Robot-assisted training of the kinesthetic sense: enhancing proprioception after stroke

What is your doctors proprioception stroke protocol? If none, Why the hell are you paying them?
http://journal.frontiersin.org/Journal/10.3389/fnhum.2014.01037/full?
Dalia De Santis¹*, Jacopo Zenzeri¹, Maura Casadio^1,2, Lorenzo Masia^1,3, Assunta Riva⁴, Pietro Morasso^1,2 and Valentina Squeri¹

• ¹Motor Learning and Robotic Rehabilitation Laboratory, Department of Robotics, Brain and Cognitive Sciences (RBCS), Istituto Italiano di Tecnologia, Genova, Italy
• ²NeuroLab, Department of Informatics, Bioengineering, Robotics and Systems (DIBRIS), University of Genova, Genova, Italy
• ³Assistive Robotics and Interactive Ergonomic Systems Laboratory, Division of Mechatronics and Design, Robotic Research Center, School of Mechanical and Aerospace Engineering (MAE), Nanyang Technological University (NTU), Singapore
• ⁴SI4LIFE – Innovation Hub for Elderly and Disabled People, Genova, Italy

Proprioception has a crucial role in promoting or hindering motor learning. In particular, an intact position sense strongly correlates with the chances of recovery after stroke. A great majority of neurological patients present both motor dysfunctions and impairments in kinesthesia, but traditional robot and virtual reality training techniques focus either in recovering motor functions or in assessing proprioceptive deficits. An open challenge is to implement effective and reliable tests and training protocols for proprioception that go beyond the mere position sense evaluation and exploit the intrinsic bidirectionality of the kinesthetic sense, which refers to both sense of position and sense of movement. Modulated haptic interaction has a leading role in promoting sensorimotor integration, and it is a natural way to enhance volitional effort. Therefore, we designed a preliminary clinical study to test a new proprioception-based motor training technique for augmenting kinesthetic awareness via haptic feedback. The feedback was provided by a robotic manipulandum and the test involved seven chronic hemiparetic subjects over 3 weeks. The protocol included evaluation sessions that consisted of a psychometric estimate of the subject’s kinesthetic sensation, and training sessions, in which the subject executed planar reaching movements in the absence of vision and under a minimally assistive haptic guidance made by sequences of graded force pulses. The bidirectional haptic interaction between the subject and the robot was optimally adapted to each participant in order to achieve a uniform task difficulty over the workspace. All the subjects consistently improved in the perceptual scores as a consequence of training. Moreover, they could minimize the level of haptic guidance in time. Results suggest that the proposed method is effective in enhancing kinesthetic acuity, but the level of impairment may affect the ability of subjects to retain their improvement in time.

Planning following stroke: a relational complexity approach using the Tower of London

No idea what this means. Your doctor will know.
http://journal.frontiersin.org/Journal/10.3389/fnhum.2014.01032/full?
Glenda Andrews¹*, Graeme S. Halford², Mark Chappell², Annick Maujean³ and David H. K. Shum²

• ¹Behavioural Basis of Health Program, Griffith Health Institute, School of Applied Psychology, Griffith University, Gold Coast, QLD, Australia
• ²Behavioural Basis of Health Program, Griffith Health Institute, School of Applied Psychology, Griffith University, Brisbane, QLD, Australia
• ³Centre for National Research on Disability and Rehabilitation Medicine (CONROD), Griffith Health Institute, Griffith University, Meadowbrook, QLD, Australia

Planning on the 4-disk version of the Tower of London (TOL4) was examined in stroke patients and unimpaired controls. Overall TOL4 solution scores indicated impaired planning in the frontal stroke but not non-frontal stroke patients. Consistent with the claim that processing the relations between current states, intermediate states, and goal states is a key process in planning, the domain-general relational complexity metric was a good indicator of the experienced difficulty of TOL4 problems. The relational complexity metric shared variance with task-specific metrics of moves to solution and search depth. Frontal stroke patients showed impaired planning compared to controls on problems at all three complexity levels, but at only two of the three levels of moves to solution, search depth and goal ambiguity. Non-frontal stroke patients showed impaired planning only on the most difficult quaternary-relational and high search depth problems. An independent measure of relational processing (viz., Latin square task) predicted TOL4 solution scores after controlling for stroke status and location, and executive processing (Trail Making Test). The findings suggest that planning involves a domain-general capacity for relational processing that depends on the frontal brain regions.

Post-stroke balance rehabilitation under multi-level electrotherapy: a conceptual review

You'll have to see what your doctor does with this to update your stroke balance protocol.
http://journal.frontiersin.org/Journal/10.3389/fnins.2014.00403/full?
Anirban Dutta^1,2*, Uttama Lahiri³, Abhijit Das⁴, Michael A. Nitsche⁵ and David Guiraud^1,2

• ¹DEMAR (INRIA Sophia Antipolis), INRIA, CNRS: UMR5506, Université Montpellier II - Sciences et Techniques, Université Montpellier I, Montpellier, France
• ²Laboratoire d'Informatique de Robotique et de Microélectronique de Montpellier, CNRS: UMR5506, Université Montpellier II - Sciences et Techniques, Montpellier, France
• ³Electrical Engineering, Indian Institute of Technology, Gandhinagar, India
• ⁴Department of Neurorehabilitation, Institute of Neurosciences, Kolkata, India
• ⁵Department of Clinical Neurophysiology, Göttingen University Medical School, Göttingen, Germany

Stroke is caused when an artery carrying blood from heart to an area in the brain bursts or a clot obstructs the blood flow thereby preventing delivery of oxygen and nutrients. About half of the stroke survivors are left with some degree of disability. Innovative methodologies for restorative neurorehabilitation are urgently required to reduce long-term disability. The ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function, and connections is called neuroplasticity. Neuroplasticity is involved in post-stroke functional disturbances, but also in rehabilitation. It has been shown that active cortical participation in a closed-loop brain machine interface (BMI) can induce neuroplasticity in cortical networks where the brain acts as a controller, e.g., during a visuomotor task. Here, the motor task can be assisted with neuromuscular electrical stimulation (NMES) where the BMI will act as a real-time decoder. However, the cortical control and induction of neuroplasticity in a closed-loop BMI is also dependent on the state of brain, e.g., visuospatial attention during visuomotor task performance. In fact, spatial neglect is a hidden disability that is a common complication of stroke and is associated with prolonged hospital stays, accidents, falls, safety problems, and chronic functional disability. This hypothesis and theory article presents a multi-level electrotherapy paradigm toward motor rehabilitation in virtual reality that postulates that while the brain acts as a controller in a closed-loop BMI to drive NMES, the state of brain can be can be altered toward improvement of visuomotor task performance with non-invasive brain stimulation (NIBS). This leads to a multi-level electrotherapy paradigm where a virtual reality-based adaptive response technology is proposed for post-stroke balance rehabilitation. In this article, we present a conceptual review of the related experimental findings.

