CVS

[Jo Bowyer]

Vertebral artery terminating in posterior inferior cerebellar artery: A normal variation with clinical significance


http://journals.plos.org/plosone/art...l.pone.0175264

Abstract

A vertebral artery (VA) terminating in a posterior inferior cerebellar artery (PICA) is often considered to be a normal variation associated with VA hypoplasia. We aimed to investigate the clinical significance of this cerebrovascular variant. A total of 80 patients with clinically evident cerebrovascular events in posterior circulation were examined by duplex sonography and magnetic resonance angiography (MRA). Eighty healthy subjects who had MRA check-up were recruited as controls. PICA termination of the VA (PICA-VA) was identified as the VA not communicating with the basilar artery (BA) but ending into a PICA. We compared the prevalence of PICA-VA and associated hemodynamic parameters between the patients with and without PICA-VA, and investigated their relationships with VA hypoplasia. The prevalence of PICA-VA was higher in the patient group than in the controls (18.7% vs. 6.3%, p = 0.015). Most measurements (73.3%) of PICA-VA did not fit the criteria of VA hypoplasia. In comparison with the non-PICA-terminating group, the PICA-VA has a smaller diameter (3.7 ± 0.7 mm vs. 3.0 ± 0.5 mm, p < 0.001), lower mean velocity (241 ± 100 mm/sec vs. 164 ± 88 mm/sec, p < 0.01), and higher pulsatility index (1.3 ± 0.5 vs. 1.9 ± 0.6, p < 0.001). Moreover, a smaller diameter of the BA (3.2 ± 0.5 mm vs. 2.5 ± 0.9 mm, p = 0.004) and the posterior cerebral artery (PCA) (2.0 ± 0.1 mm vs. 1.6 ± 0.1 mm, p = 0.006) were also noted in the PICA-VA group. The higher prevalence of PICA-VA in the patient group with smaller diameter of VA, BA and PCA reflected its clinical significance, suggesting that PICA-VA may have a detrimental impact on cerebral hemodynamics. However, the sample is small, and further studies are needed with larger sample size for confirmation.

Introduction

The vertebral arteries (VAs) are typically arising from the subclavian artery, ascending in the neck and uniting to form the single basilar artery (BA). Anatomical variations of VA may be present as complete or partial duplication, asymmetry due to unilateral hypoplasia, or termination into its principal branch, the posterior inferior cerebellar artery (PICA) [1]. PICA termination of VA (PICA-VA) is occasionally found on routine brain magnetic resonance angiography (MRA); however, only a few studies to date have reported the prevalence of this vascular variant. A review on vertebrobasilar ischemic strokes found that three of 39 patients (7.7%) had PICA-VA by pathological or angiographic examinations [2]. In a normal population, it was estimated that two percent of people had PICA-VA on the right side [3]. Nonetheless, little is known about the clinical relevance of PICA-VA in the high risk group with cerebrovascular diseases.

Anatomical variations of VA could be simultaneously associated with PICA-VA and VA hypoplasia. A hypoplastic VA which terminates into the PICA is susceptible to cervical compression, and may exhibit syndrome of rotational VA occlusion on the same side as the precipitating horizontal head rotation [4]. In addition, VA hypoplasia has been considered to be a possible predisposing factor for posterior circulation stroke [5]. In this study, we assessed hemodynamic parameters of PICA-VA by duplex sonography and MRA. We aimed to evaluate the clinical significance of PICA-VA, and to investigate its association with VA hypoplasia.

Discussion

The main finding of this study is that the prevalence of PICA-VA in patients with clinically evident cerebrovascular events in posterior circulation was significantly higher than that of healthy controls. This suggests that PICA-VA may play an important role in the occurrence of stroke or transient ischemic attack in the patient group. Because of the fact that higher pulsatility index and lower mean flow velocity have been reported in aged people, patients with white matter disease, patients of dementia and patient with traumatic head injury [9–13], thus, we consider the flow profile with higher pulsatility index and lower mean flow velocity as “unfavorable hemodynamics”. Our study revealed PICA-VA was associated with unfavorable hemodynamics, such as significant lower mean flow velocity and higher pulsatility index in the ipsilateral VA, which may explain why PICA-VA can be a risk factor for cerebrovascular disease.

