Spontaneous Carotid Dissection Research Articles

A pain in the neck

Vertebral dissection is a leading cause of stroke in young adults (age 18–45 years), and accounts for up to 25 % of ischaemic strokes in this age group. Spontaneous vertebral and carotid dissections cause approximately 2 % of all strokes. Cerebral artery dissection can result in symptoms that vary from isolated headache to a complete hemiplegia providing a diagnostic challenge. Dissection can occur either spontaneously or more commonly as a result of trauma. Cervical dissection is also associated with systemic conditions that disturb the integrity of blood vessel walls and these should be excluded by careful investigation.

Multiple spontane Dissektionen der hirnversorgenden Arterien bei Ehlers-Danlos-artiger Bindegewebserkrankung Typ III mit atypischer klinischer Manifestation

We report on a patient with spontaneous bilateral dissections of the carotid arteries and dissections of the right vertebral and basilar artery who developed cerebral infarction in the bilateral capsula interna, basal ganglia and border zones following global hypoperfusion. The patient presented atypically with psychomotoric slowing. Headache was the only symptom leading to the diagnosis of spontaneous carotid dissections. Electron microscopy of a skin biopsy sample revealed an Ehlers-Danlos-like connective tissue disease Type III, although the patient showed no typical habitus with hyperextensible skin and hypermobile joints. Spontaneous dissection of cerebral arteries is a leading cause for cerebral infarction in young patients. They can present without ischaemic symptoms and should therefore be considered in patients with atypical symptoms. Even in patients without typical habitus, connective tissue disease can be the underlying aetiology. In our case, neurological symptoms progressed in spite of sufficient anticoagulation. Stent-assisted angioplasty could not be performed due to the anatomical situation of the carotid arteries. In general, however, stent-assisted angioplasty might be an option, if anticoagulation therapy fails to prevent progression of the disease.

Carotid artery dissection in an adult with the Simpson–Golabi–Behmel syndrome

We report on the case of a 44-year-old man affected with the Simpson-Golabi-Behmel syndrome (SGBS) (OMIM 312870) presenting with ischemic stroke due to a dissection of the right internal carotid. Molecular genetic analysis revealed the p.Gly556Arg mutation in exon 8 of the gene encoding glypican 3 (GPC3). This is the second case of a GPC3 missense mutation to be reported. The only risk factor found in this patient was carotid redundancy, a deformation that is significantly associated with spontaneous carotid dissection. The natural history of SGBS in adults is poorly known, and this case raises the question of a possible vascular risk associated with the disease.

Ultrasound Diagnosis of Spontaneous Carotid Dissection With Isolated Horner Syndrome

Isolated Horner syndrome without associated cranial nerve palsies or ischemic symptoms is an important presentation of spontaneous internal carotid artery dissection (sICAD). Ultrasound is often used as a screening method in these patients because cervical MRI is not always available on an emergency basis. Current knowledge on ultrasound findings in patients with sICAD presenting with isolated Horner syndrome is limited. Patients were recruited from prospective cervical artery dissection databases of 3 tertiary care centers. Diagnosis of sICAD was confirmed by cervical MRI and MR angiography or digital subtraction angiography in all patients. Data on Doppler sonography and color duplex sonography examinations performed within 30 days of symptom onset were analyzed. We identified 88 patients with Horner syndrome as the only sign of sICAD. Initial ultrasound examination was performed in 72 patients after a mean time interval from symptom onset to examination of 11 (SD 8) days. The overall frequency of false-negative ultrasound findings was 31% (22 of 72 patients). It showed stenosis >or=80% or occlusion in 34 (47%) patients, and stenosis <or=80% in 16 (22%). It visualized mural hematoma in 7 patients and intimal flap in one. Patients with normal ultrasound were less frequently smokers (9% versus 28%, P=0.034), and had less frequently migraine without aura (9% versus 43%, P=0.012) or neck pain (18% versus 62%, P=0.003) than those with pathological ultrasound findings. Nearly one third of patients with Horner syndrome as the only sign of sICAD presented with normal ultrasound findings. These results indicate that ultrasound is not a reliable method to diagnose sICAD in patients with isolated Horner syndrome.