2015: which new directions for Alzheimer's disease?

If we had anything approaching a great stroke organization  we would know exactly how far we are along in our strategy and what the next steps were. And at 10 million stroke survivors a year we should be able to claim it as one of the biggest global public health challenges. But we have crap for stroke associations. Good luck because you are totally on your own with your recovery.
http://journal.frontiersin.org/Journal/10.3389/fncel.2014.00417/full?

Xénia Latypova and Ludovic Martin^*

• Université de Nantes, Nantes, France

Around 44 million people in the world are suffering from dementia including Alzheimer's disease (AD). It is considered as one of the biggest global public health challenges our generation cope with. At the dawn of 2015, AD medical care remains unsuccessful despite the identification of its neuropathological hallmarks one century ago. Being attentive to emerging prospects is essential because the current advances lead to substantive improvement of the medical care. We are pleased to present an issue specifically devoted to AD and to the related therapeutic strategies. The Topic Research in this issue is based on a series of original papers and reviews. The latters focus on the advances in basic and clinical research trends in AD, they provide an up-to-date information and future perspectives on this hot topic as well.

AD is a progressive disease, it occurs over a long period before the onset of symptoms which are impaired memory, apathy, and depression. The characteristics of AD consist in neurofibrillary tangles (intraneuronal aggregates of hyperphosphorylated tau proteins) and senile plaques [dense extraneuronal deposits composed of amyloid β (Aβ)]. The other features linked to these two core pathological hallmarks of AD are inflammation, oxidative stress, progressive synaptic, and neuronal loss. Nowadays, many AD molecular patterns have been screened to identify a potential therapeutic strategy. Although a myriad of evidence shows that the hippocampal volume decrease belongs to the AD earliest signs, as it is pointed out by the authors of the review paper presented in this issue, this element clearly could not be used as a diagnostic criterion (Maruszak and Thuret, 2014).

With the flood of evidence for tau pathology as key event of the disease development, the understanding of diverse tau functions and its molecular behavior is one of the major steps in the progression of our knowledge about the neurodegenerescence detected in AD. The precision of tau role in DNA protection and RNA integrity under physiological conditions or under ROS-producing stress (Violet et al., 2014) provides clarification for a mechanistic model in which tau disturbance initiates an explanation for DNA damages observed in AD. Principally, tau is a phosphoprotein. So, a complex equilibrium between tau kinases and phosphatases activities is one of the main potential therapeutic runways. Abnormal or excessive tau phosphorylation by either kinases such as GSK3β, CDK5, DYRK1A for example or other known and unknown kinases are related to AD pathogenesis. However, the identity and the strict number of tau kinases involved in AD process remain uncertain. In this way, focus at specific tau phosphorylation site(s) by a kinase multitargeting approach as potential AD therapeutic strategy has been proposed to effectively hamper the multifactorial disease progression (Hilgeroth and Tell, 2013). Since diabetes, linked itself to dysregulation of GSK3β activity, is associated in late-life with an increased risk of dementia, epidemiological and experimental studies are summarized in this issue in order to understand the effects of diabetes mellitus on tau pathogenesis. In fact, the authors discuss herein a link between tau, diabetes mellitus and the cognitive impairment (El Khoury et al., 2014). On the other hand, Peptidyl-prolyl cis-trans Isomerase NIMA-interacting 1 (Pin1), which plays a role in the balance of phosphorylation/dephosphorylation of tau, has been suspected of participating in a common mechanism between AD and hypoxia. The pathophysiological relevance of Hypoxia-inducible factor 1α (HIF-1α) pathway regulation in APP amyloidogenic metabolism has been explored in order to clarify the relationship between AD and hypoxia (Lonati et al., 2014). Among tau-based therapeutic strategies, the one which limits the spreading of tau pathology without affecting tau intracellular functions is especially attractive (Medina and Avila, 2014). Strong support for this idea comes from the importance of tau for Aβ-induced synaptotoxicity. In addition to this, high concentration of Aβ inhibits synaptic activity and in turn, it involves toxicity for the targeted synapses (Wang et al., 2013). According to this strategy, synaptic inhibitory systems could help to compensate neurotransmission imbalance (Nava-Mesa et al., 2014). Moreover, natural anti-inflammatory components, as Andrean Compound, has been studied as a preventive or adjuvant agent in AD (Maccioni et al., 2014).

Accumulation of Aβ is induced when the equilibrium between its production and clearance is disrupted. Thus, amyloid-based therapeutic strategies target this balance but numerous trials were unsuccessful for reasons of specificity or biodisponibility. However, the restoration of the microglial homeostasy and the targeting of Triggering Receptor Expressed on Myeloid cells 2 (TREM2) pathway can constitute an elegant therapeutic strategy (Zhao and Lukiw, 2013). Compounds are yet available to improve the microglia-dependent clearance of Aβ, and this strategy would benefit from in vivo experiments (Jones et al., 2014). Furthermore, diversity of gut microbiota changes through life stages and alterations of this ecosystem have been associated with diverse diseases. Therapeutic modulation of gut microbiota could constitute a promising adjuvant therapy in central neurodegenerative disorders. An opinion article proposes probiotics as a prophylactic treatment to prevent AD in its early stages (Bhattacharjee and Lukiw, 2013).

Several recent key advances in the field of AD understanding and treatment are presented in this thematic issue. Ultimately, we hope that you will enjoy as us to read these papers and reviews presented in this special issue. The coming years certainly promise a time for completion of a new era in the history of the AD understanding and emerging therapies. AD understanding is within reach. Stay tuned.

4 Ways To Reap Red Wine’s Benefits — Without Drinking It

I only had 5 glasses of red wine yesterday, 2 at a jazz concert, 3 more at a friends house after. Way less than the 52 bottles needed. I despise boiled peanuts so I'm not going down that route.
4 Ways To Reap Red Wine’s Benefits — Without Drinking It

Research has done it again: reiterated just how healthy red wine’s potent ingredient is. The polyphenol resveratrol helps you live longer! It prevents heart disease! It protects your skin! And the latest: It helps your memory.

And while there’s some truth to the antioxidant, anti-inflammatory properties of the darker vino, alcohol isn’t always your best bet for a health defense. (Plus, some research suggests that in order to rein in some of resveratrol’s touted effects, you’d have to drink 52 bottles of wine a day, which no health expert would suggest you do.)

So, consider these four ways to sneak resveratrol into your diet — we won’t tell your Malbec-loving friends.

Itadori Tea

This herbal tea popular in Japan and China has traditionally been used to fend off heart disease and strokes. But some research suggests that its high levels of resveratrol make it a perfect replacement for people who don’t drink red wine, says Ilyse Schapiro, a New York-based registered dietitian.

Peanuts (And Peanut Butter)

“Boiled peanuts actually contain more reservatrol than peanut butter,” Schapiro tells Yahoo Health. You’ll get less from a PB&J than a glass of wine, but the food is still considered a good source of the antioxidant.

