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1/15. Extracranial vertebral artery dissection causing cervical root lesion.

    The authors report an unusual manifestation of extracranial vertebral artery dissection (VAD), presenting with a predominantly motor radicular manifestation. Cervical magnetic resonance imaging (MRI) revealed the intramural hematoma in the dissected vessel wall, compressing mainly the segmental motor root and, to a lesser degree, the sensory ganglion. In the digital subtraction angiography (DSA), a circumscribed narrowing of the incriminated vessel was demonstrated. color-coded Duplex imaging (CDDI) revealed complete recanalization after a few days of anticoagulation treatment. Complete neurologic recovery was seen after 3 months. Considering the MRI data, the likely pathogenetic mechanism was compression of the nerve root by the intramural hematoma. The synopsis with similar cases in the literature points to the characteristic features, i.e., the association of neck pain with radicular motor deficit and the absence of degenerative disk disease. The respective syndrome should raise the suspicion of vertebral artery dissection, especially in young individuals.
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2/15. Vertebral artery anomaly with atraumatic dissection causing thromboembolic ischemia: a case report.

    STUDY DESIGN: A case report is presented. OBJECTIVES: To illustrate a rare cause of atraumatic vertebral artery dissection resulting from anomalous entry of the vessel at the C3 transverse foramen induced by normal physiologic head and neck motion, and to review vertebral artery anatomy and mechanisms whereby it is vulnerable to pathologic compression. SUMMARY OF BACKGROUND DATA: The vertebral artery usually enters the transverse foramen at C6. Rarely, the artery enters at C5 or C4. Only one prior case with entry at C3 has been reported. That patient experienced recurrent quadriplegia and locked-in syndrome caused by vertebral artery obstruction. A 27-year-old woman with a history of classic migraine experienced neurologic symptoms on three occasions related to physiologic neck and arm movements. Magnetic resonance angiogram was not diagnostic, but standard arteriography demonstrated anomalous vertebral artery entry into the C3 transverse foramen and focal dissection. methods: Pertinent literature and the patient's history, physical examination, and radiologic studies were reviewed. RESULTS: Standard cervico-cerebral arteriogram demonstrated focal dissection at C4 and thromboembolic complications in distal vertebral and basilar arteries. Initially, diagnosis by magnetic resonance angiogram was elusive. However, arteriography allowed prompt diagnosis followed by anticoagulation with resolution of neurologic symptoms. CONCLUSIONS: vertebral artery dissection without trauma is rare, but should be considered when neurologic symptoms accompany physiologic cervical movements. For cases in which vertebrobasilar thromboembolic ischemia is suspected, magnetic resonance angiogram may prove inadequate for demonstrating the causative vascular pathology. Therefore, standard cervico-cerebral arteriography should be performed.
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3/15. Different roles of arteriosclerosis in the rupture of intracranial dissecting aneurysms.

    AIMS: Although intracranial dissecting aneurysm (IDA) is a newly described variant of the brain aneurysms that affects mainly the vertebrobasilar arterial system, its pathogenesis remains obscure. We aimed to clarify the role of arteriosclerosis in the pathogenesis of IDA based on histopathological findings in seven autopsy cases of IDA. methods AND RESULTS: All cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited subarachnoid haemorrhage. Two types of dissection were recognized in the vertebral artery. Six of seven IDA cases showed a widespread disruption of the entire thickness of the arterial wall with the formation of a dilated pseudoaneurysm, which consisted of thin adventitia (arterial wall disruption type). Medial disruption of the arterial wall and subadventitial dissecting haemorrhage were also found, resulting in the formation of a false lumen and stenosis of the 'true' lumen of the artery. However, these lesions were connected to the site of rupture of the entire arterial wall. Within 1 day after onset of IDA, the autopsy cases showed formation of fibrin thrombus, marked leucocyte infiltration and necrosis of the arterial wall at the site of the lesion. Cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration in the lesions. These cases showed no atherosclerotic plaque, but non-atherosclerotic fibrocellular intima. The thickness of intima and media was significantly less in the vertebral artery of IDA patients than that of non-IDA patients with systemic hypertension. On the other hand, the remaining case showed severe atherosclerosis with haemorrhage into the lipid core without connection to the arterial lumen (intra-atheromatous plaque haemorrhage type). However, unusual arterioles and neovascularization of the intra-and peri-arterial walls were observed. CONCLUSIONS: Our results suggest that disruption of the entire arterial wall may be a critical event in the development of IDA and result in the medial disruption and subadventitial haemorrhage. Non-atheromatous intima might function as a protective factor in arterial wall disruption. On the other hand, atherosclerosis may predispose to intra-atheromatous plaque haemorrhage type of IDA through intramural haemorrhage originating from the newly formed vessels.
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4/15. Intravascular graft stent treatment of a ruptured fusiform dissecting aneurysm of the intracranial vertebral artery: technical case report.