Contrary to the previous belief that PICA-VA has a strong association with VA hypoplasia, we found 73.3% of our patients with PICA-VA did not fit the criteria of VA hypoplasia [14], even though it was highly associated with smaller ipsilateral VA. The mean diameter at V2 segment of PICA-VA was 3.0 ± 0.5 mm, which is higher than the most commonly used definition of VA hypoplasia with VA diameter equal or less than 2.5 mm [14]. In addition, the diameters of BA and PCA were significantly smaller in the PICA-VA group, which may represent hypogenesis of the whole vertebrobasilar system, and further contributed to posterior circulation insufficiency and stroke [7]. However, we found the prevalence of fetal-PCA, another normal cerebrovascular variant, did not increase in patients with PICA-VA.

[Jo Bowyer]

Delayed Hospital Presentation and Neuroimaging in Non-surgical Spinal Cord Infarction


http://journal.frontiersin.org/artic...017.00143/full



Background:

Lack of timely recognition and neuroimaging may be a barrier to reperfusion efforts in acute spinal cord infarction.

Methods: We performed a retrospective study of patients diagnosed with acute non-surgical spinal cord infarction at our tertiary academic center from 2001 to 2015. We studied parameters associated with time from symptom onset to initial hospital presentation and magnetic resonance imaging (MRI) of the spinal cord.

Results: We identified 39 patients among whom anterior spinal artery syndrome was the most frequent presentation (87.2%) and atherosclerosis the most common etiology (56.4%). Nearly, half of the patients presented to the emergency department on the same day of symptom onset (48.7%) but only nine (23.1%) within the first 6 h. Average time from symptom onset to spinal cord MRI was 3.2 days. We could not identify clinical, radiological, or outcome patterns associated with early vs. delayed presentation and imaging.

Discussion: Our study found a time lag from symptom onset to hospital presentation and spinal cord MRI in patients with acute spinal cord infarction. These findings point at low clinical suspicion of spinal cord syndromes and limited recognition as a potentially treatable medical emergency.

They are unusual, I haven't seen one since I was a second year student.

[Jo Bowyer]

Can machine-learning improve cardiovascular risk prediction using routine clinical data?


http://journals.plos.org/plosone/art...xonomyendocrin

Abstract

Background


Current approaches to predict cardiovascular risk fail to identify many people who would benefit from preventive treatment, while others receive unnecessary intervention. Machine-learning offers opportunity to improve accuracy by exploiting complex interactions between risk factors. We assessed whether machine-learning can improve cardiovascular risk prediction.

Methods


Prospective cohort study using routine clinical data of 378,256 patients from UK family practices, free from cardiovascular disease at outset. Four machine-learning algorithms (random forest, logistic regression, gradient boosting machines, neural networks) were compared to an established algorithm (American College of Cardiology guidelines) to predict first cardiovascular event over 10-years. Predictive accuracy was assessed by area under the ‘receiver operating curve’ (AUC); and sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) to predict 7.5% cardiovascular risk (threshold for initiating statins).

Findings


24,970 incident cardiovascular events (6.6%) occurred. Compared to the established risk prediction algorithm (AUC 0.728, 95% CI 0.723–0.735), machine-learning algorithms improved prediction: random forest +1.7% (AUC 0.745, 95% CI 0.739–0.750), logistic regression +3.2% (AUC 0.760, 95% CI 0.755–0.766), gradient boosting +3.3% (AUC 0.761, 95% CI 0.755–0.766), neural networks +3.6% (AUC 0.764, 95% CI 0.759–0.769). The highest achieving (neural networks) algorithm predicted 4,998/7,404 cases (sensitivity 67.5%, PPV 18.4%) and 53,458/75,585 non-cases (specificity 70.7%, NPV 95.7%), correctly predicting 355 (+7.6%) more patients who developed cardiovascular disease compared to the established algorithm.

