Open Heart Surgery Does Not Increase the Incidence of Ipsilateral Ischemic Stroke in Patients with Asymptomatic Severe Carotid Stenosis.

BACKGROUND AND PURPOSE: We evaluated the incidence of perioperative stroke following the institution's 2007 practice change of discontinuing combined carotid endarterectomy and open heart surgery (OHS) for patients with severe carotid stenosis. METHODS: In this retrospective cohort study, we compared 113 patients undergoing coronary artery bypass grafting, aortic valve replacement, or both from 2007 to 2011 with data collected from 2001 to 2006 from a similar group of patients. Our aim was to assess whether the practice change led to a greater incidence of stroke. RESULTS: A total of 7350 consecutive patients undergoing OHS during the specified time period were screened. Of these, 3030 had OHS between 2007 and 2011 but none were combined with carotid artery surgery (new cohort). The remaining 4320 had OHS before 2007 and 44 had combined procedures (old cohort). Of patients undergoing OHS during the 10-year period of observation, 230 had severe (>80%) carotid stenosis. In the old cohort (before 2007), carotid stenosis was associated with perioperative stroke in 2.5% of cases. None of the 113 patients having cardiac procedures after 2007 received combined carotid artery surgery; only 1 of these patients harboring severe carotid stenosis had an ischemic stroke (.9%) during the perioperative period. The difference in stroke incidence between the 2 cohorts was statistically significant (P = .002). CONCLUSION: The incidence of stroke in patients with severe carotid artery stenosis undergoing OHS was lower after combined surgery was discontinued. Combined carotid and OHS itself seems to be an important risk factor for stroke.

Spectrum and potential pathogenesis of reversible posterior leukoencephalopathy syndrome.

BACKGROUND: Controversy still exists over the etiology and pathophysiology of reversible posterior leukoencephalopathy syndrome (RPLS). This large single-center case series aims to describe the clinical and imaging features of RPLS in an attempt to deduce the etiology of the disorder and the mechanisms of brain injury. METHODS: A retrospective chart and imaging review was conducted on 59 cases of RPLS in 55 patients. RESULTS: Five RPLS imaging patterns were observed: posterior predominant (n = 40), anterior predominant (n = 7), diffuse lesion (n = 7), basal ganglia predominant (n = 3), and brainstem/cerebellum predominant patterns (n = 2). RPLS resulted in permanent neurologic deficits in 14 patients and death in 4 patients. Hypertension was seen in 57 (97%) cases, and mean arterial blood pressure exceeded 140 mm Hg in 30 (51%) cases. Follow-up magnetic resonance imaging scans revealed a significant worsening of vasogenic edema in 2 cases, both with persistent hypertension. Magnetic resonance imaging scans revealed areas of ischemia in 14 cases, all within or at areas closely adjacent to vasogenic edema. Diffuse vasculopathy was seen in 8 cases. There was a lack of correlation between the presence of vasculopathy and the degree of vasogenic edema (P = .62), but a correlation was suggested between ischemia and vasculopathy (P = .02). CONCLUSIONS: This study strongly suggests that hypertension-induced vasodilation rather than vasoconstriction-mediated hypoxia is likely the major mechanism responsible for the development of vasogenic edema, and that vasoconstriction may contribute to the development of ischemia in RPLS.

Sulcal artery syndrome after vertebral artery dissection.

Sulcal artery syndrome is a rare cause of spinal cord infarction. We describe a case of sulcal artery syndrome due to traumatic vertebral artery dissection and review the known literature on this rare syndrome.

Diagnosis and neuroimaging of acute stroke producing distal arm monoparesis.

Strokes which result in the isolated, pure motor weakness of an upper extremity are unusual and under-recognized cerebrovascular syndromes. Few reports in the literature describe the syndrome adequately or provide substantive clinical or anatomical correlation. Moreover, it may be misdiagnosed as a disorder of the peripheral nervous system because of the lack of pyramidal tract signs or the involvement of speech, the face, or lower limbs. We describe 35 patients who presented with sudden isolated pure motor weakness of an arm or hand caused by stroke, and provide clinical anatomic correlation of the lesion, stroke etiology, and outcome. Between December 1997 and November 2002, we prospectively identified 35 cases of distal arm monoparesis (DAMP) from among 4818 acute stroke and stroke related admissions to the Lehigh Valley Hospital. We included all patients with isolated weakness of one arm or hand unassociated with objective sensory, coordination, or language deficit, and no significant involvement of speech, the ipsilateral face, or leg. We examined clinical features, neuroimaging, etiology of stroke, and the prognosis of patients with the syndrome over a mean follow-up of 1.7 years. DAMP is an unusual form of cortical infarct which occurs in the parietal lobe or central sulcus region, comprising less than 1% of stroke cases. The infarcts are not caused by classical deep white matter lacunar infarctions, and are clearly delineated as superficial small cortical infarcts by magnetic resonance imaging (MRI)/diffusion-weighted imaging (DWI). Although the prognosis for recovery is uniformly good, the recurrent stroke risk was 14% over 1.7 year mean follow-up.