Invest in a Serum

“Antioxidants ingested through drinking do not directly help neutralize free radicals on the skin the way topical resveratrol does,” dermatologist Elizabeth Tanzi, MD, co-director of the Washington Institute of Dermatologic Laser Surgery in Washington, DC, tells Yahoo Health. In product form, resveratrol can help your skin. It’s also a natural anti-inflammatory and provides sun protection, says Joanna Vargas, celebrity facialist and founder of the Joanna Vargas Salon and Skincare Collection. (Studies in animals back this up.)

Supplements

Before you pop a pill, keep this in mind: Supplements aren’t regulated by the FDA. But Joseph Maroon, MD, author of The Longevity Factor: How Resveratrol and Red Wine Activate Genes for a Longer and Healthier Life, says he doesn’t see a real downside to taking a resveratrol supplement. There are virtually no side effects, he says. It’s better to eat your nutrients than take them in vitamin form, he says, but for people who struggle to incorporate polyphenol-rich foods like berries or dark chocolate into their diets, a supplement could be a good idea. Try 250 or 500 milligrams of ResVitale, available at big-name stores like GNC.

But here’s a reason to consider (moderate consumption of) red wine…

“There are about 500 other polyphenols besides resveratrol in a glass of red wine — and maybe only 1 or 2 milligrams of resveratrol,” Maroon says. So in addition to the other polyphenols, with red wine, you get the “synergism of absorption” which can provide more benefits than one polyphenol on its own. If you’re red wine-wary, consider that one of the lightest pours — Pinot Noir — is also the one richest in resveratrol, says Maroon.

Coat removal stroke protocol

Absolutely no hits from Google or YouTube. I struggle every single time I need to remove my coat. Friends jump up and start pulling on the left sleeve, which usually works once my spastic curled fingers get past the cuff. To do this by myself I have to pull my left shoulder of the coat down, reach my left arm behind my back, walk to a wall edge and have my left arm against the corner, turn my body to the right, reach with my right arm behind my back, feeling for the left arm cuff, then pulling the coat off the left arm behind my back. This usually leaves my left arm stuck back there and I have to reach around and pull it back to my side so it hangs somewhat normally. I grab the right cuff with my teeth and pull the rest of the coat off.
I can't even remember the correct way to remove a coat anymore. For such a common ADL there should be hundreds of videos demonstrating this.
Coat removal videos are about painting.
Jacket removal videos are about yellow jackets.

Promising Peptide for TBI, Heart Attack and Stroke

What is your doctor and hospital doing to see if this actually works in humans? Or are they so fucking lazy because everything in stroke is somebody elses' problem?  And your dead brain cells are the result? 

Promising Peptide for TBI, Heart Attack and Stroke

Strokes, heart attacks and traumatic brain injuries are separate diseases with certain shared pathologies that achieve a common end – cell death and human injury due to hypoxia, or lack of oxygen. In these diseases, a lack of blood supply to affected tissues begins a signaling pathway that ultimately halts the production of energy-releasing ATP molecules – a death sentence for most cells.
By employing derivatives of humanin, a naturally occurring peptide encoded in the genome of cellular mitochondria, researchers at Ben Gurion University of the Negev are working to interrupt this process, buying precious time for tissues whose cellular mechanisms have called it quits.
"The present findings could provide a new lead compound for the development of drug therapies for necrosis-related diseases such as traumatic brain injury, stroke and myocardial infarction - conditions for which no effective drug-based treatments are currently available [that work by blocking necrosis]," said Abraham Parola, a professor of biophysical chemistry at Ben Gurion University of the Negev in Beer-Sheva, Israel. Parola is presently a visiting professor of Biophysical Chemistry & Director of Natural Sciences at New York University Shanghai, and will speak about his lab's finding's this week at the Biophysical Society's 59^th annual meeting in Baltimore, Md.
The humanin derivatives work by counteracting the decrease in ATP levels caused by necrosis. The researchers tested the effectiveness of the humanin analogues AGA(C8R)-HNG17 and AGA-HNG by treating neuronal cells with these peptides prior to exposure to a necrotic agent. The experiments were a success.
Parola's previous work has dealt with membrane dynamics and the mechanism of action of anti-angiogenesis drugs, which cause starvation of malignant tumor growths by preventing the supply of nutrients and oxygen to the fast growing tissue, in addition to various other biophysical and molecular medicine and diagnostic topics.
"A recent paper published by our group suggested the involvement of cardiolipin [a phospholipid in inner mitochondrial membranes] in the necrotic process," Parola said. "During this work we stumbled along humanin and were intrigued by its anti-apoptotic effect, and extended it to anti-necrotic effect."
Parola and his colleagues also performed in vivo studies by treating mice that had had traumatic brain injuries with an HNG17 analogue, which successfully reduced cranial fluid buildup and lowered the mice's neuronal severity scores, a metric in which a higher number corresponds with greater degrees of neurological motor impairment.
As the peptides Parola and his colleagues used are derivatives of naturally occurring humanin, an ideal treatment might involve a drug delivery system with the HNG17 as the lead compound, a process aided by the ability of the peptides to penetrate the cell membrane without the use of additional reagents.
Future work for Parola and his colleagues includes further exploration of ischemic activity in liver cirrhosis, as induced by acetaminophen activity, in addition to searching for a synergistic effect between humanin and other anti-necrotic agents, such as protease inhibitors, to increase its clinical potential.

Prehospital use of magnesium sulfate as neuroprotection in acute stroke.

How does this one compare to  these 31 hyperacute possibilities I'm going to insist my doctor give me the first week. 
Exactly when is your doctor going to start clinical trials to prove efficacy of therapies in the first week? Or is your doctor a lazy bastard because it is  somebody elses' problem?
 Prehospital use of magnesium sulfate as neuroprotection in acute stroke.

Saver JL¹, Starkman S, Eckstein M, Stratton SJ, Pratt FD, Hamilton S, Conwit R, Liebeskind DS, Sung G, Kramer I, Moreau G, Goldweber R, Sanossian N; FAST-MAG Investigators and Coordinators.

Collaborators (1220)

Author information

Abstract

BACKGROUND:

Magnesium sulfate is neuroprotective in preclinical models of stroke and has shown signals of potential efficacy with an acceptable safety profile when delivered early after stroke onset in humans. Delayed initiation of neuroprotective agents has hindered earlier phase 3 trials of neuroprotective agents.

METHODS:

We randomly assigned patients with suspected stroke to receive either intravenous magnesium sulfate or placebo, beginning within 2 hours after symptom onset. A loading dose was initiated by paramedics before the patient arrived at the hospital, and a 24-hour maintenance infusion was started on the patient's arrival at the hospital. The primary outcome was the degree of disability at 90 days, as measured by scores on the modified Rankin scale (range, 0 to 6, with higher scores indicating greater disability).

