• P. Mordasini,M. El-Koussy,C. Brekenfeld,G. Schroth,U. Fischer,J. Beck,and J. Gralla. Applicability of Tableside Flat Panel Detector CT Parenchymal Cerebral Blood Volume Measurement in Neurovascular Interventions: Preliminary Clinical Experience AJNR Am J Neuroradiol 2011 originally published online on September 29, 2011, 10.3174/ajnr.A2715.
  

CBV is a vital perfusion parameter in estimating the viability of brain parenchyma (eg, in cases of ischemic stroke or after interventional vessel occlusion). Recent technologic advances allow parenchymal CBV imaging tableside in the angiography suite just before, during, or after an interventional procedure. The aim of this work was to analyze our preliminary clinical experience with this new imaging tool in different neurovascular interventions.

FPD-CBV measurement was performed on a biplane FPD angiographic system. Eighteen patients (11 women, 7 men) were examined (age range, 18–86 years; median, 58.7 years). In the 10 patients with stroke, the extent of intracranial hypoperfusion was evaluated. The remaining 8 patients had an intracranial hemorrhage; periprocedural CBV was evaluated during the course of interventional treatment.

In the 18 cases studied, 23 CBV measurements were performed. Twenty acquisitions were of sufficient diagnostic quality. The remaining 3 acquisitions failed technically, 1 due to motion artifacts and 2 due to injection technique and/or hardware failure.

FPD-CBV measurement in the angiography suite provides a feasible and helpful tool for peri-interventional neuroimaging. It extends the intraprocedural imaging modalities to the level of tissue perfusion. However, the technique has technical limitations and shows room for improvement in the future.

CME ARTICLE

Neurologic/Head and Neck Imaging:

• Rajiv Mangla,
• Balasubramanya Kolar,
• Jeevak Almast,
• and Sven E. Ekholm

Border Zone Infarcts: Pathophysiologic and Imaging Characteristics Radiographics September-October 2011 31:1201-1214; doi:10.1148/rg.315105014

The causal mechanisms and anatomic locations of external (cortical) and internal (subcortical) border zone infarcts are reviewed, and their appearances at MR imaging, CT, and transcranial Doppler US are described in detail.

Border zone or watershed infarcts are ischemic lesions that occur in characteristic locations at the junction between two main arterial territories. These lesions constitute approximately 10% of all brain infarcts and are well described in the literature. Their pathophysiology has not yet been fully elucidated, but a commonly accepted hypothesis holds that decreased perfusion in the distal regions of the vascular territories leaves them vulnerable to infarction. Two types of border zone infarcts are recognized: external (cortical) and internal (subcortical). To select the most appropriate methods for managing these infarcts, it is important to understand the underlying causal mechanisms. Internal border zone infarcts are caused mainly by hemodynamic compromise, whereas external border zone infarcts are believed to result from embolism but not always with associated hypoperfusion. Various imaging modalities have been used to determine the presence and extent of hemodynamic compromise or misery perfusion in association with border zone infarcts, and some findings (eg, multiple small internal infarcts) have proved to be independent predictors of subsequent ischemic stroke. A combination of several advanced techniques (eg, diffusion and perfusion magnetic resonance imaging and computed tomography, positron emission tomography, transcranial Doppler ultrasonography) can be useful for identifying the pathophysiologic process, making an early clinical diagnosis, guiding management, and predicting the outcome.

http://www.springerlink.com/content/64rr0h3827k1g5p7/

Patients with acute stroke with large vessel occlusion and carotid stenosis have been stented and then thrombolysed, or the stenosis simply left as it is, in the past. However, a problem arises if a visible clot sticks in the lumen at the stenotic site. No need to worry. You can stent this as well and then perform thrombolysis, as done by the authors of this paper. Of course one needs to use a distal filter device!

Abstract

Introduction 

Carotid stenosis with intraluminal thrombus is associated with a high risk of early recurrent stroke. We evaluated the feasibility and outcome of carotid stenting in acute ischemic stroke patients with carotid stenosis and intraluminal thrombus.

Methods 

Among 295 consecutive acute ischemic stroke patients who were referred for intra-arterial thrombolytic (IAT) therapy, six patients with carotid stenosis and intraluminal thrombus were treated by stent assisted angioplasty. The clinical characteristics, feasibility, and clinical outcomes were assessed.

Results 

All patients had severe stenosis of the underlying carotid bulb (mean, 86.8%; range, 71–99%) with adjacent intraluminal thrombus. Stent assisted angioplasty resulted in successful recanalization in all six patients. Thrombus was captured with the filter device in four patients. Three patients with tandem occlusion of the ipsilateral proximal middle cerebral artery were successfully recanalized with intra-arterial urokinase. No patients suffered procedure related complications or symptomatic hemorrhage. Four patients showed good long-term outcome (3 month mRS; 0–2).

Conclusions 

Stent assisted angioplasty is a feasible treatment option for acute ischemic stroke patients caused by carotid stenosis with intraluminal thrombus and may be effective in preventing early recurrent stroke.