Spontaneous Dissection of the Carotid and Vertebral Arteries: the 10-year UCSD Experience

The etiology of spontaneous dissection of the carotid and vertebral arteries without antecedent trauma remains unclear. The goal of this 10-year review was to examine factors regarding presentation, diagnosis, treatment, and outcome for all patients at our institution who were diagnosed with spontaneous carotid dissections (SCD) or spontaneous vertebral dissections (SVD) with no prior trauma history. A retrospective chart analysis was performed involving all discharges from UCSD Medical Center from 1995 to 2005. Patients were selected for inclusion based on the diagnosis of carotid or vertebral dissection with no associated traumatic or iatrogenic cause for their presentation. Characteristics of these patients' medical risk factors, presenting symptoms, diagnostic method and time, treatment, and outcomes were analyzed. A total of 20 patients (10 male, age 44.8 +/- 12.9 yrs; 10 female, age 39.6 +/- 14.9 yrs) were included for study. These patients represented 12 cases of SCD and nine SVD. On presentation, a majority of patients with both SVD and SCD reported headache as their primary complaint while a significantly higher rate of nausea (25% vs. 67%, p < 0.01) was reported in SVD. SVD was associated with a significantly longer diagnostic time (11 hr vs. 16 hr, p < 0.01). The most commonly performed diagnostic exam in both SCD and SVD was magnetic resonance angiography (MRA). Anticoagulation was the primary treatment in 11 of 12 SCD and all nine SVD. One patient with persistent, symptomatic bilateral carotid dissection after anticoagulation was treated with stent placement resulting in unilateral intracranial hemorrhage (ICH). Length of stay was significantly longer in SVD (5 d vs. 7 d, p < 0.02). A significantly higher incidence of persistent neurologic deficits on discharge was seen in SCD (71% vs. 33%, p < 0.02). Radiographic evidence of cerebral infarction on discharge had a stronger correlation with clinical deficits in SCD. Although there were only two cases, those treated with endovascular therapy in the setting of SCD suffered complications related to the intervention. On discharge, there did not seem to be a correlation between persistent neurologic deficits and radiographic evidence of infarction in SVD reflecting that recovery after these episodes may not be predictable based on the appearance of the infarction.

Commentary

BACKGROUNDAngioplasty and stenting of various lesions of the carotid artery is gaining in popularity. Our knowledge of the efficacy and limitations of this promising technology is incomplete. Although Horner’s syndrome and its variants have been described after traumatic, spontaneous, or surgical carotid dissection, it has not been reported after carotid artery stenting.CASE DESCRIPTIONA 36-year-old woman presented with left neck and ear pain and a 3-year history of rushing noises in her left ear. Angiography demonstrated evidence of dissection of the left internal carotid artery at the skull base with a pseudoaneurysm.The pseudoaneurysm was treated with a 6-mm diameter self-expanding stent in a 4-mm diameter left internal carotid artery. A few hours later, she developed partial Horner’s syndrome with a subtle ipsilateral ptosis and miosis without anhidrosis. Angiography performed on the next day did not demonstrate further dissection or aneurysm growth but did show distention of the artery wall because of the stent. She did not develop any further sequelae.CONCLUSIONThis case suggests that stretching of the artery wall may result in stretching of surrounding structures. The sympathetic fibers surrounding the internal carotid artery are clearly sensitive to this degree of stretch. Possible complications associated with stretch injury must be considered when choosing the stent diameter.

Accuracy of colored duplex ultrasound diagnosis of spontaneous carotid dissection cause and ischemia

Conclusion: Color duplex ultrasound has high sensitivity and specificity for diagnosis of spontaneous internal carotid artery dissection that causes neurologic symptoms. Summary: Carotid duplex ultrasound is frequently used in evaluation of patients with possible carotid artery dissection. The authors sought to determine the overall accuracy of color duplex ultrasound to diagnose spontaneous internal carotid artery dissection in patients with a first episode of carotid distribution ischemia. Patients with a first episode of carotid territory stroke, transient ischemic attack, or retinal ischemia underwent an electrocardiogram (ECG), color duplex ultrasound of the cervical carotid arteries, and clinical and hematologic examinations. Brain computed tomography (CT) scanning was performed in individuals with stroke or transient ischemic attacks, and echocardiography and 24-hour ECG monitoring were used in selective cases. Patients were included if they were <65 years, color duplex ultrasound showed a probable internal carotid artery dissection (stenosed or occluded internal carotid artery), or they had no determined etiology of cerebral ischemia. Included patients also underwent cervical magnetic resonance imaging (MRI) and MR angiography (MRA) and possibly cerebral catheter angiography as well. Those who performed the color duplex ultrasound studies were blinded to the results of the MRI and angiographic studies. The study screened 1652 patients, and 177 were included. Of the 1475 excluded patients, 818 were >65 years, 1081 had another cause of carotid artery ischemia, and 58 had intercranial hemorrhage. Internal carotid artery dissection was diagnosed by carotid duplex ultrasound in 77 of the 177 patients. The etiology of ischemia was undetermined in the remaining 100 patients. Cervical MRI and MRA indicated 74 of the 177 patients had spontaneous internal carotid artery dissection. There were three false-negative and six false-positive color duplex ultrasound examinations. Therefore, sensitivity, specificity, positive, and negative predictive values for diagnosis of spontaneous internal carotid artery dissection using carotid artery duplex ultrasound in patients with carotid territory ischemic symptoms were 96%, 94%, 92%, and 97%, respectively. Comment: The very high negative predictive value for excluding spontaneous carotid artery dissection with color duplex ultrasound essentially allows withholding of treatment for internal carotid artery dissection in patients in which that diagnosis is suspected but in whom the duplex ultrasound shows no evidence of dissection. Positive predictive value is also excellent, but because such patients will be treated with anticoagulation, or perhaps other interventions, patients in whom internal carotid artery dissection is diagnosed by duplex should have a confirmatory study before treatment is initiated.