RESULTS:

Among the 1700 enrolled patients (857 in the magnesium group and 843 in the placebo group), the mean (±SD) age was 69±13 years, 42.6% were women, and the mean pretreatment score on the Los Angeles Motor Scale of stroke severity (range, 0 to 10, with higher scores indicating greater motor deficits) was 3.7±1.3. The final diagnosis of the qualifying event was cerebral ischemia in 73.3% of patients, intracranial hemorrhage in 22.8%, and a stroke-mimicking condition in 3.9%. The median interval between the time the patient was last known to be free of stroke symptoms and the start of the study-drug infusion was 45 minutes (interquartile range, 35 to 62), and 74.3% of patients received the study-drug infusion within the first hour after symptom onset. There was no significant shift in the distribution of 90-day disability outcomes on the global modified Rankin scale between patients in the magnesium group and those in the placebo group (P=0.28 by the Cochran-Mantel-Haenszel test); mean scores at 90 days did not differ between the magnesium group and the placebo group (2.7 in each group, P=1.00). No significant between-group differences were noted with respect to mortality (15.4% in the magnesium group and 15.5% in the placebo group, P=0.95) or all serious adverse events.

CONCLUSIONS:

Prehospital initiation of magnesium sulfate therapy was safe and allowed the start of therapy within 2 hours after the onset of stroke symptoms, but it did not improve disability outcomes at 90 days. (Funded by the National Institute of Neurological Disorders and Stroke; FAST-MAG ClinicalTrials.gov number, NCT00059332.).

The potential therapeutic effects of THC on Alzheimer's disease

For your doctors' knowledge. This won't be enough to get through the stupidity of Schedule I classification of marijuana. Every single congressperson is going to need to get alzheimers and be successfully treated like this before they legalize it.  I personally will travel to Colorado.
http://www.ncbi.nlm.nih.gov/pubmed/25024327

Cao C¹, Li Y², Liu H¹, Bai G², Mayl J³, Lin X¹, Sutherland K⁴, Nabar N⁵, Cai J².

Author information

Abstract

The purpose of this study was to investigate the potential therapeutic qualities of Δ9-tetrahydrocannabinol (THC) with respect to slowing or halting the hallmark characteristics of Alzheimer's disease. N2a-variant amyloid-β protein precursor (AβPP) cells were incubated with THC and assayed for amyloid-β (Aβ) levels at the 6-, 24-, and 48-hour time marks. THC was also tested for synergy with caffeine, in respect to the reduction of the Aβ level in N2a/AβPPswe cells. THC was also tested to determine if multiple treatments were beneficial. The MTT assay was performed to test the toxicity of THC. Thioflavin T assays and western blots were performed to test the direct anti-Aβ aggregation significance of THC. Lastly, THC was tested to determine its effects on glycogen synthase kinase-3β (GSK-3β) and related signaling pathways. From the results, we have discovered THC to be effective at lowering Aβ levels in N2a/AβPPswe cells at extremely low concentrations in a dose-dependent manner. However, no additive effect was found by combining caffeine and THC together. We did discover that THC directly interacts with Aβ peptide, thereby inhibiting aggregation. Furthermore, THC was effective at lowering both total GSK-3β levels and phosphorylated GSK-3β in a dose-dependent manner at low concentrations. At the treatment concentrations, no toxicity was observed and the CB1 receptor was not significantly upregulated. Additionally, low doses of THC can enhance mitochondria function and does not inhibit melatonin's enhancement of mitochondria function. These sets of data strongly suggest that THC could be a potential therapeutic treatment option for Alzheimer's disease through multiple functions and pathways.

We don't care enough to want you to give us constructive feedback - stroke associations

The only one I have seen that seems to want feedback is the British Stroke Association.
Here at the Stroke Association we are looking for a representative sample of people affected by stroke to take part in a reader panel to provide feedback and advice on our written information publications and help us to be really sure that they are meeting the needs of stroke survivors and their carers.
Reader panel members will be sent a range of publications by post or email to read at regular intervals throughout the year and will be asked to provide a range of feedback, via a method appropriate to your needs.
Another failure in our stroke world. Someday our stroke leaders will realize they are failing survivors. Probably because the associations are for doctors and researchers, not survivors.

ASA - Nope

NSA - Nope

WSO - Nope

A great writeup from Seth Godin;

We don't care enough to give you constructive feedback

FDA Okays VEGF Drug for Diabetic Retinopathy

VEGF may be useful for us. Have your doctor read my 23 posts on the subject and explain why you don't already have a stroke protocol  for this.
http://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/49919?

Forever Young(er): potential age-defying effects of long-term meditation on gray matter atrophy

How many decades before your doctor creates a stroke protocol around this? 5? 10? Don't do this on your own, you know how dangerous meditation is without your doctors prescription to control it.
http://journal.frontiersin.org/journal/10.3389/fpsyg.2014.01551/abstract

Eileen Luders^1*, Nicolas Cherbuin² and Florian Kurth¹

• ¹Department of Neurology, School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA
• ²Centre for Research on Ageing Health and Wellbeing, Australian National University, Canberra, ACT, Australia

While overall life expectancy has been increasing, the human brain still begins deteriorating after the first two decades of life and continues degrading further with increasing age. Thus, techniques that diminish the negative impact of aging on the brain are desirable. Existing research, although scarce, suggests meditation to be an attractive candidate in the quest for an accessible and inexpensive, efficacious remedy. Here, we examined the link between age and cerebral gray matter re-analyzing a large sample (n = 100) of long-term meditators and control subjects aged between 24 and 77 years. When correlating global and local gray matter with age, we detected negative correlations within both controls and meditators, suggesting a decline over time. However, the slopes of the regression lines were steeper and the correlation coefficients were stronger in controls than in meditators. Moreover, the age-affected brain regions were much more extended in controls than in meditators, with significant group-by-age interactions in numerous clusters throughout the brain. Altogether, these findings seem to suggest less age-related gray matter atrophy in long-term meditation practitioners.

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Influence of visual and auditory biofeedback on partial body weight support treadmill training of individuals with chronic hemiparesis: a randomized controlled clinical trial.

Finally, a trial published that had a negative result.
http://europepmc.org/abstract/med/25634107

(PMID:25634107)

• Abstract
• Citations
• BioEntities
• Related Articles
• External Links

Brasileiro A, Gama G, Trigueiro L, Ribeiro T, Silva E, Galvão É, Lindquist A

Department of Physical Therapy Federal University of Rio Grande do Norte, Natal‑RN, Brazil - raquellindquist@ufrnet.br.

European Journal of Physical and Rehabilitation Medicine [2015]

Type: Journal Article

Abstract

Highlight Terms Diseases(1)

BACKGROUND: Stroke is an important causal factor of deficiency and functional dependence worldwide.

