Explore the vast range of titles available.

Cerebral angiography is associated with a small but definite risk of neurological complications with an unknown incidence of clinically silent embolism. We assessed the neurological complication rate compared with the frequency of silent embolism after angiography We used diffusion-weighted magnetic resonance imaging (MRI) before and after angiography to assess embolic events. 100 consecutive angiographies (66 diagnostic and 34 interventional procedures) were done on 91 patients. Patients underwent neurological assessment before, immediately after, and 1 day after angiography. Before angiography, no abnormalities were seen on diffusion-weighted MRI. Diffusion-weighted MRI showed 42 bright lesions in 23 patients after 23 procedures (17 diagnostic, six interventional) in a pattern consistent with embolic events. There was no new neurological deficit after any angiographic procedure. After diagnostic angiography in patients with a history of vasculopathy, the frequency of lesions was significantly higher than in patients without vascular risk factors (12 [44%] of 27 vs five [13%] of 39 patients, p=0·03). In diagnostic angiography, the appearance of lesions was significantly correlated with whether vessels were difficult to probe (p=0·01), amount of contrast medium needed (p<0·01), fluoroscopy time (p<0·01), and use of additional catheters (p=0·02). After diagnostic and interventional cerebral angiography, embolic events are more frequent than the apparent neurological complication rate. In diagnostic procedures, the incidence of embolism is closely related to a vascular risk profile.

Cervical artery dissection (CAD) accounts for up to one fifth of ischemic strokes occurring before 45 years. Their increasing recognition is probably due to an increased clinical awareness of this condition in patients with painful ischemic events. The internal carotid artery is the most commonly affected vessel. Cerebral ischemia is the most serious consequence of a CAD. It may be due to hemodynamic factors or emboli. The enlargement of the artery may lead to a direct compression of the lower cranial nerves. CAD typically occurs in young adults with a mean age of 40 years with a male:female ratio of 1.5. After exclusion of traumatic cases, the average annual incidence rate of CAD is 2.6 per 100,000, but the reported incidence figures in the literature are likely to be an underestimation of the incidence of CAD. A spontaneous dissection is assumed when no or only minor trauma preceded the onset. However, the differentiation between spontaneous and traumatic dissections is artificial because of a continuum between both forms. The pathogenesis of dissections remains unknown in most cases. However, traumas and primary diseases of the arterial wall are the main predisposing factors. The clinical presentation of spontaneous dissections of the internal carotid artery includes cerebral ischemia, cervical or cranial pain, Homer’s syndrome and cranial nerve palsy; CAD may also be silent. Brainstem ischemic deficits and occipital pain are the most common findings in vertebral artery dissections, but these features may be biased because the most benign and the most severe cases may escape detection. The favorable natural history of CAD emphasizes the need for a noninvasive approach to the detection, monitoring and follow-up. This noninvasive approach can be obtained by means of CT scan, MRI, magnetic resonance angiography and ultrasonography, although angiography remains the gold standard for the diagnosis of arterial dissections. Follow-up studies suggest a fairly good overall prognosis in adults and in children. In many centers, CAD are treated by heparin at the acute stage, although the benefit of such a potentially dangerous treatment has never been proven by a randomized trial.

OBJECTIVES To examine the association between intraoperative cerebral microembolic signals (MES) and postoperative neuropsychological deficit in patients with valve replacement (VR) and patients with coronary artery bypass grafting (CABG). METHODS Neuropsychological examination (10 tests) was performed 1–2 days before and 2 months after surgery (VR (n=26) and CABG (n=14)). The intraoperative number of cerebral MES were monitored from the right middle cerebral artery using transcranial Doppler. RESULTS A higher number of cerebral MES were detected in VR patients with neurological deficit (6/26) compared with those without deficit (20/26) (MES median number 2083 v645, p=0.04). No such difference was found in patients with CABG (2/14v 12/14) (MES median number 50 v 112, p=0.2). CONCLUSION A high number of MES were detected in patients with VR with neuropsychological deficit. In patients with CABG with such a deficit, a low number of MES were detected. This difference in number may be explained by relatively more gaseous emboli in the first and more solid in the second. However, the results in the patients with CABG should be interpreted with caution due to the few patients in this subgroup.

Keywords: Cardiopulmonary bypass, adverse effects, Cerebral embolism, etiology, Cerebral embolism, physiopathology, Embolism, fat

The only randomized data on heparin treatment in acute cerebral sinus venous thrombosis (CSVT) are derived from a small number of patients. The rate of intracranial hemorrhages as a complication of high-dose heparin treatment is still unknown. This retrospective study evaluates the clinical features, neuroimaging monitoring and outcome of 42 patients with proven CSVT. Diagnosis was established by DSA, CT, MR tomography and MR angiography. All patients received heparin intravenously guided by doubling the aPTT value for 3 weeks, followed by oral anticoagulation. Partial or complete recanalization was found in 36 cases. 40 patients improved clinically, in 26 of them complete recovery was observed. One patient deteriorated and developed an apallic syndrome, one further patient died of septic multiorgan failure. Only in one patient was hemorrhagic transformation of infarcted brain tissue observed but without clinical deterioration.