Keywords  Carotid stenosis – Angioplasty – Stent – Thrombolytic therapy

http://www.springerlink.com/content/u315778702g1jj86/

Jee-Hyun Kwon, Shang Hun Shin, Young Cheol Weon, Jae Cheol Hwang and Seung Kug Baik. Intra-arterial adjuvant tirofiban after unsuccessful intra-arterial thrombolysis of acute ischemic stroke: preliminary experience in 16 patients. NeuroradiologyVolume 53, Number 10, 779-785, DOI: 10.1007/s00234-011-0939-y

Intra-arterial chemical thrombolytic therapy of acute stroke is rapidly gaining strides. However, the drugs and their dosage to be used is far from clear, with ever neurointerventionist using a different protocol. Even then, few points are becoming lucid;

1. Fibrin busting drugs e.g tPA or urokinase is not effective in a substantial number of patients

2. Antiplatelets are vey handy in intra-arterial thrombolysis

3. Intra-arterial heparin also can be handy in many instances

Reports of  groups using antiplatelets have been published.

A recent one studied 16 patients with failed thrombolysis after IA urokinase, in whom tirofiban was used. They achieved good recanalisation rates. However, 6 patients had ICH, which to my mind does not really augur well for this idea, even though the authors themselves say that it is a good result.

Probably we need to design a chemical IA thrombolysis dosage using both Urokinase/tPA and antiplatelets rather than using one after the other has failed.

Abstract

Introduction 

Intra-arterial (IA) thrombolysis with plasminogen activator is well-known, but the use of IA tirofiban as an adjuvant for IA thrombolysis is not well-known. We investigated the feasibility of IA tirofiban as an adjuvant after unsuccessful IA recanalization with urokinase (UK) for acute ischemic stroke.

Methods 

We retrospectively analyzed all 16 consecutive patients (11 men and five women; mean age, 61.3 years; range, 36–85 years) who were treated with IA tirofiban after isolated IA thrombolysis with UK or bridging therapy with systemic recombinant tissue plasminogen activator (rt-PA; 0.6 mg/Kg) and IA UK for acute ischemic stroke. Outcome measures included angiographic recanalization (thrombolysis in cerebral infarction, TICI), symptomatic and asymptomatic intracerebral hemorrhage (ICH), mortality, and functional independence at 3 months (modified Rankin Scale, 0–2).

Results 

Among the 16 patients treated with IA tirofiban as an adjuvant, 10 patients had conventional dose (<25 ug/kg, bolus) and six patients had high dose (≥25 ug/kg, bolus) of IA tirofiban after unsuccessful IA thrombolysis whether systemic rt-PA used or not. Successful angiographic recanalization (TICI grade 2b or 3) was achieved in 13 patients (13/16) and a functional independence at 3 months in eight patients (8/16). Three months after therapy, three patients had died. There were two patients of symptomatic ICH and four asymptomatic ICH.

Conclusion 

Conventional dose of IA tirofiban as an adjuvant during IA thrombolysis for acute ischemic stroke seems feasible. However, further dose escalation studies should be performed regarding the IA use of tirofiban for acute ischemic stroke.

Keywords  Acute ischemic stroke – Intra-arterial – Tirofiban – Thrombolysis

    Click to open the article in the journal website

Charlotte Rosso, Olivier Colliot, Romain Valabrègue, Sophie Crozier, Didier Dormont, Stéphane Lehéricy and Yves Samson. Tissue at risk in the deep middle cerebral artery territory is critical to stroke outcome. Neuroradiology Volume 53, Number 10, 763-771, DOI: 10.1007/s00234-011-0916-5

We have often seen that patients with predominant cortical ischemia do well over time however, the ones with large deep white matter infarcts have poor outcomes. A growing body of evidence has been accumulating the same. In this recent article, the authors have used voxel based ADC mapping and diffusion tensor imaging to establish this fact.

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Abstract

Introduction 

The clinical efficacy of thrombolysis in stroke patients is explained by the increased rate of recanalization, which limits infarct growth. However, the efficacy could also be explained by the protection of specific sites of the brain. Here, we investigate where is this outcome-related tissue at risk using voxel-based analysis.

Methods 

We included 68 acute stroke patients with middle cerebral artery (MCA) occlusion on the admission MRI performed within 6 h of symptoms onset (H6) and 16 controls. MCA recanalization was assessed using the magnetic resonance angiography performed at day 1 (D1). Apparent diffusion coefficient (ADC) changes were analyzed using a voxel-based method between patients vs. controls group at admission (H6) in non-recanalized vs. recanalized and in 3-month poor vs. good outcome patients at D1.

Results 

Complete or partial MCA recanalization was observed in 52 of 68 patients. Good outcome at 3 months occurred in 40 patients (59%). In non-recanalized patients, ADC was decreased in the deep MCA and watershed arterial territory (the lenticular nucleus, internal capsule, and the overlying periventricular white matter). This decrease was not observed in recanalized patients at D1 or patients at H6. Fiber tracking suggested that the area is crossed by the cortico-spinal, cerebellar, and intra-hemispheric association tracts. Finally, this area almost co-localized with the area associated with poor outcome.

Conclusions 

A clinically relevant area of tissue at risk may occur in patients with MCA infarcts at the level of deep white matter fiber tracts. These findings suggest that neuroprotection research should be refocused on white matter.

Keywords  Stroke – Recanalization – Outcome – MRI – DWI