Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Monday, January 22, 2018

Barb in Gloucester

Front of Barb and Toms house
Visited Barb Polan last weekend, a short train ride from Boston.
Looking at their back yard, if I lived there I would have broken numerous bones trying to get around. My living space there would be the third floor with a view of the ocean, regardless of how difficult it would be to climb the steps. It was fun being there.
Back yard, that top window would be mine. Barbs' dog Turbo
Barb, walking past neighbors house

New Horizons for Stroke Medicine: Understanding the Value of Social Media

Since you haven't found or contacted me your use of social media is appalling.  And since no stroke doctor, therapist, hospital or stroke board member has ever contacted me they are all failing at this social media thing.
Jose Maria Cabrera-Maqueda, Jatinder S. Minhas
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Social media (SM) has provided individuals and organizations with an openly accessible platform encouraging participation and engagement in different forms of media (blogs, photos, infographics, and videos). In the past decade, there has been an exponential increase in platforms supporting user-driven content all encouraging differing degrees of SM interaction. Despite the initial SM revolution being based on social interaction, increasingly medical professionals are harboring such streams of communication to further medical knowledge and develop professional networks. An example of a SM platform is Twitter, a well-established microblogging tool,1 which supports communities2 of medical professionals interacting regularly. Importantly, data support an increasing coverage of biomedical literature on Twitter (≈10% of all published literature).3 Stroke medicine is constantly evolving to adapt to new technologies, which have supported new therapies and new diagnostic tools. However, little is known about the benefit of new technologies to our ways of communicating. In this article, we discuss how stroke trainees in particular could benefit from using SM to communicate and improve their educational, professional, and academic development. Furthermore, we provide for the first time Twitter analytic data from an international stroke trainee-based meeting to demonstrate real-world value to trainees and importantly organizations.

Benefits to Patients

In the past decade, several medical and surgical specialties have developed international SM platforms to disseminate a variety of professional and patient relevant outputs. These include online journal clubs, anonymized cases, and patient-friendly information. Interestingly, patients seem to value online health communities in which both physicians and patients participate. The benefits are colocated information from both medical experts and experiential experts. In an online 95 stroke patient community, patients’ reasons for use of such a platform included medical activities (gathering information about disease or being informed about scientific research …
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Cognitive and Mood Assessment Tools for Use in Stroke

My mood after my doctor not telling me anything about my recovery prospects or stroke protocols being used to get recovered was not good.  My next doctor will not be let off without a complete dressing down of their lack of knowledge. If 10 million stroke survivors a year started dressing down their doctors for not knowing anything about recovery we might start getting somewhere.
Terence J. Quinn, Emma Elliott, Peter Langhorne
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Should Stroke Physicians Assess Cognition and Mood?

It would seem intuitive that for a brain disease, such as stroke, the examination of memory, thinking, and mood would be fundamental to the clinical assessment. Yet in contemporary stroke practice, we have tended to focus on the physical manifestations of stroke and neuropsychological aspects have received little, if any, attention.1 Thankfully the landscape is changing, and there is an increasing recognition of the importance of the psychological consequences of stroke and a growing evidence base and standardization around assessment.24 The stroke physician cannot be expected to take on the role of the neuropsychology specialist, and there will always be cases where expert input is required. However, a basic appreciation of how to approach cognitive and mood assessment should now be mandatory for all working in stroke care.
In this review, we discuss assessment of cognitive function and mood. We have drawn on evidence from recent research, particularly systematic review.3 We do not offer a comprehensive critique of all cognitive and mood assessment tools. Rather, we suggest a framework for assessment that emphasizes the need for differing approaches to testing at differing points in the stroke pathway (Figure 1).
Figure 1.
Neuropsychological assessment throughout the stroke pathway. Schematic illustrating a potential approach to neuropsychological assessment at various stages in the stroke pathway. The tests named are given as examples rather than recommendations. Note how all elements are used to inform the clinical diagnosis. Note also that the early assessments focus on prestroke cognition, delirium, and stroke impairments rather than detailed cognitive assessment. CAM-ICU indicates Confusion Assessment Method for the Intensive Care Unit; CES-D, Centre for Epidemiologic Studies Depression; E-ADL, Extended Activities of Daily Living; HR-QoL, Health-Related Quality of Life; IQCODE, Informant Questionnaire for Cognitive Decline in the Elderly; MoCA, Montreal Cognitive Assessment (mini-MoCA, short form of …

Neuroimaging Identifies Patients Most Likely to Respond to a Restorative Stroke Therapy

Until you idiots come up with 3d representations of dead and damaged areas you will never be able to predict recovery.
Jessica M. Cassidy, George Tran, Erin B. Quinlan, Steven C. Cramer


