervention with primary stenting for extracranial vertebral artery stenosis is a promising potential treatment.
Address correspondence to Dr G. Classification and natural history of clinically identifiable subtypes of cerebral infarction. Read it at Google Books - Find it at Amazon. Related articles: Anatomy: Brain.
Related articles: Anatomy: Spine. Promoted articles advertising. Figure 1: vertebral artery Figure 1: vertebral artery. Figure 2: vertebral artery Figure 2: vertebral artery. Figure 4: brainstem arterial territories Figure 4: brainstem arterial territories. Figure 5: development from the aortic arches Gray's illustration Figure 5: development from the aortic arches Gray's illustration. Case 1: vertebral arteries: 3D recon Case 1: vertebral arteries: 3D recon.
Case 2: aortic origin Case 2: aortic origin. Case 3 Case 3. Case 4: V4 segments uniting to form basilar artery Case 4: V4 segments uniting to form basilar artery. Case 5: fenestration Case 5: fenestration. Case 7: tortourous course of vertebral arteries Case 7: tortourous course of vertebral arteries. Case partial duplication Case partial duplication. Case variant origin course of the left vertebral artery Case variant origin course of the left vertebral artery.
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