Carotid Occlusion (carotid + occlusion)

Distribution by Scientific Domains


Selected Abstracts


Models of white matter injury: Comparison of infectious, hypoxic-ischemic, and excitotoxic insults

DEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 1 2002
Henrik Hagberg
Abstract White matter damage (WMD) in preterm neonates is strongly associated with adverse outcome. The etiology of white matter injury is not known but clinical data suggest that ischemia-reperfusion and/or infection-inflammation are important factors. Furthermore, antenatal infection seems to be an important risk factor for brain injury in term infants. In order to explore the pathophysiological mechanisms of WMD and to better understand how infectious agents may affect the vulnerability of the immature brain to injury, numerous novel animal models have been developed over the past decade. WMD can be induced by antenatal or postnatal administration of microbes (E. coli or Gardnerella vaginalis), virus (border disease virus) or bacterial products (lipopolysaccharide, LPS). Alternatively, various hypoperfusion paradigms or administration of excitatory amino acid receptor agonists (excitotoxicity models) can be used. Irrespective of which insult is utilized, the maturational age of the CNS and choice of species seem critical. Generally, lesions with similarity to human WMD, with respect to distribution and morphological characteristics, are easier to induce in gyrencephalic species (rabbits, dogs, cats and sheep) than in rodents. Recently, however, models have been developed in rats (PND 1,7), using either bilateral carotid occlusion or combined hypoxia-ischemia, that produce predominantly white matter lesions. LPS is the infectious agent most often used to produce WMD in immature dogs, cats, or fetal sheep. The mechanism whereby LPS induces brain injury is not completely understood but involves activation of toll-like receptor 4 on immune cells with initiation of a generalized inflammatory response resulting in systemic hypoglycemia, perturbation of coagulation, cerebral hypoperfusion, and activation of inflammatory cells in the CNS. LPS and umbilical cord occlusion both produce WMD with quite similar distribution in 65% gestational sheep. The morphological appearance is different, however, with a more pronounced infiltration of inflammatory cells into the brain and focal microglia/macrophage ("inflammatory WMD") in response to LPS compared to hypoperfusion evoking a more diffuse microglial response usually devoid of cellular infiltrates ("ischemic WMD"). Furthermore, low doses of LPS that by themselves have no adverse effects in 7-day-old rats (maturation corresponding to the near term human fetus), dramatically increase brain injury to a subsequent hypoxic-ischemic challenge, implicating that bacterial products can sensitize the immature CNS. Contrary to this finding, other bacterial agents like lipoteichoic acid were recently shown to induce tolerance of the immature brain suggesting that the innate immune system may respond differently to various ligands, which needs to be further explored. MRDD Research Reviews 2002;8:30,38. © 2002 Wiley-Liss, Inc. [source]


Intracerebral large artery disease in Aicardi,Goutières syndrome implicates SAMHD1 in vascular homeostasis

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 8 2010
VENKATESWARAN RAMESH
Aim, To describe a spectrum of intracerebral large artery disease in Aicardi,Goutières syndrome (AGS) associated with mutations in the AGS5 gene SAMHD1. Method, We used clinical and radiological description and molecular analysis. Results, Five individuals (three males, two females) were identified as having biallelic mutations in SAMHD1 and a cerebral arteriopathy in association with peripheral vessel involvement resulting in chilblains and ischaemic ulceration. The cerebral vasculopathy was primarily occlusive in three patients (with terminal carotid occlusion and basal collaterals reminiscent of moyamoya syndrome) and aneurysmal in two. Three of the five patients experienced intracerebral haemorrhage, which was fatal in two individuals. Post-mortem examination of one patient suggested that the arteriopathy was inflammatory in origin. Interpretation, Mutations in SAMHD1 are associated with a cerebral vasculopathy which is likely to have an inflammatory aetiology. A similar disease has not been observed in patients with mutations in AGS1 to AGS4, suggesting a particular role for SAMHD1 in vascular homeostasis. Our report raises important questions about the management of patients with mutations in SAMHD1. [source]


Long-term follow-up of patients with asymptomatic occlusion of the internal carotid artery with good and impaired cerebral vasomotor reactivity

