Eagle syndrome: A case report of stylocarotid syndrome with internal carotid artery dissection.

Eagle syndrome is defined by an elongated styloid process or a calcified stylohyoid ligament that impinges on surrounding structures and causes a variety of symptoms. Classically, Eagle syndrome presents as neck, throat, or ear pain. The vascular variant, stylocarotid syndrome, can present as headache, transient ischemic attack, or stroke. Carotid artery dissection is a rare complication of stylocarotid syndrome. We report a case of stylocarotid syndrome in a 60-year-old man who presented with a right internal carotid artery (ICA) dissection and focal neurological deficits. Computed tomography with three-dimensional reformatting was used in the evaluation of his pathology. His dissecting right ICA was stented with subsequent symptom resolution. Improved recognition of the relationship between an elongated styloid or calcified stylohyoid ligament and symptomatology may lead to optimal etiology recognition and directed treatment.

Expanding Endovascular Therapy of Very Small Ruptured Aneurysms with the 1.5-mm Coil.

BACKGROUND: Very small ruptured aneurysms (≤3 mm) demonstrate a significant risk for procedural rupture with endovascular therapy. Since 2007, 1.5-mm-diameter coils have been available (Micrus, Microvention, and ev3), allowing neurointerventionalists the opportunity to offer patients with very small aneurysms endovascular treatment. In this study, we review the clinical and angiographic outcome of patients with very small ruptured aneurysms treated with the 1.5-mm coil. METHODS: This is a retrospective cohort study in which we examined consecutive ruptured very small aneurysms treated with coil embolization at a single institution. The longest linear aneurysm was recorded, even if the first coil was sized to a smaller transverse diameter. Very small aneurysms were defined as ≤3 mm. Descriptive results are presented. RESULTS: From July 2007 to March 2015, 81 aneurysms were treated acutely with coils in 78 patients presenting with subarachnoid hemorrhage. There were 5 patients with 3-mm aneurysms, of which the transverse diameter was ≤2 mm in 3 patients. In all 5 patients, a balloon was placed for hemostatic prophylaxis in case of rupture, and a single 1.5-mm coil was inserted for aneurysm treatment without complication. Complete aneurysm occlusion was achieved in 1 patient, residual neck in 2, and residual aneurysm in 2 patients. Aneurysm recanalization was present in 2 patients with an anterior communicating artery aneurysm; a recoiling attempt was unsuccessful in 1 of these 2 patients due to inadvertent displacement and distal coil embolization, but subsequent surgical clipping was successful. Another patient was retreated by surgical clipping for a residual wide-neck carotid terminus aneurysm. One patient died of ventriculitis 3 weeks after presentation; all 4 other patients had an excellent outcome with no rebleed at follow-up (mean 21 months, range 1-62). CONCLUSION: The advent of the 1.5-mm coil may be used in the endovascular treatment of patients with very small ruptured aneurysms, providing a temporary protection to the site of rupture in the acute phase. If necessary, bridging with elective clipping may provide definitive aneurysm treatment.

The safety of anticoagulation in patients with intracranial aneurysms.

BACKGROUND AND PURPOSE: Little is known about the safety of long-term anticoagulation in patients with unruptured saccular intracranial aneurysms, although case reports of anticoagulation in patients with fusiform and saccular aneurysms have been published. The goal of this study was to estimate the rate of subarachnoid hemorrhage (SAH) due to aneurysm rupture in patients with intracranial saccular aneurysms receiving therapeutic doses of anticoagulation. METHODS: This was a retrospective case series of patients with intradural aneurysms receiving therapeutic doses of anticoagulation (defined as a dose that achieves a target INR >2.0 or the equivalent dose of another anticoagulant). The primary outcome was SAH due to aneurysm rupture while receiving anticoagulation treatment. The rate of SAH due to aneurysm rupture was calculated among patients with aneurysms documented on imaging. RESULTS: 42 patients with 48 intradural aneurysms on anticoagulation were identified. Their mean age was 67 years (range 40-83) and 28 (67%) were women. The mean aneurysm size was 5.1±3.6 mm and 40 (83%) aneurysms were in the anterior circulation. The mean±SD follow-up was 495±749 days per patient. Twelve patients had their aneurysms coiled, clipped or surgically wrapped before the period of anticoagulation. Three patients had clipping or coiling of their aneurysms during the period of anticoagulation. Six patients had a history of aneurysm rupture prior to anticoagulation, of which two were treated by coiling and four by clipping. Among the 48 aneurysms, 32 were never coiled or clipped prior to anticoagulation. No anticoagulated patients with known aneurysms developed SAH during 57 patient-years of follow-up. The patients with untreated aneurysms had 31 patient-years of follow-up and those who underwent clipping, coiling or surgical wrapping of their aneurysms had 26 patient-years of follow-up while receiving anticoagulation (for a combined total of 57 years of follow up). CONCLUSIONS: The risk of aneurysm rupture is not increased in patients receiving systemic anticoagulation. However, these results should be interpreted with caution given the small sample size in this study and the need for a prospective study to confirm these findings.