OBJECTIVE: To determine the immediate effects of visual and auditory biofeedback, combined with partial body weight supported (PBWS) treadmill training on the gait of individuals with chronic hemiparesis.

DESIGN: Randomized controlled trial.

SETTING: Outpatient rehabilitation hospital.

POPULATIONS: Thirty subjects with chronic hemiparesis and ability to walk with some help.

METHODS: Participants were randomized to a control group that underwent only PBWS treadmill training; or experimental I group with visual biofeedback from the display monitor, in the form of symbolic feet as the subject took a step; or experimental group II with auditory biofeedback associated display, using a metronome at 115% of the individual's preferred cadence. They trained for 20 minutes and were evaluated before and after training. Spatio-temporal and angular gait variables were obtained by kinematics from the Qualisys Motion Analysis system.

RESULTS: Increases in speed and stride length were observed for all groups over time (speed: F=25.63; P<0.001; stride length: F=27.18; P<0.001), as well as changes in hip and ankle range of motion - ROM (hip ROM: F=14.43; P=0.001; ankle ROM: F=4.76; P=0.038), with no time*groups interaction. Other spatio-temporal and angular parameters remain unchanged.

CONCLUSIONS: Visual biofeedback and auditory biofeedback had no influence on PBWS treadmill training of individuals with chronic hemiparesis, in short term. Additional studies are needed to determine whether, in long term, the biofeedback will promote additional benefit to the PBWS treadmill training.

CLINICAL REHABILITATION IMPACT: The findings of this study indicate that visual and auditory biofeedback does not bring immediate benefits on PBWS treadmill training of individuals with chronic hemiparesis. This suggest that, for additional benefits are achieved with biofeedback, effects should be investigated after long-term training, which may determine if some kind of biofeedback is superior to another to improve the hemiparetic gait.

9 Nutrients Which Should Be In Your Diet for Good Mental Health

Is your doctor and hospital following this for your post-stroke diet protocol?
http://www.spring.org.uk/2015/02/9-nutrients-which-should-be-in-your-diet-for-good-mental-health.php?
Doctors, nutritionists, psychologists, psychiatrists and others all question the lack of attention paid to nutrition in mental health, in the review, published in The Lancet Psychiatry (Sarris et al., 2015).
Studies have shown clear links between the following nine nutrients (among others) and brain health:

1. omega-3s,
2. B vitamins (particularly folate and B12),
3. choline,
4. iron,
5. zinc,
6. magnesium,
7. S-adenosyl methionine (SAMe),
8. vitamin D,
9. and amino acids.

More at link.

The trouble with tDCS? Electrical brain stimulation may not work after all

A single session of tDCS may have no detectable effect on cognitive function in most people.  I'm sure a single session of PT will have no effect on most people.

Have your doctor validate all this research;

Single Session of Dual-tDCS Transiently Improves Precision Grip and Dexterity of the Paretic Hand After Stroke

Effect of Anodal Versus Cathodal Transcranial Direct Current Stimulation on Stroke Rehabilitation

Jumper Cables for the Mind

Effect of Anodal Versus Cathodal Transcranial Direct Current Stimulation on Stroke Rehabilitation: A Pilot Randomized Controlled Trial 

Transcranial brain stimulation after stroke

Noninvasive brain stimulation shown to impact walking patterns

 

The newest one:

The trouble with tDCS? Electrical brain stimulation may not work after all

Hawks freshman shows grit in recovering from stroke

Once again tPA does not provide full recovery. How many more times will tPA need to be shown to fail before something better is found?
http://www.philly.com/philly/sports/colleges/st_josephs/20150206_Hawks_freshman_shows_grit_in_recovering_from_stroke.html

UMd Professors Get $100,000 to Build Rehab Robot For Stroke Patients - wrist

You can compare to these already out there;

Wrist Rehabilitation Assisted by an Electromyography-Driven Neuromuscular Electrical Stimulation Robot After Stroke

 Myoelectrically controlled wrist robot for stroke rehabilitation

Design and control of a 2 degree of freedom upper limb robotic rehabilitation device

 

Rome doctors use robotic glove, videogame on stroke patients

Can surface neuromuscular electrical stimulation of the wrist and hand combined with routine therapy facilitate recovery of arm function in patients with stroke?

 The newest one here:

UMd Professors Get $100,000 to Build Rehab Robot For Stroke Patients - wrist

Bedding and pillows improve positioning in stroke patients

How does this interact with the Head of Bed positioning? How many years will this take to get rolled out to your hospital? 50? 100?

HOBOE (Head-of-Bed Optimization of Elevation) Study: association of higher angle with reduced cerebral blood flow velocity in acute ischemic stroke.

The influence of positioning upon cerebral oxygenation after acute stroke: a pilot study

The new one here:

Bedding and pillows improve positioning in stroke patients

Many patients with a cerebral injury cannot move independently. Every year, 45,000 new stroke patients are affected in such a way. They have to be repositioned at regular intervals for a long period of time in order to prevent pressure ulcers that may develop as a result of patients’ physical immobility. Heidrun Pickenbrock et al., in a topical original article in Deutsches Ärzteblatt International, compare two positioning methods for immobile patients. They found that lying in the so called neutral position is more comfortable for affected patients, and that mobility of hips and shoulders is improved compared with when the conventional method is used.
In the study, more than 218 immobile patients with a brain injury were placed in a conventional position or the neutral position for two hours. The positions differ primarily in terms of the load placed on certain body sections. In the neutral position, the body parts are aligned in order to prevent overextension and shortening of muscles and tendons. A survey among participating patients showed that the neutral position is experienced as more comfortable than the conventional position. Furthermore, a study of passive mobility showed that the hip and shoulder joints were more mobile after patients had been placed in the neutral position than after conventional positioning.
http://www.aerzteblatt.de/pdf.asp?id=167249

 

 

Scientists Discover a Key Pathway That Protects Cells Against Death by Stress

What is your doctor doing to protect you against the stress of no stroke protocols for getting to 100% recovery? You're under a lot of stress about recovery so DEMAND this protection against cell death.