Conclusions


Machine-learning significantly improves accuracy of cardiovascular risk prediction, increasing the number of patients identified who could benefit from preventive treatment, while avoiding unnecessary treatment of others.

[Jo Bowyer]

Recovery from stroke after more than 20 years

https://motorimpairment.neura.edu.au...roke-20-years/

A paper recently published in the Journal of Neurophysiology provides another example. It features a case of delayed partial recovery from weakness and paralysis produced by a devastating stroke, with improvements in hand function more than two decades after the initial event (Sörös et al. 2017).

[Jo Bowyer]

Atrial fibrillation and blood pressure: more than just a number

https://www.sciencedaily.com/release...0828095030.htm

The range of variability in a patient's systolic blood pressure (SBP) from visit to visit was strongly associated with their risk of adverse outcomes, reported Dr Marco Proietti, MD, from the Institute of Cardiovascular Sciences, University of Birmingham.

"Our findings suggest that consistency in blood pressure control, beyond the single measurement, is very important, and this appears to be the case across all types of AF patients, irrespective of age, blood pressure history, blood pressure level or clotting risk," said Dr. Proietti.

"Interventions aimed at reducing blood pressure variability over the long term, such as optimizing the medications and improving adherence are strongly needed," he added.

The study was a post-hoc analysis of the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial, a prospective randomized comparison of two treatment strategies in patients with AF.

[Jo Bowyer]

Constraint-induced aphasia therapy in post-stroke aphasia rehabilitation: A systematic review and meta-analysis of randomized controlled trials


http://journals.plos.org/plosone/art...l.pone.0183349

Abstract

Background


Constraint-induced aphasia therapy (CIAT) has been widely used in post-stroke aphasia rehabilitation. An increasing number of clinical controlled trials have investigated the efficacy of the CIAT for the post-stroke aphasia.

Purpose


To systematically review the randomized controlled trials (RCTs) concerning the effect of the CIAT in post-stroke patients with aphasia, and to identify the useful components of CIAT in post-stroke aphasia rehabilitation.

Methods


A computerized database search was performed through five databases (Pubmed, EMbase, Medline, ScienceDirect and Cochrane library). Cochrane handbook domains were used to evaluate the methodological quality of the included RCTs.

Results


Eight RCTs qualified in the inclusion criteria. Inconsistent results were found in comparing the CIAT with conventional therapies without any component from the CIAT based on the results of three RCTs. Five RCTs showed that the CIAT performed equally well as other intensive aphasia therapies, in terms of improving language performance. One RCT showed that therapies embedded with social interaction were likely to enhance the efficacy of the CIAT.

Conclusion


CIAT may be useful for improving chronic post-stroke aphasia, however, limited evidence to support its superiority to other aphasia therapies. Massed practice is likely to be a useful component of CIAT, while the role of “constraint” is needed to be further explored. CIAT embedded with social interaction may gain more benefits.

[Mabo]

Usefull artikel

[Jo Bowyer]

Acute chest pain evaluation using coronary computed tomography angiography compared with standard of care: a meta-analysis of randomised clinical trials.

https://www.ncbi.nlm.nih.gov/pubmed/...form=hootsuite

[Jo Bowyer]

Cerebral ischemia comes in waves

http://stm.sciencemag.org/content/9/408/eaao6127.full


Abstract

Subarachnoid blood induces spreading depolarizations, which are associated with cortical infractions.

Cortical spreading depolarizations are waves of electrical silence caused by massive coordinated neuronal depolarizations that have been shown to occur in different types of acute brain injury, including subarachnoid hemorrhage (SAH). During brain injury, the presence of cortical spreading depolarizations has been associated with brain hypoxia and poor clinical outcomes; however, their causes and clinical impact in SAH are not well understood. Hartings et al. used a swine model of SAH and studied subdural electrocorticography recordings in 23 patients with aneurysmal SAH to determine causes and clinical consequences of cortical spreading depolarizations.