Accuracy of colored duplex ultrasound diagnosis of spontaneous carotid dissection cause and ischemia

Background and Purpose—Spontaneous dissection of the cervical internal carotid artery (sICAD) is mainly assessed with MRI and magnetic resonance angiography (MRA), which are not always at hand. In contrast, color duplex sonography (CDS) is readily available. We undertook this prospective study to examine the accuracy of CDS to diagnose sICAD in patients with first carotid territory ischemia. Methods—Consecutive patients with first carotid territory stroke or transient ischemic attack or retinal ischemia underwent clinical and laboratory examinations, ECG, CDS of the cerebral arteries, cranial computed tomography in case of stroke or transient ischemic attack, and echocardiography and 24-hour ECG in selected cases. Patients were included, if they were 65 years of age, CDS showed a probable sICAD (cervical internal carotid artery stenosed or occluded), or had no determined etiology of ischemia. All of the included patients underwent cervical MRI and MRA cerebral catheter angiography. The sonographer was blinded to the results of MRI and angiography studies. Results—We included 177 of 1652 screened patients. Excluded patients (n 1475) were 65 years old (n 818), had another determined cause of ischemia (n 1475), and had intracranial hemorrhage (n 58). CDS diagnosed sICAD in 77 of 177 patients, and the etiology of ischemia was undetermined in the remaining 100 patients. Cervical MRI and angiography showed 74 sICAD; there were 6 falsely positive and 3 falsely negative CDS findings. Thus, sensitivity, specificity, and positive and negative predictive values for CDS diagnosis of patients with sICAD causing carotid territory ischemia was 96%, 94%, 92%, and 97%, respectively. Conclusions—Color duplex ultrasound allows the reliable exclusion of sICAD in patients with carotid territory ischemia, whereas diagnosis of CDS of sICAD must be confirmed with cervical MRI and MRA. (Stroke. 2006;37:000-000.)

Acute Therapy and Prevention of Stroke in Spontaneous Carotid Dissection

No randomized and controlled study has evaluated acute stroke therapy and antithrombotic agents for stroke prevention in patients with spontaneous cervical artery dissection (CAD). CAD was not a contraindication for including cases with acute ischemic stroke in trials evaluating systemic fibrinolysis with recombinant tissue plasminogen activator (rt-PA). Small case series have reported successful systemic and local intra-arterial thombolysis without clinical signs of rupture of the dissected vessel. Thus, thrombolysis seems to be a therapeutic option in acute CAD causing ischemic stroke, although it remains unclear whether rt-PA increases the obstruction of the dissected vessel by enlarging the wall hematoma or diminishes the obstruction by enhancing the recanalization of the thrombus adhering to the dissection. Meta-analyses have shown no benefit of anticoagulation compared to aspirin in stroke prevention of patients with CAD. It is also unclear, whether long-term antithrombotic therapy is necessary. Many centers and ours maintain the antithrombotic therapy for 3 to 6 months. Dissections of the internal carotid artery (ICAD) have a benign long-term prognosis with low stroke rates that are not related to the persistence of severe carotid stenosis or occlusion. These results suggest that surgical or endovascular therapy of ICA stenosis or occlusion related to ICAD should only be taken into consideration in the very rare patients with stroke recurrence in spite of an optimal medical treatment. Cervical aneurysms caused by CAD have an excellent long-term outcome with a low stroke risk, and no vessel rupture has been reported. Thus, surgical or endovascular therapy should be restricted to the very rare cases developing ischemic symptoms in the vascular territory supplied by the dissected aneurysm in spite of antithrombotic therapy.

