Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, December 10, 2021

Reclassifications of ischemic stroke patterns due to variants of the Circle of Willis

How did you miss telling us the 100% recovery protocols based upon these Circle of Willis variants?

Laziness? Incompetence? Or just don't care? No leadership? No strategy? Not my job.

 Your job is to solve stroke, this does nothing.

Reclassifications of ischemic stroke patterns due to variants of the Circle of Willis

First Published October 5, 2021 Research Article Find in PubMed 

Variants of the Circle of Willis (vCoW) may impede correct identification of ischemic lesion patterns and stroke etiology. We assessed reclassifications of ischemic lesion patterns due to vCoW.

We analyzed vCoW in patients with acute ischemic stroke from the 1000+ study using time-of-flight magnetic resonance angiography (TOF MRA) of intracranial arteries. We assessed A1 segment agenesis or hypoplasia in the anterior circulation and fetal posterior cerebral artery in the posterior circulation. Stroke patterns were classified as one or more-than-one territory stroke pattern. We examined associations between vCoW and stroke patterns and the frequency of reclassifications of stroke patterns due to vCoW.

Of 1000 patients, 991 had evaluable magnetic resonance angiography. At least one vCoW was present in 37.1%. VCoW were more common in the posterior than in the anterior circulation (33.3% vs. 6.7%). Of 238 patients initially thought to have a more-than-one territory stroke pattern, 20 (8.4%) had to be reclassified to a one territory stroke pattern after considering vCoW. All these patients had fetal posterior cerebral artery and six (30%) additionally had carotid artery disease. Of 753 patients initially presumed to have a one-territory stroke pattern, four (0.5%) were reclassified as having more-than-one territory pattern.

VCoW are present in about one in three stroke patients and more common in the posterior circulation. Reclassifications of stroke lesion patterns due to vCoW occurred predominantly in the posterior circulation with fetal posterior cerebral artery mimicking multiple territory stroke pattern. Considering vCoW in these cases may uncover symptomatic carotid disease.

Identifying stroke lesion patterns and affected territories supplied by neck arteries is an essential component in determining ischemic stroke etiology. More-than-one territory stroke patterns suggest a proximal embolic source, e.g. of cardiac or aortal origin, whereas single territory stroke patterns point to large or small vessel disease.1 Assigning stroke lesions to the corresponding arterial territories is usually carried out using pre-set brain maps due to practicality.2 However, since the Circle of Willis (CoW) connects all three major cerebral territories (left anterior, right anterior, and posterior), classifying stroke lesion patterns based solely on brain maps without considering variants of the Circle of Willis (vCoW) may lead to false assignment of affected arterial territories.3 Taking vCoW into account may lead to clinically relevant reclassifications of stroke patterns.

Establishing the frequency of different vCoW could help to distinguish stroke locations that are more prone to misclassifications. Here, we analyzed the frequency of two vCoW in patients with ischemic stroke using time-of-flight magnetic resonance angiography (TOF MRA): (a) agenesis or hypoplastic A1 segment of the ACA in the anterior circulation (anterior vCoW) and (b) fetal posterior cerebral artery (fPCA) in the posterior circulation. Furthermore, we examined stroke lesion patterns (classified as one and more-than-one territory stroke pattern) in patients with complete Circle of Willis (cCoW) and vCoW. Finally, we examined the rate of reclassifications from more-than-one territory to one territory and vice versa, following reattributions of stroke lesions to the corresponding cerebral artery after identifying vCoW.

Study design and study population

MRI data were obtained from the prospective observational cohort study 1000+ (Clinical trials.gov identifier: NCT00715533), which was approved by the ethics committee of the Charité – Universitätsmedizin Berlin (EA4/026/08). The study enrolled consecutively admitted patients with transient ischemic attack or ischemic stroke to our stroke unit (Department of Neurology, Charité – Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany) from February 2011 to April 2013.4 The inclusion criteria were onset of acute ischemic stroke symptoms within the last 24 h of admission to the emergency department, meeting general MRI eligibility criteria and age ≥18 years.4 Additionally, only patients with a complete MRA were included into the current subanalysis.