Scientists Discover a Key Pathway That Protects Cells Against Death by Stress

When it comes to protecting cells from death brought on by the calamities of environmental stress, the human body is particularly ingenious. From cellular components that suck up misfolded proteins to a vigilant immune system, the ways we protect our cells (and ourselves) are many and mysterious.
Scientists from the Florida campus of The Scripps Research Institute (TSRI) have now uncovered the workings of another cell-protection device, one that may play a major role in a number of age-related diseases, including diabetes and Parkinson’s, Alzheimer’s and Huntington’s diseases.
The study, led by Srinivasa Subramaniam, a TSRI assistant professor, and Solomon H. Snyder, a neuroscience professor at Johns Hopkins University School of Medicine, was published February 5 in the journal Cell Reports.
More or Less Acceleration
The study focuses on a new pathway through which Rheb, a regulator that many believe is active in the brain’s ability to change in response to learning, actually plays two roles, rather than one—stimulating and inhibiting protein synthesis.
The interplay between the two roles may be the key that enables cells to alter protein synthesis and protect the cell in response to varying environmental stresses.
“We found Rheb acts like the gas pedal in a car,” Subramaniam said. “It can either increase translation or decrease it. And because translation is a fundamental process that is affected in a lot of diseases, we now think that Rheb may act like a switch in some disease states—helping to turn them off and on.”
Rheb is known to bind and activate mTOR, a developmentally important gene that integrates signals from multiple pathways and regulates critical cell functions such as protein synthesis. Besides its role as an activator of mTOR, which plays a major role in conditions from diabetes to neurodegenerative disease, the mTOR-independent role of Rheb is less known. The new study defines crucial mTOR-independent effects of Rheb. Results showed that, when stressed, Rheb instead inhibits protein synthesis by amplifying the phosphorylation (adding a phosphate group to a protein to alter its function) of another protein known eIF2a. As a result, cell resources can be conserved rather than squandered when the environment is challenging.
“We don’t really understand the full role of the Rheb-mTOR pathway, but we have uncovered a new fundamental process of Rheb that is independent of mTOR and very intriguing,” said Neelam Shahani, a member of Subramaniam’s lab who was co-first author of the study with Richa Tyagi of Johns Hopkins University School of Medicine. “Rheb can inhibit protein synthesis, and we know that protein misfolding via environmental stress factors is present in a lot of diseases.”
Subramaniam noted that, intriguingly, an earlier study had suggested the Rheb pathway had been implicated in Alzheimer’s disease. “We also want to look at Rheb’s role in other neurodegenerative diseases,” he said.
In addition to Subramaniam, Snyder, Shahani and Tyagi, authors of the study, “Rheb Inhibits Protein Synthesis by Activating the PERK-eIF2α Signaling Cascade,” include Max Ferretti, William Pryor, Supriya Swarnkar and Katrin Karbstein of TSRI; Lindsay Gorgen of Florida Atlantic University; as well as Paul F. Worley and Po Yu Chen of Johns Hopkins University School of Medicine.
This work was supported by the State of Florida, the O'Keeffe Neuroscience Scholar Award and the United States Public Health Service (DA000266).

Cognitive Rehabilitation After Traumatic Brain Injury A Reference for Occupational Therapists

Send your Occupational therapist after this to see if anything can be used for your stroke protocols.
http://otj.sagepub.com/content/35/1/5.abstract?

1. Jaclyn A. Stephens, OTR/L, CBIS1
2. Karen-Nicole C. Williamson1
3. Marian E. Berryhill, PhD1

1. ¹University of Nevada, Reno, USA

1. Jaclyn A. Stephens, Program in Cognitive and Brain Sciences, Department of Psychology, University of Nevada, 1664 N. Virginia St., Mail Stop 296, Reno, NV 89557, USA. Email: jaclynanne09@gmail.com

Abstract

Nearly 1.7 million Americans sustain a traumatic brain injury (TBI) each year. These injuries can result in physical, emotional, and cognitive consequences. While many individuals receive cognitive rehabilitation from occupational therapists (OTs), the interdisciplinary nature of TBI research makes it difficult to remain up-to-date on relevant findings. We conducted a literature review to identify and summarize interdisciplinary evidence-based practice targeting cognitive rehabilitation for civilian adults with TBI. Our review summarizes TBI background, and our cognitive remediation section focuses on the findings from 37 recent (since 2006) empirical articles directly related to cognitive rehabilitation for individuals (i.e., excluding special populations such as veterans or athletes). This manuscript is offered as a tool for OTs engaged in cognitive rehabilitation and as a means to highlight arenas where more empirical, interdisciplinary research is needed.

Brilliant Harvard Psychologist Explains How To Achieve Long-Term Happiness In This Popular TED Talk

Make sure your doctor gives you  happiness protocols after s/he doesn't have any way to get you to 100% recovery as a consolation prize.
http://www.upworthy.com/brilliant-harvard-psychologist-explains-how-to-achieve-long-term-happiness-in-this-popular-ted-talk?c=upw1

New Test Claims It Can Tell If You Will Develop Alzheimer's... But Do You Want To Know?

Of course I would want to know. I know there is no clinically proven way to prevent dementia, so I'll have to rely on my unproven ways to prevent dementia. Hey, it is better than anything your doctor will give you.

My complete list here:
Dementia prevention 19 ways

http://www.forbes.com/sites/nicolefisher/2015/02/06/a-new-test-can-tell-you-if-you-will-develop-alzheimers-but-do-you-want-to-take-it/? 

 

Changing the Trajectory of Alzheimer's Disease

At least the Alzheimers Association has some intelligent people that can put together a report like this. We in stroke however have absolutely nothing like this, which seems odd that with three major stroke organizations, ASA, NSA, WSO; not one has anyone intelligent enough to produce such a report. I'm sure we could prove that stroke will affect more people and have a greater financial impact. But we have NO leaders that are even willing to try to tackle all the problems in stroke.

Do you want to be known as the stroke leaders that did nothing but twiddle your thumbs?

NSA President - Mr. Lopez

AHA President - Dr. Arnett

WSO President - Dr. Davis

Changing the Trajectory of Alzheimer's Disease

Changing the Trajectory of Alzheimer's Disease: How a Treatment by 2025 Saves Lives and Dollars presents information about the current trajectory and economic impact of Alzheimer's disease, and describes an alternate trajectory if, in 2025, a treatment became available to delay the onset of Alzheimer's. > Summary > Quick Facts > Appendices

Summary

Changing the Trajectory of Alzheimer's Disease: How a Treatment by 2025 Saves Lives and Dollars calculates that a treatment introduced in 2025 that delays the onset of Alzheimer's by five years would reduce the number of individuals affected by the disease by 5.7 million by mid-century and save all payers, including Medicare, Medicaid and families, more than $220 billion within the first five years.
The report reinforces the value of reaching the 2025 goal set by the National Plan to Address Alzheimer's Disease under the National Alzheimer's Project Act (NAPA). If the federal government were to invest $2 billion per year as recommended by the scientific community, then it would recoup its investment within the first three years after a treatment became available.
A treatment introduced in 2025 that delays the onset of Alzheimer's would cut the number of people in 2050 who have the disease by 42 percent — from 13.5 million to 7.8 million. The Alzheimer's Association's report also shows the positive impact of adequate funding and the potential consequences of under-funding.

• In 2015, the costs to all payers for the care of people living with Alzheimer's disease and other dementias will total an estimated $226 billion, with Medicare and Medicaid paying 68 percent of the costs. Without a treatment costs are projected to increase to more than $1.1 trillion in 2050.
• Reaching the 2025 goal would save payers $220 billion over the first five years and $367 billion in 2050 alone. Savings to Medicare and Medicaid would account for nearly 60 percent of the savings.
• People living with Alzheimer's and other dementias and their families would save $54 billion over the first five years in their out-of-pocket costs if the 2025 goal is met.