Fresh and clotted blood was injected into the subarachnoid space in gyrencephalic swine brains to create a model of SAH. Intracranial electrodes were placed to measure the number of cortical spreading depolarizations. Infusion of fresh blood resulted in continuous, repetitive spreading depolarizations and infusion of clotted blood caused spreading depolarizations associated with cortical infarctions. Twenty-three aneurysmal SAH patients underwent subdural electrocorticography and magnetic resonance imaging to detect spreading depolarizations and cerebral ischemia. 86% of patients with ischemic lesions had cortical spreading depolarizations compared with only 9% of those who had no lesions. The findings in the animal model in conjunction with the observation that SAH patients with early infarcts have more spreading depolarizations suggest that spreading depolarizations might contribute to cerebral ischemia in SAH.

The main limitation of the study is that although SAH was shown to lead to cortical spreading depolarizations and ischemic injury, the mediators of this injury were not investigated thoroughly. Cortical spreading depolarizations occur after acute brain injuries of different types. A better understanding of the mechanisms underlying the relationship between cortical spreading depolarization and ischemic processes is needed to develop targeted interventions for preventing ischemic damage.

[Jo Bowyer]

The association between cigarette smoking and inflammation: The Genetic Epidemiology Network of Arteriopathy (GENOA) study


http://journals.plos.org/plosone/art...l.pone.0184914

Abstract

To inform the study and regulation of emerging tobacco products, we sought to identify sensitive biomarkers of tobacco-induced subclinical cardiovascular damage by testing the cross-sectional associations of smoking with 17 biomarkers of inflammation in 2,702 GENOA study participants belonging to sibships ascertained on the basis of hypertension. Cigarette smoking was assessed by status, intensity (number of cigarettes per day), burden (pack-years of smoking), and time since quitting. We modeled biomarkers as geometric mean (GM) ratios using generalized estimating equations (GEE). The mean age of participants was 61 ±10 years; 64.5% were women and 54.4% African American. The prevalence of smoking was 12.2%. After adjusting for potential confounders, 6 of 17 biomarkers were significantly higher among current smokers at a Bonferroni adjusted p-value threshold (p<0.003). High sensitivity C-reactive protein was the most elevated biomarker among current smokers when compared to never smokers [GM ratio = 1.39 (95% CI: 1.23, 1.57); p <0.001]. Among former smokers, each pack-year of cigarettes smoked was associated with a 0.4% higher serum level of hsCRP [GM ratio = 1.004 (95% CI: 1.001, 1.006); p = 0.002] and each 5-year lapsed since quitting was associated with a 4% lower serum level of hsCRP [GM ratio = 0.96 (95% CI: 0.93, 0.99); p = 0.006]. However, we found no significant association of smoking intensity or burden with biomarkers of inflammation among current smokers. HsCRP appears to be the most sensitive biomarker of inflammation associated with cigarette smoking of those investigated, and could be a useful biomarker of smoking-related injury for the study and regulation of emerging tobacco products.

[Jo Bowyer]

Training for muscle endurance after stroke

https://motorimpairment.neura.edu.au...urance-stroke/

Muscle endurance is an understudied aspect of function with high relevance to stroke rehabilitation. The magnitude of improvement in muscle endurance (178%) was unexpected, but suggests that this component of post-stroke function can be robustly improved across a relatively short training period, provided appropriate exercise dose-intensity and a regimen geared towards endurance gains. Many everyday tasks depend on repetitive submaximal contractions (muscle endurance). Thus, health practitioners should evaluate this component of health and implement training programs to improve it. Additional studies are needed to determine how gains in muscle endurance translate into improvements in community- and home-based function.

There are plenty of opportunities for use of the home and surrounding environment as a strength and conditioning gym, I often do a home visit in order to get them started.