Carotid artery stenting is a recently introduced treatment in symptomatic atherosclerotic carotid artery disease with acceptable complication rates. The major risk is perioperative embolic stroke. Transcranial Doppler ultrasonography (TCD) can be used to identify embolic signals and guide therapy. We present a case of symptomatic embolization in a 72-year-old female following carotid stent deployment complicated by haemodynamic changes. Despite concurrent dual antiplatelet medication significant symptomatic embolization occurred even after restoration of the blood pressure, and modulation of the rate of embolization was achieved using dextran-40 guided by TCD monitoring. The patient recovered from an initially profound hemiparesis and dysphasia to minor sensory changes. Microemboli are common following carotid artery stenting and there appears to be a threshold phenomenon associated with prolonged embolization and progression to cerebral infarction. TCD can be used to detect particulate microemboli and therefore may be useful in guiding antithrombotic therapy in this setting. Dextran-40 has been shown to reduce the embolic load following carotid endarterectomy and was used to good effect in this patient in terms of both embolic load and clinical outcome. This is the first case of embolization following carotid stenting successfully treated with dextran-40, and offers a further option for therapeutic intervention in microembolism detected by TCD and stresses the importance of perioperative monitoring of embolic load for postoperative stroke risk.

The mechanisms of thrombus formation in atherosclerotic cerebral arteries are still controversial, although intraplaque haemorrhage and rupture of the atheromatous plaques have been proposed. A histopathological analysis of segments of the thrombosed large intracranial arteries was carried out on eight patients who died within 28 days after brain infarction. The study revealed occlusive thrombi in six and mural thrombi in two, developing mostly at the site of greatest stenosis or just distal to it. The histological characteristics of the thrombosed arteries were plaque rupture in three, intramural haemorrhage in one, ulceration in one, and thrombosis in the absence of plaque rupture or intramural haemorrhage in three. Occlusive emboli distal to the site of cerebral artery thrombosis (intracranial artery-to-artery thromboembolism) were observed in two. The following conclusions were drawn from the study: 1) plaque rupture or intraplaque haemorrhage is not a sine qua non for cerebral artery thrombosis; 2) occlusions occur at the site of greatest luminal compromise or just distal to it, and 3) non-occlusive mural thrombosis can occur in the absence of plaque rupture and eventually lead to local occlusion or distal embolisation.

The purpose of this retrospective study was to demonstrate the MRI features of cerebral manifestations in patients with fat embolism syndromes in comparison with cerebral CT (CCT). Magnetic resonance imaging was performed according to standard protocols revealing multiple small non-confluent hyperintense intracerebral lesions larger than 2 mm on proton-density and T2-weighted images to various extents in three of four patients with clinically suspected cerebral fat embolism. Cerebral CT was negative in all patients. Our findings confirm that MRI can detect cerebral fat embolism with a higher sensitivity than CCT. Thus, MRI should be the first choice for imaging of cerebral fat embolism.

Background: We determined clinical predictive factors of in-hospital embolic recurrence in presumed cardioembolic stroke patients by means of multivariate analysis based on clinical and neuroimaging prognostic variables assessed within 48 h of stroke onset. Methods: Data of 347 consecutive patients with presumed cardioembolic stroke included in a prospective stroke registry were collected. Demographic characteristics, clinical events, and outcome in the recurrent and nonrecurrent embolization group were compared. The independent predictive value of each variable on the development of early embolic recurrence was analyzed in two multiple liner regression models – one based on eight demographic, anamnestic, and clinical variables and another based on 10 clinical, neuroimaging, and outcome variables. Results: In-hospital recurrent embolization was diagnosed in 25 (6.9%) patients. The latency period was 12.1 days. The overall in-hospital mortality was 70.8% in the recurrent embolization group and 24.4% in the nonrecurrent embolization group (p < 0.001). Alcohol abuse, the combination of hypertension, valvular heart disease, and atrial fibrillation, nausea and vomiting, and previous cerebral infarction were predictors of recurrent embolization in the model based on clinical variables. In addition to these four variables, cardiac events were selected in the model based on clinical, neuroimaging, and outcome variables. Conclusions: A small number of clinical features that can be easily obtained on the patient’s initial assessment may help clinicians to identify a subgroup of patients with cardioembolic stroke at the highest risk of developing early recurrent brain or systemic embolization.