    OBJECTIVE AND IMPORTANCE: An innovative stenting technique to treat a difficult case of a fusiform aneurysm of the intracranial vertebral artery (VA), with restoration of the vessel lumen, is described. CLINICAL PRESENTATION: A 58-year-old patient experienced sudden pain in the upper cervical spine, followed by a severe headache. He underwent computed tomographic evaluation, which demonstrated subarachnoid hemorrhage in the prepontine cistern. A fusiform aneurysm of the distal right VA and critical stenosis of the left VA were detected in digital subtraction angiograms. The patient experienced a new subarachnoid hemorrhaging episode, and urgent endovascular treatment was planned. INTERVENTION: The patient underwent angioplastic and stenting procedures in the left VA, with good results. Forty-eight hours later, an endovascular procedure was performed to treat the right VA aneurysm. We decided to use a graft stent (Jostent graft stent; Jomed, Conroe, TX) instead of a balloon to preserve the arterial lumen. The complete procedure was well tolerated by the patient, and he was discharged, without symptoms, 48 hours later. CONCLUSION: The patient was discharged, without neurological deficits, 48 hours after completion of the endovascular procedure, with clopidogrel (75 mg/d) and aspirin (325 mg/d) therapy. This treatment was discontinued after 4 weeks. According to our search of the medical literature, this is the first clinical case in which an intracranial fusiform aneurysm was permanently sealed with a graft stent.
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5/15. A case of segmental mediolytic arteriopathy involving both intracranial and intraabdominal arteries.

    Segmental mediolytic arteriopathy (SMA) is an uncommon nonatherosclerotic and nonvasculitic arteriopathy. This disease is characterized by lytic degeneration of the arterial media, intramural dissection and thrombosed or ruptured aneurysm. SMA mainly involves the intraabdominal arterial system, resulting in intraabdominal and retroperitoneal hemorrhage. However, only a few cases of SMA with involvement of intracranial arteries have been reported. Here, we present a case of SMA developing subarachnoid hemorrhage due to dissection of the internal carotid and vertebral arteries. This patient was a 48-year-old male who died 13 days after admission for sudden loss of consciousness. Computed tomography showed subarachnoid hemorrhage. At autopsy, the affected vessels included the right vertebral, left internal carotid, superior mesenteric, bilateral renal and left external iliac arteries. Histopathologically, the arteries showed segmental lytic degeneration and disappearance of medial smooth muscle cells, medial dissection and formation of pseudo-aneurysms, the wall of which consisted of a thin membrane of the adventitia. These histopathological features mimicked an entire wall dissection type of intracranial dissecting aneurysm, which exclusively affects the vertebro-basilar system. Thus, SMA should be considered a possible underlying disease in patients with spontaneous dissection of intracranial arteries.
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6/15. Ruptured dissecting aneurysm of the vertebral artery associated with occlusive internal carotid artery dissection--case report.

    A 64-year-old male presented with subarachnoid hemorrhage. Angiography showed a dissecting aneurysm of the right vertebral artery (VA), and severe stenosis of the right internal carotid artery (ICA). He was treated conservatively in the early stage. Repeat angiography showed enlargement of the dissecting aneurysm of the VA and partial resolution of the stenosis of the right ICA. Intraaneurysmal coil embolization with proximal coil occlusion was performed following a balloon occlusion test. The postoperative course was uneventful. Based on the neuroradiological findings, the stenotic lesion of the right ICA was considered to be due to dissection. Analysis of serial changes in dissecting lesions in the craniocervical arteries is important for the correct choice of treatment, especially in patients with multi-vessel dissections. The surgical options should be determined on an individual basis.
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7/15. Simultaneous bilateral internal carotid and vertebral artery dissection following chiropractic manipulation: case report and review of the literature.

    Single-vessel cervical arterial dissections typically occur in young adults and are a common cause of cerebral ischemia and stroke. Although the pathogenesis of multivessel dissection is unclear, it is thought to be a consequence of underlying collagen vascular disease. We present a 34-year-old previously healthy man who developed bilateral internal carotid and vertebral artery dissection following chiropractic manipulation.
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8/15. Endovascular management of symptomatic vertebral artery dissection achieved using stent angioplasty and emboli protection device.