Aneurysms of the Carotid Artery

Carotid artery aneurysms are an uncommon but important problem. The available data suggests that, untreated, these aneurysms lead to neurologic symptoms from embolization. Pseudoaneurysms of the carotid artery result from injury or may be the long-term sequelae of a spontaneous carotid dissection. While open surgery has been the primary mode of treatment, these aneurysms are being treated more commonly with endovascular approaches. This trend is partly the result of the increasing experience with the endovascular treatment of carotid artery stenosis. The endovascular approach offers advantages in other situations where open access to the distal extent of the aneurysm is difficult or neck radiation leads to concerns about wound healing. This article outlines the etiology, new diagnostic modalities, and treatment of aneurysms of the carotid artery.

Invited commentary

Drs Edgell, Abou-Chebl, and Yadav report a small but fascinating series of seven patients undergoing carotid stenting for the management of complications of spontaneous carotid dissection. With their experience and meticulous technique, the authors have achieved excellent results in patients facing potentially devastating strokes. The article should be read carefully. The authors are not reporting the use of stenting in all, or even in most, cases of spontaneous dissection. In their experience only 7 (5%) of approximately 135 patients presenting with spontaneous dissection were selected for intervention. In fact, the title of the article is misleading. The authors are not reporting on the endovascular management of spontaneous carotid dissection, but rather on the endovascular management of complications of spontaneous carotid dissection. It is generally accepted, and the authors re-emphasize, that 85% to 90% of patients with spontaneous dissection recover very well with medical management alone. Furthermore, in most cases, arterial recanalization and remodeling occur after dissection with restoration of a reasonable luminal diameter. Recurrent dissection is unusual, and the overall prognosis usually quite good. The small subset of patients selected for stenting in this series included those with expanding or symptomatic pseudoaneurysms or with severe flow compromise due to multivessel involvement. Other scenarios in which intervention seems reasonable include ongoing symptoms despite anticoagulation and contraindication to anticoagulation. Although this article addresses only patients with complications of spontaneous dissection, it provokes two significant questions. First, what is the role of stenting in patients who present with traumatic carotid dissection? In these patients, neurologic deficits may occur after an asymptomatic period of several hours or even days, and anticoagulation is often contraindicated. Should stenting be used early in these patients to prevent delayed neurologic sequelae and lessen concern over anticoagulation? Second, should we consider changing the default algorithm in the management of uncomplicated spontaneous dissection? The authors’ results are so good in very compromised patients that it is tempting to think that stenting for uncomplicated dissection might result in an improvement over the 85% to 90% favorable results with traditional medical therapy. Obviously, only a randomized prospective trial can properly answer this question. Although they reported only on the management of complicated spontaneous carotid dissections, the authors have demonstrated in very high-risk patients the potential of a new treatment for carotid dissection that calls into question our current management paradigm for lower-risk patients. Aggressive early stenting of traumatic and spontaneous carotid dissections now warrants careful study.

Progressive Symptomatic Carotid Dissection Treated With Multiple Stents

Internal carotid artery (ICA) dissection remains a major cause of stroke in the young. Although systemic anticoagulation and antiplatelet therapy allow healing of the dissection in most patients, medical treatment can fail or be contraindicated. In selected cases of carotid dissections, the use of endovascular stent-assisted angioplasty has been reported to permit reconstruction of the extracranial ICA. We report a case of symptomatic spontaneous carotid dissection which progressively extended from the cervical to the supraclinoid segments of the ICA in a 48-year-old patient under anticoagulant therapy. Because of failed medical therapy and further transient ischemic attacks (TIAs), the patient was treated by 5 tandem stents deployed in an overlapping fashion from the terminal ICA to the cervical segment. Postprocedure angiography demonstrated reconstitution of the luminal diameter of the ICA. The patient progressively improved and no further TIAs were observed. At 8-month follow-up, the vessel remained patent with a slight intra-extracranial reduction in size suggesting myointimal hyperplasia. Neurological exam was normal. The successful angiographic and clinical results observed in our case of intra-extracranial stenting of a long dissection contributes to the literature of carotid dissection treated with multiple stents. The excellent mid-term follow-up in our patient confirms the efficacy of this treatment and good tolerance to multiple stents. To our knowledge this is the first case of spontaneous dissection treated with stenting including the distal supraclinoid segment, through an extensive proximally dissected artery.