[Jo Bowyer]

What Happens When Nerve Cells Stop Working?


http://neurosciencenews.com/neural-breakdown-7599/

A stroke is just one example of a condition when communication between nerve cells breaks down. Micro-failures in brain functioning also occur in conditions such as depression and dementia. In most cases, the lost capacity will return after a while. However, consequential damage will often remain so that the functional capability can only be restored through lengthy treatment — if at all. For this reason, researchers at Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) have been investigating what happens during such breakdown phases and looking at possible ways of preventing damage and speeding up the healing processes. Their findings have been recently published in Scientific Reports.

The research team headed by Jana Wrosch of FAU’s Chair of Psychiatry and Psychotherapy found that significant alterations occurred in neural cells while the communication pathways were blocked. Neuron networks reconnect during such periods of inactivity and become hypersensitive. If we imagine that normal communication pathways are motorways, when they are blocked a form of traffic chaos occurs in the brain whereby information is re-routed in disorganised form along what can be called side streets and minor routes. Additional synapses are generated everywhere and begin operating. When the signal is reinstated, the previously coordinated information routes no longer exist and, as in the case of a child, the appropriate functions need to be learned from scratch. Since they are receiving no normal signals during the phase of brain malfunction, the nerve cells also become more sensitive in an attempt to find the missing input. Once the signals return, this means they may overreact.

[Jo Bowyer]

Body fat distribution, in particular visceral fat, is associated with cardiometabolic risk factors in obese women

http://journals.plos.org/plosone/art...l.pone.0185403

[Jo Bowyer]

Gut bacteria metabolism may factor into hypertension

https://www.sciencedaily.com/release...1003144516.htm

[Jo Bowyer]

Is two better than one? Muscle vibration plus robotic rehabilitation to improve upper limb spasticity and function: A pilot randomized controlled trial

http://journals.plos.org/plosone/art...l.pone.0185936
Abstract

Even though robotic rehabilitation is very useful to improve motor function, there is no conclusive evidence on its role in reducing post-stroke spasticity. Focal muscle vibration (MV) is instead very useful to reduce segmental spasticity, with a consequent positive effect on motor function. Therefore, it could be possible to strengthen the effects of robotic rehabilitation by coupling MV. To this end, we designed a pilot randomized controlled trial (Clinical Trial NCT03110718) that included twenty patients suffering from unilateral post-stroke upper limb spasticity. Patients underwent 40 daily sessions of Armeo-Power training (1 hour/session, 5 sessions/week, for 8 weeks) with or without spastic antagonist MV. They were randomized into two groups of 10 individuals, which received (group-A) or not (group-B) MV. The intensity of MV, represented by the peak acceleration (a-peak), was calculated by the formula (2πf)2A, where f is the frequency of MV and A is the amplitude. Modified Ashworth Scale (MAS), short intracortical inhibition (SICI), and H_max/M_max ratio (HMR) were the primary outcomes measured before and after (immediately and 4 weeks later) the end of the treatment. In all patients of group-A, we observed a greater reduction of MAS (p = 0.007, d = 0.6) and HMR (p<0.001, d = 0.7), and a more evident increase of SICI (p<0.001, d = 0.7) up to 4 weeks after the end of the treatment, as compared to group-B. Likewise, group-A showed a greater function outcome of upper limb (Functional Independence Measure p = 0.1, d = 0.7; Fugl-Meyer Assessment of the Upper Extremity p = 0.007, d = 0.4) up to 4 weeks after the end of the treatment. A significant correlation was found between the degree of MAS reduction and SICI increase in the agonist spastic muscles (p = 0.004). Our data show that this combined rehabilitative approach could be a promising option in improving upper limb spasticity and motor function. We could hypothesize that the greater rehabilitative outcome improvement may depend on a reshape of corticospinal plasticity induced by a sort of associative plasticity between Armeo-Power and MV.

This doesn't surprise me.

I prefer hands on vibration along with a walkytalky physiotherapist though, I reckon that I can mulititask better than a robot and tailor the intervention to the patient in real time.