    Extracranial vertebral artery (VA) dissection may lead to significant arterial stenosis, occlusion, or pseudoaneurysm formation with subsequent hemodynamic and embolic infarcts. To prevent thromboembolic complications, anticoagulation with intravenous heparin followed by oral warfarin has been recommended for all patients with acute dissections, regardless of the type of symptoms, unless there are contra-indications. Nevertheless, anticoagulation is not innocuous, may be contra-indicated or may be ineffective to prevent symptoms or dissection progression. Because it is effective and less invasive than other surgical procedures, endovascular treatment of VA dissection has recently attracted interest. We present a case of a traumatic VA dissection, presenting with multiple embolic infarctions that was managed with protected stent-assisted angioplasty. Protected stent-assisted VA angioplasty has not been previously reported and appears to be a safe, effective and immediate method of restoring vessel lumen integrity and should be considered in the therapy of selected cases of VA dissection.
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9/15. recurrence of a vertebral artery dissecting pseudoaneurysm after successful stent-supported coil embolization: case report.

    OBJECTIVE AND IMPORTANCE: Dissecting aneurysms of the intracranial vertebral artery are increasingly recognized as a cause of subarachnoid hemorrhage. We present a case involving technical success of the stent-supported coil embolization but with recurrence of the dissecting pseudoaneurysm of the intracranial vertebral artery. The implications for the endovascular management of ruptured dissecting pseudoaneurysms of the intracranial vertebral artery are discussed. CLINICAL PRESENTATION: A 36-year-old man with a remote history of head injury had recovered functionally to the point of independent living. He experienced the spontaneous onset of severe head and neck pain, which progressed rapidly to obtundation. A computed tomographic scan of the head revealed subarachnoid hemorrhage centered in the posterior fossa. The patient underwent cerebral angiography, which revealed dilation of the distal left vertebral artery consistent with a dissecting pseudoaneurysm. INTERVENTION: Transfemoral access was achieved under general anesthesia, and two overlapping stents (3 mm in diameter and 14 mm long) were placed to cover the entire dissected segment. Follow-up angiography of the left vertebral artery showed the placement of the stents across the neck of the aneurysm; coil placement was satisfactory, with no residual aneurysm filling. Approximately 6 weeks after the patient's initial presentation, he developed the sudden onset of severe neck pain. A computed tomographic scan showed no subarachnoid hemorrhage, but computed tomographic angiography revealed that the previously treated left vertebral artery aneurysm had recurred. Angiography confirmed a recurrent pseudoaneurysm around the previously placed Guglielmi detachable coils. A test balloon occlusion was performed for 30 minutes. The patient's neurological examination was stable throughout the test occlusion period. Guglielmi detachable coil embolization of the left vertebral artery was then performed, sacrificing the artery at the level of the dissection. After the procedure was completed, no new neurological deficits occurred. On the second day after the procedure, the patient was discharged from the hospital. He was alert, oriented, and able to walk. CONCLUSION: We appreciate the value of preserving a parent vessel when a dissecting pseudoaneurysm of the intracranial vertebral artery ruptures in patients with inadequate collateral blood flow, in patients with disease involving the contralateral vertebral artery, or in patients with both. However, our case represents a cautionary note that patients treated in this fashion require close clinical follow-up. We suggest that parent vessel occlusion be considered the first option for treatment in patients who will tolerate sacrifice of the parent vessel along its diseased segment. In the future, covered stent technology may resolve this dilemma for many of these patients.
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10/15. Endovascular management of spontaneous bilateral symptomatic vertebral artery dissections.

    Extracranial vertebral artery (VA) dissection may lead to significant arterial stenosis, occlusion, or pseudoaneurysm formation with subsequent hemodynamic and embolic infarcts. To prevent thromboembolic complications, anticoagulation with intravenous heparin followed by oral warfarin has been recommended for all patients with acute dissections, regardless of the type of symptoms. Nevertheless, anticoagulation is not innocuous and may be associated with hemorrhagic transformation of a cerebral infarction or may be ineffective to prevent symptoms or dissection progression. We present a case of a bilateral spontaneous extracranial VA dissection presenting with multiple embolic infarctions. The dominant VA was reconstructed with multiple in-tandem stents and the contralateral VA, proved to be the source of emboli, was occluded with coils. Stent-assisted VA angioplasty has rarely been reported in the management of spontaneous dissections and appears to be a safe, effective and immediate method of restoring vessel lumen integrity and should be considered in the therapy of selected cases of VA dissection.
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