IV thrombolysis in patients with acute stroke due to spontaneous carotid dissection

The authors reviewed the histories of 33 patients (ages 44 to 50 years) treated with IV thrombolysis for acute stroke due to spontaneous cervical carotid artery dissection. Median NIH Stroke Scale (NIHSS) score on admission was 15. No new or worsened local signs, subarachnoid hemorrhage, pseudoaneurysm formation, or rupture of the cervical ICA were observed. At 3 months, median NIHSS was 7 and median modified Rankin Scale (mRS) 2.5; mRS < or = 2 was observed in 17 patients.

Upper cranial nerve palsy resulting from spontaneous carotid dissection

Upper cranial nerve palsy has a variety of causes such as cerebral and nerve ischemia, diabetes, infectious and non-infectious meningitis, subarachnoid hemorrhage and intracranial aneurysm. CASE 1 : A 45-year-old man suffered from holocephalic headaches and a right-sided neck pain for two weeks. He presented to our emergency department because of a sudden ptosis of the right eye. On admission neurological examination revealed a right sided Horner's syndrome and hypesthesia of the right side of the face. Magnetic resonance angiography identified a circumscribed dissection of the right extracranial internal carotid artery originating from the carotid bifurcation. Conventional angiography 2 weeks later showed a nearly recanalized artery. CASE 2 : A 55-year-old previously healthy man without cardiovascular risk factors developed right sided neck pain when loading a seeder with several sacks of crop. A few hours later he noticed a left-sided weakness. On admission a severe left sided hemiparesis and a mild neglect were present. Duplex sonography revealed a right-sided distal internal carotid artery (ICA) occlusion. The next morning the patient complained of double vision; he had a right-sided pupil-sparing oculomotor palsy. The diagnosis of ICA dissection was confirmed by conventional angiography, at that time showing a partially recanalized ICA without involvement of the cavernous region by the dissection. ICA dissection must be included in the differential diagnosis of upper cranial nerve palsy and should be assessed by duplex ultrasound and magnetic resonance imaging. A possible explanation is nerve ischemia due to a transient or permanent interruption of the blood supply by compression of the vasa nervorum originating from the intracranial carotid artery.

Mechanism of ischemic infarct in spontaneous carotid dissection.

It is unclear whether stroke in patients with spontaneous dissection of the cervical internal carotid artery (ICAD) is due to thromboembolism or impaired hemodynamics. This study investigated the mechanism of stroke in ICAD by examining brain imaging and cerebrovascular findings of such patients. We retrospectively evaluated the prospectively collected brain CT, MR, and ultrasound findings of 141 consecutive patients with 143 ICADs causing ischemic stroke. Eleven patients were not included because they had an inappropriate temporal bone window (n=6) or were treated with thrombolysis (n=5). Thus, the data of 130 patients (76 men, 54 women) with 131 ICADs were analyzed. All patients had territorial infarcts; 6 patients (5%) also had border-zone infarct patterns. Territorial infarcts affected the middle cerebral artery (MCA) in 130 of 131 cases (99%) and the anterior cerebral artery (ACA) in 1 case (1%). Additional vascular territories were affected in 8 patients with MCA infarcts (ACA, n=5 [4%]; posterior cerebral artery, n=3 [2%]). The pattern (hemodynamic versus thromboembolic) and extent of infarction were not influenced by vascular findings (MCA stenosis or occlusion, ACA occlusion, degree of obstruction in the dissected ICA, pattern of cross-flow in 115 patients with >80% ICA stenosis or occlusion). This study suggests that thromboembolism, not hemodynamic infarction, is the essential stroke mechanism in ICAD.

Ceguera secundaria a neuropatía óptica isquémica por una disección carotídea espontánea: Caso clínico

In young and middle age subjects, spontaneous carotid dissection is an increasingly recognized cause of ischemic stroke. Their usual presentation is facial pain with a Horner syndrome and a contra lateral paresis. Blindness has been reported as a presenting symptom in only a few cases. We report a 50 years old man who presented with amblyopia in the left eye, without periocular pain. Fundoscopy showed papilledema and a peripapillar hemorrhage, compatible with an ischemic optic neuropathy. A magnetic resonance angiography confirmed a left carotid dissection.