Periprocedural management of acute ischemic stroke intervention.

Periprocedural medical management is an important aspect in optimizing the outcome of patients who undergo endovascular treatment for acute ischemic stroke. Blood pressure, fluid hydration, and antithrombotics are some of the elements that need to be tailored carefully to the patient according to the patency of his or her cerebral vasculature, the extent of his or her infarct, and the potential for hemorrhagic transformation. This article reviews the medical care of acute stroke patients before and after endovascular therapy.

Treatment of high risk symptomatic intracranial atherosclerosis with balloon mounted coronary stents and Wingspan stents: single center experience over a 10 year period.

BACKGROUND: Stenting of symptomatic intracranial atherosclerosis remains under investigation, yet this option to potentially avert subsequent stroke has been offered at select centers under humanitarian device exemption and off-label use for several years. METHODS: Retrospective case series of consecutive patients undergoing stenting with Wingspan and balloon mounted coronary stents for symptomatic intracranial atherosclerosis at a single institution. Recurrent symptomatic ischemia in the territory of the stented artery was ascertained. Rates of recurrent ischemic stroke were calculated per patient-year of follow-up and were compared with medically treated patients in the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial. RESULTS: During the 10 year study period, 41 cases of intracranial stenting were identified. Stenoses were severe (>70%) in 88% of patients. Stenting procedures occurred a median of 14 days from the most recent symptomatic event. 19 Wingspan stents and 22 balloon mounted coronary stents were deployed. Four strokes occurred within 24 h of stenting, seven within 1 month and eight within 3 months. By 3 months after stenting, no further strokes occurred during up to 2 years of follow-up. Patients had 0.194 ischemic strokes per person-year of follow-up, compared with 0.083 ischemic strokes per person-year of follow-up in the aspirin arm of WASID and 0.065 ischemic strokes per person-year of follow-up in the warfarin arm of WASID. CONCLUSIONS: Stenting of symptomatic intracranial atherosclerosis in a high risk subset of cases with advanced degree of luminal stenosis may be associated with an increased early risk of recurrent ischemic stroke.

Asymmetric posterior reversible encephalopathy syndrome complicating hemodynamic augmentation for subarachnoid hemorrhage-associated cerebral vasospasm.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) is a rare complication of hemodynamic augmentation for subarachnoid hemorrhage (SAH)-associated vasospasm. The roles of hyperperfusion and hypoperfusion in the genesis of PRES remain uncertain. METHODS: Case report. RESULTS: We admitted a 35-year-old woman with Hunt & Hess grade II SAH secondary to rupture of a right middle cerebral artery (MCA) aneurysm. This was surgically clipped. Beginning on hospital day 3, she developed recurrent symptomatic vasospasm of the right MCA despite hemodynamic augmentation to a MAP as high as 130 mmHg and endovascular therapy. On hospital day 7, after 36 h of sustained MAP 120-130 mmHg, her level of arousal progressively declined, culminating in stupor and two generalized tonic-clonic seizures. MRI showed widespread, yet markedly asymmetric changes consistent with PRES largely sparing the right MCA territory. After the MAP was decreased to 85-100 mmHg, she had no further seizures. 2 days later she was fully alert with mild left hemiparesis. CONCLUSIONS: PRES is a rare complication of hemodynamic augmentation that should be considered in the differential diagnosis of delayed neurological decline in patients with aneurysmal SAH-associated cerebral vasospasm. The markedly asymmetric distribution of PRES lesions with sparing of the territory affected by vasospasm supports the hypothesis that hyperperfusion underlies the pathophysiology of this disorder.

HDL-C and LDL-C: their role in stroke pathogenesis and implications for treatment.

Elevated serum low-density lipoprotein cholesterol (LDL-C) and low serum high-density lipoprotein cholesterol (HDL-C) are risk factors for atherosclerotic ischemic stroke. The National Cholesterol Education Panel and the American Heart Association have released guidelines for the treatment of dyslipidemia that stress LDL-C reduction using HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors (statins) and are applicable to individuals who have had or are at a high risk of having a stroke. Treatment of low HDL-C is a secondary goal of these guidelines and can be best achieved by using extended-release niacin (alone or in combination with statins) and fibrates. Early and aggressive treatment of dyslipidemia is an important component of a multimodality approach to stroke prevention.