Tom Wujec: Got a wicked problem? First, tell me how you make toast

Ask every stroke medical person you know how to make toast. Then ask them how to solve the problem of getting every stroke survivor to 100% recovery.  Then have them do the actual work. We need to have our medical staff solve this fucking roblem, they are being paid for this. I hate having my complete recovery being dumped in my lap because solving stroke problems is hard and no one wants to work hard.
http://www.ted.com/talks/tom_wujec_got_a_wicked_problem_first_tell_me_how_you_make_toast?

Vascular Dementia Caused by Plaque Build-Up in Arteries

You can compare this Mayo clinic explanation of atherosclerosis to an earlier one I pointed to.
Vascular dementia and artery plaque by Mayo Clinic
You can see a video of how plaque forms here:
Inflammation In Atherosclerotic Plaque Formation 
You can see from both of these that the real solution is to stop the original inflammation in the first place. Reducing cholesterol is a secondary solution and a poor one at that.

Positive Affect and Markers of Inflammation: Discrete Positive Emotions Predict Lower Levels of Inflammatory Cytokines

What stroke protocol is your doctor following to make sure you experience awe every day? 

Positive Affect and Markers of Inflammation: Discrete Positive Emotions Predict Lower Levels of Inflammatory Cytokines

Stellar, Jennifer E.; John-Henderson, Neha; Anderson, Craig L.; Gordon, Amie M.; McNeil, Galen D.; Keltner, Dacher

Emotion, Jan 19 , 2015, No Pagination Specified.

Current issue feed

Negative emotions are reliably associated with poorer health (e.g., Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002), but only recently has research begun to acknowledge the important role of positive emotions for our physical health (Fredrickson, 2003). We examine the link between dispositional positive affect and one potential biological pathway between positive emotions and health—proinflammatory cytokines, specifically levels of interleukin-6 (IL-6). We hypothesized that greater trait positive affect would be associated with lower levels of IL-6 in a healthy sample. We found support for this hypothesis across two studies. We also explored the relationship between discrete positive emotions and IL-6 levels, finding that awe, measured in two different ways, was the strongest predictor of lower levels of proinflammatory cytokines. These effects held when controlling for relevant personality and health variables. This work suggests a potential biological pathway between positive emotions and health through proinflammatory cytokines.

Why Happiness is the Wrong Pursuit

Is your hospital psychiatrist/psychologist helping you pursue happiness the right way?
http://www.dailygood.org/story/963/why-happiness-is-the-wrong-pursuit-christine-carter/
I liked this quote;

If you want happiness for an hour -- take a nap. If you want happiness for a day -- go fishing. If you want happiness for a year -- inherit a fortune. If you want happiness for a lifetime -- help someone else.

- Chinese Proverb -

The distinctly different brains of “SuperAgers”

What is your doctor doing to get your brain close in makeup to these “SuperAgers”?  ANYTHING AT ALL?

The distinctly different brains of “SuperAgers” 

Scientists are gaining insights into the cognitive abilities of "SuperAgers" and why their memories are more resilient against the ravages of time than are other older people's. ABC News reports today on new research:

The SuperAgers were picked to be studied because all were over age 80 and had the memory capability of a person 20 to 30 years their junior according to the study recently published in the Journal of Neurology.
To understand how SuperAgers managed to keep their mental ability intact, researchers performed a battery of tests on them, including MRI scans on 12 SuperAgers and post-mortem studies on five other SuperAgers to understand the make-up of their brains.
“The brains of the SuperAgers are either wired differently or have structural differences when compared to normal individuals of the same age,” Changiz Geula, a study senior author and a research professor at the Cognitive Neurology and Alzheimer’s Disease Center, said in a prepared statement. “It may be one factor, such as expression of a specific gene, or a combination of factors that offers protection.”

The article goes on to explain that participants' unusual brain signature had three common components in comparison to normal people of similar ages: notably fewer tangles (a primary marker of Alzheimer’s disease), a thicker region of the cortex and a significant supply of a neuron called von Economo, which is linked to higher social intelligence.
Previously: What brain scans reveal about "super agers", The secret to living longer? It's all in the 'tude and Healthy aging the focus of Stanford study

Non-physical practice improves task performance in an unstable, perturbed environment: motor imagery and observational balance training

I'm sure your doctor can use this to update your stroke protocols.
http://journal.frontiersin.org/Journal/10.3389/fnhum.2014.00972/full?
Wolfgang Taube^1*, Michael Lorch², Sibylle Zeiter³ and Martin Keller¹

• ¹Department of Medicine, Movement and Sport Science, University of Fribourg, Fribourg, Switzerland
• ²Department of Sport Science, University of Freiburg, Freiburg, Germany
• ³Department of Medicine, Human Movement and Sport Sciences, Universities of Geneva and Lausanne, Geneva, Switzerland

For consciously performed motor tasks executed in a defined and constant way, both motor imagery (MI) and action observation (AO) have been shown to promote motor learning. It is not known whether these forms of non-physical training also improve motor actions when these actions have to be variably applied in an unstable and unpredictable environment. The present study therefore investigated the influence of MI balance training (MI_BT) and a balance training combining AO and MI (AO+MI_BT) on postural control of undisturbed and disturbed upright stance on unstable ground. As spinal reflex excitability after classical (i.e., physical) balance training (BT) is generally decreased, we tested whether non-physical BT also has an impact on spinal reflex circuits. Thirty-six participants were randomly allocated into an MI_BT group, in which participants imagined postural exercises, an AO+MI_BT group, in which participants observed videos of other people performing balance exercises and imagined being the person in the video, and a non-active control group (CON). Before and after 4 weeks of non-physical training, balance performance was assessed on a free-moving platform during stance without perturbation and during perturbed stance. Soleus H-reflexes were recorded during stable and unstable stance. The post-measurement revealed significantly decreased postural sway during undisturbed and disturbed stance after both MI_BT and AO+MI_BT. Spinal reflex excitability remained unchanged. This is the first study showing that non-physical training (MI_BT and AO+MI_BT) not only promotes motor learning of “rigid” postural tasks but also improves performance of highly variable and unpredictable balance actions. These findings may be relevant to improve postural control and thus reduce the risk of falls in temporarily immobilized patients.

MicroTransponder Invited to Present Stroke Clinical Trial Results at the International Stroke Conference, with U.S. Stroke Study to Follow

Vagus nerve stimulation. If you are close to one of the study sites I'm 100% positive your doctor will not be telling you about it. You are on your own with your recovery. Some movement would disqualify me and anyone else whose upper limb is in the dead brain area.