Stroke severity was assessed using the National Institutes of Health Stroke Scale (NIHSS) with higher scores indicating greater severity (range: 0–42). Functional outcome at discharge was evaluated by modified Rankin Scale (mRS), a seven-point scale ranging from “0” (no neurological deficit) to “6” (death). We also recorded history of arterial hypertension, diabetes mellitus, hypercholesterinemia, coronary heart disease, atrial fibrillation, and smoking. Only patients with a diffusion weighted imaging (DWI) lesion that were previously included in the substudy by Erdur et al. (n = 1000) were analyzed in this substudy.3

Neuroimaging and assessment of the variants of the Circle of Willis

All exams were acquired using 3-Tesla magnetic resonance imaging (MRI); Tim Trio 3T whole-body system (Siemens Healthcare, Erlangen, Germany) using a 12-channel receive radiofrequency (RF) coil (Siemens Healthcare). Extracranial neck arteries were either assessed by MRA, computed tomography angiography (CTA), or duplex ultrasound. The CoW was assessed using TOF MRA; voxel size 0.52 × 0.52 × 0.65 mm, matrix size 312 × 384 × 127 voxels, TR/TE = 22/3.86 ms, respectively, acquisition time 3:50 and flip angle 18°.

LSM mapped and characterized all lesions on DWI, FLAIR, and anatomical variations of cerebral vessels while blind to all clinical data except name and sex under continuous supervision by HE. All inconclusive imaging findings were discussed by HE, LSM, JBF and CHN for definitive allocation.

Stroke lesion patterns and vCoW were previously evaluated in a substudy by Erdur et al. using the data from the 1000+ study.3 The current work represents a subanalysis of this data set. We examined the frequency of two vCoW that occur most commonly.5,6 In the anterior circulation, we assessed the agenesis or hypoplasia of the A1 segment of the anterior cerebral artery (ACA) – anterior vCoW. This variant was identified when one A1 segment was significantly narrower than the contralateral A1 segment or absent. Consecutively, blood supply to the A2 segment ipsilateral to the underdeveloped A1 segment was manly provided from the contralateral A1 segment via anterior communicating artery (AComA). In the posterior circulation, we defined fPCA where posterior communicating artery (PComA) was significantly larger than the P1-segment of the ipsilateral posterior cerebral artery (PCA). Vice versa, the adult PCA was defined as P1-segment of the PCA being larger than the ipsilateral PComA. In cases with nearly the same diameters of the PComA und P1-segment, the posterior circulation was labeled as transitional, as previously described in the literature.7

We conducted separate comparisons of patients with vCoW and cCoW in the posterior and anterior circulation in terms of demographics, medical history, stroke severity (NIHSS on admission), and early functional outcome (mRS at discharge). Patients with only transitional posterior circulation were excluded from the comparison of vCoW due to the small sample size and because it was not possible to assign transitional PCA to either adult PCA or fetal PCA variant, owing to distinct hemodynamics of each variant. Patients with fPCA on one side and either adult or transitional PCA on the other side were considered as fPCA patients for this particular analysis.

Hyperintense lesions in the DWI and low apparent diffusion coefficient (ADC) were considered as acute ischemic lesions. Chronic ischemic lesions were assessed using fluid attenuated inversion recovery (FLAIR) sequence. Only acute ischemic lesions were considered for determining stroke patterns and affected arterial territories. Arterial territories were divided into left and right anterior (middle cerebral artery (MCA) + ACA territory of each side, originating from the internal carotid artery (ICA)) and posterior territory (PCA territories and vertebrobasilar system). Allocating stroke lesions to the corresponding arterial territories was initially performed using brain maps according to Tatu et al. with no regard to possible vCoW.2,3

Stroke lesion patterns were classified as one and more-than-one territory stroke pattern. We examined the frequency of different stroke patterns with no regard to vCoW. After identifying vCoW, we examined the rate of reclassifications from more-than-one territory to one territory stroke pattern. For example, in a patient with ipsilateral temporal and occipital lesions, the lesions were labeled as more-than-one territory pattern. This had to be corrected to a one territory pattern after ipsilateral fPCA was identified (Figure 1). Reversely, reclassification from one to more-than-one territory pattern was conducted in cases where simultaneous PCA strokes and cerebellar strokes were seen and had been considered to belong to the same (posterior) territory. However, in patients with fPCA, the PCA stroke belonged to the anterior circulation, and consequently, a reclassification into more-than-one territory group was conducted (Figure 2). In addition, we examined how often ipsilateral fPCA is present in patients with isolated lesions in the PCA territory. In the presence of fPCA, isolated lesions in the PCA territory were re-allocated from the posterior to the (ipsilateral) anterior vascular territory. 

More at link.

 
 

No comments:

Post a Comment