Background and Purpose—Patient heterogeneity reduces statistical power in clinical trials of restorative therapies. Valid predictors of treatment responsiveness are needed, and several have been studied with a focus on corticospinal tract (CST) injury. We studied performance of 4 such measures for predicting behavioral gains in response to motor training therapy.
Methods—Patients with subacute-chronic hemiparetic stroke (n=47) received standardized arm motor therapy, and change in arm Fugl-Meyer score was calculated from baseline to 1 month post-therapy. Injury measures calculated from baseline magnetic resonance imaging included (1) percent CST overlap with stroke, (2) CST-related atrophy (cerebral peduncle area), (3) CST integrity (fractional anisotropy) in the cerebral peduncle, and (4) CST integrity in the posterior limb of internal capsule.
Results—Percent CST overlap with stroke, CST-related atrophy, and CST integrity did not correlate with one another, indicating that these 3 measures captured independent features of CST injury. Percent injury to CST significantly predicted treatment-related behavioral gains (r=−0.41; P=0.004). The other CST injury measures did not, neither did total infarct volume nor baseline behavioral deficits. When directly comparing patients with mild versus severe injury using the percent CST injury measure, the odds ratio was 15.0 (95% confidence interval, 1.54–147; P<0.005) for deriving clinically important treatment-related gains.
Conclusions—Percent CST injury is useful for predicting motor gains in response to therapy in the setting of subacute-chronic stroke. This measure can be used as an entry criterion or a stratifying variable in restorative stroke trials to increase statistical power, reduce sample size, and reduce the cost of such trials.

Serum Hepatocyte Growth Factor Is Probably Associated With 3-Month Prognosis of Acute Ischemic Stroke

No clue what use this is to your recovery or prediction of stroke risk.
Zhengbao Zhu, Tan Xu, Daoxia Guo, Xinfeng Huangfu, Chongke Zhong, Jingyuan Yang, Aili Wang, Chung-Shiuan Chen, Yanbo Peng, Tian Xu, Jinchao Wang, Yingxian Sun, Hao Peng, Qunwei Li, Zhong Ju, Deqin Geng, Jing Chen, Yonghong Zhang, Jiang He
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Background and Purpose—Serum hepatocyte growth factor (HGF) is positively associated with poor prognosis of heart failure and myocardial infarction, and it can also predict the risk of ischemic stroke in population. The goal of this study was to investigate the association between serum HGF and prognosis of ischemic stroke.
Methods—A total of 3027 acute ischemic stroke patients were included in this post hoc analysis of the CATIS (China Antihypertensive Trial in Acute Ischemic Stroke). The primary outcome was composite outcome of death or major disability (modified Rankin Scale score ≥3) within 3 months.
Results—After multivariate adjustment, elevated HGF levels were associated with an increased risk of primary outcome (odds ratio, 1.50; 95% confidence interval, 1.10–2.03; Ptrend=0.015) when 2 extreme quartiles were compared. Each SD increase of log-transformed HGF was associated with 14% (95% confidence interval, 2%–27%) increased risk of primary outcome. Adding HGF quartiles to a model containing conventional risk factors improved the predictive power for primary outcome (net reclassification improvement: 17.50%, P<0.001; integrated discrimination index: 0.23%, P=0.022). The association between serum HGF and primary outcome could be modified by heparin pre-treatment (Pinteraction=0.001), and a positive linear dose–response relationship between HGF and primary outcome was observed in patients without heparin pre-treatment (Plinearity<0.001) but not in those with heparin pre-treatment.
Conclusions—Serum HGF levels were higher in the more severe stroke at baseline, and elevated HGF levels were probably associated with 3-month poor prognosis independently of stroke severity among ischemic stroke patients, especially in those without heparin pre-treatment. Further studies from other samples of ischemic stroke patients are needed to validate our findings.