Posterior reversible encephalopathy syndrome: clinicoradiological spectrum and therapeutic strategies.

Posterior reversible encephalopathy syndrome (PRES) is a clinical syndrome of encephalopathy, headache, visual disturbance, and seizures. In most cases, symptoms present acutely or subacutely in the setting of accelerated hypertension, eclampsia, autoimmune disease, immunosuppressive treatment, or cancer chemotherapy. One essential feature of PRES is the presence of reversible cerebral vasogenic edema that has a predominantly posterior distribution on brain imaging. Atypical imaging features are commonly described, including involvement of the anterior brain or brainstem and the coexistence of ischemia or hemorrhage. In most cases, both clinical and radiological findings are reversible, although permanent imaging abnormalities and residual neurological sequelae can be seen in a minority of patients. The syndrome is thought to be caused by a breakdown of the blood-brain barrier and an extravasation of the intravascular fluid. Treatment of hypertension and seizures, and withdrawal of causative agents are the mainstays of therapy in PRES.

Thrombolytic therapy for ischemic stroke secondary to paradoxical embolism in pregnancy: a case report and literature review.

INTRODUCTION: Thrombolysis for acute ischemic stroke has been rarely administrated during pregnancy. Paradoxical embolism through a patent foramen ovale (PFO) or pulmonary arteriovenous malformation (AVM) is an identified risk factor for ischemic stroke. CASE REPORT: We report a 24-year-old woman at 11 weeks gestation who developed a sudden onset of dysarthria, hemiparesis, and hemisensory loss. She was diagnosed as having an ischemic stroke in the left middle cerebral artery (MCA) territory. She was treated with intra-arterial recombinant tissue plasminogen activator with subsequent resolution of her neurological deficits. Further workup revealed the presence of a PFO with a large right-to-left shunt. After being put on antithrombotic therapy, she presented again at 13 gestational weeks with a new ischemic infarction in the vertebrobasilar territory. Her PFO was closed percutaneously under ultrasonic guidance but the right-to-left shunt persisted. After a normal delivery, she was found to have a large pulmonary AVM which was successfully resected without complication. CONCLUSIONS: This report describes the successful usage of intra-arterial tissue plasminogen activator for acute ischemic stroke during early pregnancy. In patients with presumed paradoxical embolism, careful attention should be paid to rule out a coexistence of PFO and pulmonary AVM.

Cardiac surgery, carotid stenosis, and stroke prevention.

Stroke following cardiac surgery is a major source of morbidity and mortality. In patients undergoing cardiac surgery, the presence of severe carotid stenosis is associated with a higher incidence of postoperative stroke. Carotid revascularization procedures, such as carotid endarterectomy and stenting, are frequently performed under such circumstances in an effort to reduce the incidence of stroke. The available literature suggests that most postoperative strokes are not directly related to carotid stenosis. Synchronous carotid revascularization and cardiac surgery renders a higher risk of cardiovascular complications. In this article, we summarize the incidences of postoperative stroke and carotid stenosis in this population, discuss the pathogenesis of stroke in these patients, and propose strategies for managing patients undergoing cardiac surgery with severe carotid stenosis.

Strokes after cardiac surgery and relationship to carotid stenosis.

OBJECTIVE: To critically examine the role of significant carotid stenosis in the pathogenesis of postoperative stroke following cardiac operations. DESIGN: Retrospective cohort study. SETTING: Single tertiary care hospital. PARTICIPANTS: A total of 4335 patients undergoing coronary artery bypass grafting, aortic valve replacement, or both. MAIN OUTCOME MEASURES: Incidence, subtype, and arterial distribution of stroke. RESULTS: Clinically definite stroke was detected in 1.8% of patients undergoing cardiac operations during the same admission. Only 5.3% of these strokes were of the large-vessel type, and most strokes (76.3%) occurred without significant carotid stenosis. In 60.0% of cases, strokes identified via computed tomographic head scans were not confined to a single carotid artery territory. According to clinical data, in 94.7% of patients, stroke occurred without direct correlation to significant carotid stenosis. Undergoing combined carotid and cardiac operations increases the risk of postoperative stroke compared with patients with a similar degree of carotid stenosis but who underwent cardiac surgery alone (15.1% vs 0%; P = .004). CONCLUSIONS: There is no direct causal relationship between significant carotid stenosis and postoperative stroke in patients undergoing cardiac operations. Combining carotid and cardiac procedures is neither necessary nor effective in reducing postoperative stroke in patients with asymptomatic carotid stenosis.