MicroTransponder Invited to Present Stroke Clinical Trial Results at the International Stroke Conference, with U.S. Stroke Study to Follow

MicroTransponder, Inc., (http://www.microtransponder.com) a privately-held medical device company is pleased to announce the successful completion of its 20-patient stroke trial using the Vivistim® System. The results of this ground breaking clinical trial for stroke patients who experience limited upper limb mobility following a stroke will be presented during an oral presentation at the International Stroke Conference on Feb. 12 at 2:42 PM in Nashville, Tennessee. The International Stroke Conference is one of the largest gathering of stroke clinicians in the world and is sponsored by the American Heart Association. (http://www.strokeconference.org)
The 20-patient study focused on stroke patients with limited upper limb function following their stroke. The lack of upper limb mobility impeded the ability to do daily tasks and live independently. The study was conducted at 2 stroke centers in the United Kingdom. The principle investigator for the study was Dr. Jesse Dawson, and he explained, “We saw dramatic improvements in these patients over the 6-week treatment period. Some patients were able to resume daily activities like driving, swimming, grocery shopping, cooking, and taking care of young children.”
Based on these successful trial results, MicroTransponder has planned a 20-patient follow up U.S. stroke study. The initial sites will be in Dallas, Texas, Houston, Texas, and Minneapolis, Minnesota. Enrollment is now open and the sites are seeking stroke patients who have recently had a stroke and are still experiencing upper limb movement limitations although they must still have some movement. More information is available at http://www.vnsstroketrial.com.
The Vivistim® System has been developed to treat stroke patients that experience an upper-limb deficit following their stroke. It consists of a small implanted battery and wires that internally connect to the vagus nerve in the neck. During the rehabilitative therapy, the patient receives a small amount of neurostimulation to the vagus nerve to strengthen the neural pathways in the brain. This paired treatment method is based on years of neuroscience research published in peer-reviewed academic journals. More information can be found on http://www.MicroTransponder.com
The invitation for an oral presentation at the International Stroke Conference is an important milestone for the Company notes CEO Frank McEachern, “We are honored to be able to present our clinical trial results to one of the largest gatherings of stroke clinicians in the world. Our mission is to bring this therapy to as many stroke patients as possible. Currently, they have very few options if traditional therapy is not effective.” To support additional U.S. clinical trials and further commercialization work, MicroTransponder plans to raise $5 million in funding this summer. Additional information can be found at http://www.MicroTransponder.com
About MicroTransponder, Inc.
MicroTransponder Inc. (http://www.microtransponder.com) is a medical device development company with a strong neuroscience research focus. An experienced team of scientists and engineers has developed and continue developing neurostimulation technology platforms to treat various forms of neurological diseases, including post stroke motor rehabilitation and tinnitus. MicroTransponder has a substantial neurostimulation-focused R&D program which is able to quickly translate scientific discoveries into clinical therapies.

Exercise, exercise, exercise

For all these benefits what exact stroke protocols is your doctor giving you post-stroke? No protocols is a definite sign of incompetence.

Exercise in the Elderly: BDNF and Executive Function

Can Physical Exercise Improve Cognitive Abilities?

Another study on exercise keeping us young - and other fitness trends

 

Paddleboarding in Lake Michigan

Someday I'll do this but during the summer. I still haven't found my drysuit and a wetsuit like his would be impossible to put on one-handed. This is only about 1.5 hours away.
https://www.youtube.com/watch?feature=player_embedded&v=BTR2kUGKxSM

Karol Garrison stand up paddleboarding among the Lake Michigan ice floes in St. Joseph, Michigan on Jan. 11, 2015. Photo by Joshua Nowicki.

One in three people would risk shorter life rather than take daily pill to avoid heart disease

Considering the side effects from statins I don't see this as unusual.

http://www.alphagalileo.org/ViewItem.aspx?ItemId=149267&CultureCode=en
One in three people say they would risk living a shorter life instead of taking a daily pill to prevent cardiovascular disease, according to new research in Circulation: Cardiovascular Quality and Outcomes, an American Heart Association journal.
Researchers at the University of California San Francisco (UCSF) and the University of North Carolina at Chapel Hill surveyed 1,000 people (average age 50) via the Internet hypothetically asking how much time they were willing to forfeit at the end of their lives to avoid taking daily medication. They were also asked the amount of money they would pay and the hypothetical risk of death they were willing to accept to avoid taking medications to prevent cardiovascular disease.
The survey showed:

• More than 8 percent of participants were willing to trade as much as two years of life to avoid taking daily medication for cardiovascular disease; while roughly 21 percent would trade between one week and a year of their lives.  
• About 70 percent said they wouldn’t trade any weeks of their lives to avoid taking a CVD pill daily
• About 13 percent of participants said they would accept minimal risk of death to avoid taking a pill daily; 9 percent said they’d risk a 10 percent chance; and about 62 percent weren’t willing to gamble any risk of immediate death.  
• About 21 percent said they would pay $1,000 or more to avoid taking a pill each day for the rest of their lives, but 43 percent said they wouldn’t pay any amount. 

“What we were really trying to measure is how much the act of taking a pill — obtaining it, remembering to take it and actually taking it — interferes with one’s quality of life,” said Robert Hutchins, M.D., M.P.H., lead author and resident physician in UCSF’s Department of Medicine, Division of General Internal Medicine. “Even ignoring the side-effects of pills, the act of having to take a daily pill can have a large effect on an individual’s quality of life."
“When you consider that many adults are on numerous pills, the effect is often magnified for that person,” he said. “On a population level, even for the small reductions in quality of life like those found in this study, that effect multiplied across millions of people can have very large effects on the cost-effectiveness of that drug for a population.”
While Hutchins and co-authors, believe this is the largest study to date to quantify the utility of taking such medications, they note that the survey was hypothetical. Researchers used a time trade-off method as their primary goal, with the standard gamble and willingness-to-pay as secondary aims.
The standard gamble technique measures an individual’s preference under uncertain situations — in this case whether they may one day require cardiovascular medications and whether they would take them or risk CVD or related death.
Although the survey stipulated that participants wouldn’t have to pay for pills and to ignore any potential side effects, researchers aren’t certain that these issues didn’t affect responses.
“It is important to note that our survey only measured individuals’ preferences at one point in time,” Hutchins said. “However, the fact that we did not see large differences gives us confidence that this effect is probably not large.”
The respondents were 59 percent female and 63 percent Caucasian. Almost a third didn’t have college degrees and 51 percent had incomes between $25,000 and $75,000.
The mean utility – the value of taking just one daily pill for CVD prevention, such as statins or even aspirin – was found to be approximately 0.990 to 0.994. Utility refers to potential value of preventative services including disease prevention, cost effectiveness, quality of life and adverse effects.
The study’s findings are useful for policymakers evaluating preventive interventions, specifically the cost effectiveness of those interventions for cardiovascular disease, Hutchins said.
http://newsroom.heart.org/news/one-in-three-people-would-risk-shorter-life-rather-than-take-daily-pill-to-avoid-heart-disease?preview=9fc0c22d4003b55a01be79d9cf1932a6