Spontaneous carotid dissection presenting lower cranial nerve palsies

Cranial nerve palsy in internal carotid artery (ICA) dissection occurs in 3–12% of all patients, but in 3% of these a syndrome of hemicranias and ipsilateral cranial nerve palsy is the sole manifestation of ICA dissection, and in 0.5% of cases there is only cranial nerve palsy without headache. We present two cases of lower cranial nerve palsy. The first patient, a 49-year-old woman, developed left eleventh and twelfth cranial nerve palsies and ipsilateral neck pain. The angio-RM showed an ICA dissection with stenosis of 50%, beginning about 2 cm before the carotid channel. The patient was treated with oral anticoagulant therapy and gradually improved, until complete clinical recovery. The second patient, a 38-year-old woman, presented right hemiparesis and neck pain. The left ICA dissection, beginning 2 cm distal to the bulb, was shown by ultrasound scanning of the carotid and confirmed by MR angiogram and angiography with lumen stenosis of 90%. Following hospitalisation, 20 days from the onset of symptoms, paresis of the left trapezius and sternocleidomastoideus muscles became evident. The patient was treated with oral anticoagulant therapy and only a slight right arm paresis was present at 10 months follow-up. Cranial nerve palsy is not rare in ICA dissection, and the lower cranial nerve palsies in various combinations constitute the main syndrome, but in most cases these are present with the motor or sensory deficit due to cerebral ischemia, along with headache or Horner’s syndrome. In the diagnosis of the first case, there was further difficulty because the cranial nerve palsy was isolated without hemiparesis, and the second case presented a rare association of hemiparesis and palsy of the eleventh cranial nerve alone. Compression or stretching of the nerve by the expanded artery may explain the palsies, but an alternative cause is also possible, namely the interruption of the nutrient vessels supplying the nerve, which in our patients is more likely.

Horner’s syndrome after carotid artery stenting:: Case report

BACKGROUND Angioplasty and stenting of various lesions of the carotid artery is gaining in popularity. Our knowledge of the efficacy and limitations of this promising technology is incomplete. Although Horner’s syndrome and its variants have been described after traumatic, spontaneous, or surgical carotid dissection, it has not been reported after carotid artery stenting. CASE DESCRIPTION A 36-year-old woman presented with left neck and ear pain and a 3-year history of rushing noises in her left ear. Angiography demonstrated evidence of dissection of the left internal carotid artery at the skull base with a pseudoaneurysm. The pseudoaneurysm was treated with a 6-mm diameter self-expanding stent in a 4-mm diameter left internal carotid artery. A few hours later, she developed partial Horner’s syndrome with a subtle ipsilateral ptosis and miosis without anhidrosis. Angiography performed on the next day did not demonstrate further dissection or aneurysm growth but did show distention of the artery wall because of the stent. She did not develop any further sequelae. CONCLUSION This case suggests that stretching of the artery wall may result in stretching of surrounding structures. The sympathetic fibers surrounding the internal carotid artery are clearly sensitive to this degree of stretch. Possible complications associated with stretch injury must be considered when choosing the stent diameter.

Intraoperative stenting of the internal carotid artery after unsuccessful eversion endarterectomy

Stenting Of The Internal Carotid Artery (ICA) Has Been Shown To Be Feasible In Atherosclerotic Lesions, In Restenosis After Carotid Endarterectomy, And In Spontaneous Carotid Dissections. To Correct An Intimal Flap That Detached Distal Occlusion Of The Ica After Eversion Carotid Endarterectomy, As Shown With Intraoperative Completion Angiography, We Successfully Used Stenting Of The Ica With A Self-EXPANDABLE Stainless Steel Stent Placed During Surgery Through The Common Carotid Artery. (J Vasc Surg 1999;30:355-6.)

A strangled wife

neurointerventional unit for cervical and cerebral angiography. She had been seen at another hospital 3 weeks earlier with sudden onset of weakness of her left arm. She had been treated for hypertension and hyperthyroidism. Upon arrival she was awake, alert, and oriented, with normal cognition and speech. The function of her cranial nerves was intact with no signs of Horner’s syndrome. Motor examination showed left pronator drift, decreased left hand and arm strength, and poor rapid finger movements. Sensory examination was normal to all modalities. Auscultation revealed a carotid bruit on the left side. A computed tomograph scan showed right middle frontal and opercular gyrus infarcts (figure, A). Carotid angiography showed bilateral symmetrical stenoses of the internal carotid arteries at the level of C2–C3 (figure, B, C). There was no evidence of atherosclerosis. A filling defect suggestive of an embolus was shown in the ascending frontal branch of the right middle cerebral artery. Renal angiography showed no evidence of fibromuscular dysplasia. The angiographic appearances of the carotid lesions were consistent with healed spontaneous or traumatic carotid dissections.