EUROPEAN JOURNAL OF NEUROLOGY, Issue 10 2010
I. Kimiagar
Background:, Cerebral hemodynamic status might be prognostic for either the symptomatic or asymptomatic course of carotid occlusive disease. It is determined by evaluating cerebral vasomotor reactivity (VMR). We assessed VMR in asymptomatic patients with total occlusion of the internal carotid artery (ICA) and followed them to evaluate the role of impaired VMR in predicting ischaemic stroke (IS). Methods:, Thirty-five patients (21 men, mean age ± SD 68 ± 7.5 years) with unilateral asymptomatic ICA occlusion were studied by transcranial Doppler and the Diamox test (intravenous 1.0 g acetazolamide) and followed for 48 months or until reaching the end-points of IS, transient ischaemic attack, or vascular death. VMR% was evaluated by recording the percent differences in peak systolic blood flow velocities in each middle cerebral artery at baseline and after Diamox administration. Results:, Based on VMR% calculations, 14 (40%) patients had good VMRs and 21 (60%) had impaired VMRs. The global annual risk of ipsilateral ischaemic events was 5.7%. The annual ipsilateral ischaemic event risk was 1.8% in patients with good VMRs, whilst it was 7.1% in patients with impaired VMRs. An impaired VMR was significantly correlated with ipsilateral IS (Kaplan,Meier log rank statistic, P = 0.04). Conclusions:, Our results support the value of VMR assessment for identifying asymptomatic patients with carotid occlusion who belong to a high-risk subgroup for IS. New trials using extracranial-to-intracranial bypass surgery in patients with asymptomatic ICA occlusion and impaired VMRs are warranted. [source]


Bilateral common carotid occlusion without neurological deficit

JOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 4 2002
Serdar Karaköse
Summary A 40-year-old man presented with pain and numbness in his right arm. On his clinical examination, no neurological deficit was found. Bilateral common carotid artery duplex sonography scan demonstrated no flow in either lumen. No abnormality was recognized on brain CT. On cerebral digital substraction angiogram, total occlusion of the brachiocephalic trunk and left carotid artery were shown. There was a modest stenosis in the left vertebral artery. Collateral circulation feeding the intracranial carotid system mainly originated from the left vertebrobasilar system. Previous cases of bilateral carotid occlusion are reviewed and discussed. [source]


Aortic Dissection Presenting as an Acute Ischemic Stroke for Thrombolysis

JOURNAL OF NEUROIMAGING, Issue 3 2005
Ken Uchino MD
ABSTRACT Thrombolysis for the treatment of acute ischemic stroke requires careful selection of patients. The authors report a case of aortic dissection presenting with acute ischemic stroke for which emergent ultrasonographic evaluation was helpful in the diagnosis and subsequent treatment. The patient presented with acute middle cerebral artery ischemic stroke symptoms and complained of bilateral ear and chest pain. Chest x-ray, cardiac enzymes, and transthoracic echocardiogram were normal, and she was considered for thrombolytic therapy. Carotid ultrasound revealed right common carotid occlusion that led to the diagnosis of aortic dissection, confirmed by chest computed tomography. An experienced sonographer with skills to perform rapid intra- and extracranial examinations may help to change the treatment plan for acute stroke patients. [source]


RISK FACTORS FOR PERI-OPERATIVE STROKE COMPLICATING CAROTID ENDARTERECTOMY: SELECTIVE ANALYSIS OF A PROSPECTIVE AUDIT OF 1000 CONSECUTIVE OPERATIONS

ANZ JOURNAL OF SURGERY, Issue 1 2000
J. E. Frawley
Background: The aim of the present study was to investigate the role of potential clinical risk factors in the causation of peri-operative stroke associated with carotid endarterectomy. With the change in carotid endarterectomy practice from the use of a shunt to high-dose thiopental for cerebral protection (a previously undocumented method), it was essential to identify accurately the causes of all peri-operative strokes. Methods: A prospective audit was undertaken of 1000 carotid endarterectomies in which the causes and pathology of all peri-operative strokes were documented. The roles of advanced age, female gender, hypertension, previous stroke, contralateral carotid stenosis > 70%, and contralateral carotid occlusion as potential causes of peri-operative stroke were defined. Results were statistically analysed using odds ratio and Fisher's exact test. Results: None of the potential risk factors was statistically significant for peri-operative stroke. Female gender was associated with a significant risk of peri-operative stroke due to operative site thrombosis. Complications at the endarterectomy site were the commonest cause of stroke. Conclusions: Prospective audit is a useful tool for identifying causes of peri-operative stroke and indicating the need for modifications to surgical clinical management which might improve outcomes for carotid endarterectomy. [source]