Optimal Blood Pressure After Intracerebral Hemorrhage Still a Moving Target

So you are still screwed if you have a hemorrhage, once again a guinea pig in an unregistered one person clinical trial.
Alejandro A. Rabinstein
See related article, p 348
If you have been following the literature in recent years and feel confused about how to manage acute hypertension in patients with intracerebral hemorrhage (ICH), you are not alone. Two similar randomized controlled trials reaching seemingly different conclusions can confuse anybody.1,2 However, as always, the devil is in the details. It is not just about the blood pressure (BP) target, but also about how and when you reach it.
The INTERACT-2 trial (The Second Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial) evaluated nearly 2800 patients with acute hypertension within 6 hours of ICH onset randomized to target systolic BP <140 or <180 mm Hg.1 Hypertension could be treated with any drugs available, and patients were treated to remain below their BP target for 7 days. Death and moderate or severe disability at 90 days (modified Rankin score of 3–6) did not differ significant between the 2 arms (odds ratio, 0.87 with systolic BP <140 mm Hg; 95% confidence interval, 0.75–1.01; P=0.06), but functional outcomes were better in the intensive treatment arm on a prespecified ordinal shift analysis of the modified Rankin score. Serious adverse events were similar in the 2 groups. On the basis of these results, the AHA guidelines on management of ICH were modified to recommend treating acute hypertension to keep a systolic BP <140 mm Hg.3
Yet, ATACH-2 (Antihypertensive Treatment of Acute Cerebral Hemorrhage-II) was subsequently completed and moved us back to the drawing board. This trial randomized patients with acute ICH and hypertension to the same 2 systolic BP targets (ie, <140 or <180 mm Hg), but antihypertensive treatment had to be initiated within 4.5 hours of hematoma onset and intravenous nicardipine had to be used as first-line medication. The BP target was maintained for 24 hours.2 After enrollment of 1000 patients (planned n=1280), the trial was terminated because of futility after a prespecified interim analysis demonstrated that the rates of death or severe disability (modified Rankin score of 4–6) at 90 days were similar in both arms (relative risk, 1.04 with systolic BP <140 mm Hg; 95% confidence interval, 0.85–1.27; P=0.72 on analysis adjusted for prognostic factors). Unlike INTERACT-2, ATACH-2 showed no difference in the ordinal distribution of modified Rankin scores and instead showed an increase in renal adverse events within 7 days on the intensive treatment arm, which could have been caused by excessive BP lowering on the first day.
Then what have we learned from these 2 trials? Although the target systolic BPs were the same in both trials, actual BP reduction was faster and more pronounced in ATACH-2—average systolic BP over the first 24 hours was 120 to 130 mm Hg in ATACH-2 versus 135 to 145 mm Hg in INTERACT-2—and this degree of reduction may have been too much. In fact, systolic BP <130 mm Hg was also associated with worse prognosis in a secondary analysis of INTERACT-2.4 Taken along with the lack of effect from intensive BP lowering on reducing hematoma expansion observed in both trials, these combined findings argue against overzealous BP lowering during the first few hours after an ICH.
The study by Chung et al5 published on this issue of Stroke contributes another piece to this puzzle. This study evaluated BP variability within the first 24 to 26 after ICH among 386 patients enrolled in the FAST-MAG trial (Field Administration of Stroke Therapy-Magnesium) with a particular interest on BP changes during the first 4 to 6 hours (ie, the hyperacute phase). The first available BP was obtained by paramedics in the field at a median of 23 minutes after symptom onset. The results demonstrate a strong dose-dependent association of greater BP variability with unfavorable functional outcomes (modified Rankin score of 3–6) at 90 days. The association was particularly strong for BP variability during the hyperacute period, to the point that patients in the highest quintile of hyperacute BP variability had a 3- to 4-fold increase in the risk of unfavorable outcome even after adjustment for age, initial severity, and mean systolic BP. Of note, mean systolic BPs during the first 6 hours ranged mostly between 155 and 165 mm Hg, and neither mean systolic BP nor maximal systolic BP during this hyperacute period was associated with unfavorable functional outcome.
Although the analysis by Chung et al5 could not be adjusted for all major prognostic factors (missing were hematoma volume, hematoma location, and intraventricular hemorrhage), the associations seem solid. Greater BP variability was also associated with worse clinical outcomes in INTERACT-2 and SAMURAI-ICH (Stroke Acute Management With Urgent Risk-Factor Assessment and Improvement–Intracerebral Hemorrhage),6,7 although these trials did not include consistent information on the BP during the first few hours. Thus, cumulative evidence suggests that BP variability should be avoided, especially very early after an ICH.
What the study by Chung et al5 cannot tell us is to what degree the BP changes were induced by BP-lowering medications. Neither does it provide information on early neurological decline related to the BP changes, which actually were not more common in the intensive treatment arms of INTERACT-2 or ATACH-2. Also, as acknowledged by the investigators and especially considering the limitations of the adjusted analysis, the data cannot conclusively determine whether the association of greater hyperacute BP variability with worse outcome reflects a detrimental effect of the BP fluctuations or simply shows that BP fluctuations are more prominent in patients with more severe hematomas.
The optimal management of acute hypertension after ICH remains undefined. Large randomized trials did not provide consistent evidence that aiming for one particular BP target is broadly beneficial and informed us that very rapid and aggressive BP reduction can be harmful. Meanwhile, exploratory analyses like the one reported by Chung et al5 indicate that excessive BP fluctuations portend poor outcome and suggest that avoiding these fluctuations could represent a valid therapeutic target. As we keep learning, we should follow the advice of the old sages who always preached the merits of moderation and lower BP after ICH neither too fast nor too low.