New Breakthrough in Hemorrhagic Stroke Treatment

The writeup doesn't make sense, clots vs. hemorrhagic in the title.
http://www.strokesmart.org/new-hemorrhagic-stroke-treatment
The following refers to a clot removal.
Read about a stroke patient who benefitted from this procedure. Dr. Shah says that this surgery should be performed within 8 hours of the stroke occurring.

Ginseng: a promising neuroprotective strategy in stroke

Is anyone ever going to write up a stroke protocol for this kind of stuff?  My god, neurons are dying by the trillions every day because our stroke medical people will not get off their asses and put this together.  This is not somebody else's problem to solve, it's yours. So buckle down and put some f*cking neuroprotective stroke protocols together.  My ideas here:
these 31 hyperacute possibilities I'm going to insist my doctor give me the first week. 

http://journal.frontiersin.org/article/10.3389/fncel.2014.00457/full? 

Vaibhav Rastogi^1,2, Juan Santiago-Moreno¹ and Sylvain Doré^1,2,3,4*

• ¹Departments of Anesthesiology, Center for Translational Research in Neurodegenerative Disease, University of Florida College of Medicine, Gainesville, FL, USA
• ²Departments of Neurology, Center for Translational Research in Neurodegenerative Disease, University of Florida College of Medicine, Gainesville, FL, USA
• ³Departments of Psychiatry, Center for Translational Research in Neurodegenerative Disease, University of Florida College of Medicine, Gainesville, FL, USA
• ⁴Departments of Neuroscience, Center for Translational Research in Neurodegenerative Disease, University of Florida College of Medicine, Gainesville, FL, USA

Ginseng is one of the most widely used herbal medicines in the world. It has been used in the treatment of various ailments and to boost immunity for centuries; especially in Asian countries. The most common ginseng variant in traditional herbal medicine is ginseng, which is made from the peeled and dried root of Panax Ginseng. Ginseng has been suggested as an effective treatment for a vast array of neurological disorders, including stroke and other acute and chronic neurodegenerative disorders. Ginseng’s neuroprotective effects are focused on the maintenance of homeostasis. This review involves a comprehensive literature search that highlights aspects of ginseng’s putative neuroprotective effectiveness, focusing on stroke. Attenuation of inflammation through inhibition of various proinflammatory mediators, along with suppression of oxidative stress by various mechanisms, including activation of the cytoprotective transcriptional factor Nrf2, which results in decrease in reactive oxygen species, could account for its neuroprotective efficacy. It can also prevent neuronal death as a result of stroke, thus decreasing anatomical and functional stroke damage. Although there are diverse studies that have investigated the mechanisms involved in the efficacy of ginseng in treating disorders, there is still much that needs to be clarified. Both in vitro and in vivo studies including randomized controlled clinical trials are necessary to develop in-depth knowledge of ginseng and its practical applications.

Introduction

Ginseng is a broad term that refers to a group of 11 species of perennial plants belonging to the Panax genus under the family Araliaceae. The commercially available herbal formulations of ginseng are extracted from the root of these plants. It has been used for more than 2000 years mainly in China, Korea and Japan. The most commonly used herbal derivative of ginseng is Korean ginseng which is derived from the peeled, steamed, and dried root of Panax ginseng also commonly known as Korean ginseng. Although there are other variants of ginseng that contain many of the same compounds and medicinal properties, we will mainly focus on Panax ginseng and its constituents. The chemical constituents of ginseng include triterpene saponins, polysaccharides, peptidoglycans, nitrogen-containing compounds, fatty acids, carbohydrates and phenolic compounds (Sticher, 1998). It also contains essential oil-containing polyacetylenes and sesquiterpenes (Sticher, 1998). Ginsenosides are the major active components in ginseng; they are a form of triterpene glycosides (saponins). Of the 150 ginsenosides that have been isolated from ginseng, 40 have been found in Panax ginseng alone (Christensen, 2009). These mainly include Rb1, Rb2, Rc, Rd, Rg1, Rg2, Rh1, and Re (Attele et al., 1999).

The Greek word “panax” means “cure-all” and true to its name, ginseng has proven to have a wide variety of medicinal uses. Ginseng can improve pulmonary lung function in stable chronic obstructive pulmonary disorder patients (An et al., 2011). Korean ginseng has been shown to provide symptomatic relief in the patients with complaints of erectile dysfunction (Hong et al., 2002). A large number of carcinomas, including those associated with smoking, could potentially be prevented by the regular use of ginseng (Yun and Choi, 1995). Ginseng’s efficacy in type-2 diabetics has been illustrated by the fact that the patients had a decrease in the fasting blood glucose, weight loss and HbA1c (glycated hemoglobin) along with improvement in mood and psychophysical performance (Sotaniemi et al., 1995). Ginseng also possesses numerous cardiovascular benefits that are mainly due to its cardioprotective and anti-hypertensive effects; it can also attenuate myocardial hypertrophy and heart failure (Karmazyn et al., 2011).

Ginseng is also known to affect various aspects of neurodevelopmental, neurodegenerative and neuropsychiatric disorders (Kim et al., 2013). Stroke is the 4th leading cause of death in United States with an estimated 1 death every 4 min. Stroke recurs in 1 out of every 4 stroke patients. Approximately 87% of strokes are a result of ischemic insult and 13% are hemorrhagic strokes. Subarachnoid hemorrhage (SAH) accounts for approximately 3% of all strokes, has an incidence rate of 30,000 cases per year (King, 1997) and is mostly seen after brain aneurysm rupture or in traumatic brain injury (TBI) patients. Stroke is also one of the leading causes of long term disability (Go et al., 2013). These are reasons for stroke’s high magnitude of mortality and morbidity. From this information, one can see that present preventive and treatment strategies are not sufficient to curb this health menace. Because of this, there is a need to look for other treatment modalities and ginseng has shown promising evidence in this regard.

The adorable yet advanced Robear designed to take care of elderly people

I could see all kinds of uses for survivors.  Hopefully there is some morality built in compared to the robot in the movie, Robot and Frank.
http://www.hexapolis.com/2015/02/28/the-adorable-yet-advanced-robear-designed-to-take-care-of-elderly-people/ 

 

Neurogenesis: How To Grow New Brain Cells

Exercise is the easy part, mating is quite a bit harder, requires a willing partner.
http://www.spring.org.uk/2015/02/neurogenesis-how-to-grow-new-brain-cells.php
Selected paragraphs:
Maya Opendak, who co-authored the study, said:

“New neurons may serve as a means to fine-tune the hippocampus to the predicted environment.
In particular, seeking out rewarding experiences or avoiding stressful experiences may help each individual optimize his or her own brain.”

Grow new brain cells

Rewarding experiences, like exercise and mating, have been shown to grow new brain cells in mice.

Intensive PT in Stroke: More Not Necessarily Better

But is this because the results were based on subjective reporting by the patients rather than looking at objective criteria? I don't care if objective criteria doesn't exist yet. Create them!!!
http://www.medscape.com/viewarticle/840485
Intensive physiotherapy focusing on the arms and hands of stroke patients accelerated some patient-reported improvements at the end of the therapy period but was not associated with any significant benefit over usual care at 1 year, new research shows.
Presenting the primary results of the ICARE phase 3 stroke rehabilitation trial, at the International Stroke Conference (ISC) 2015, Carolee Winstein, PhD, professor of biokinesiology and physical therapy at the University of Southern California, Los Angeles, concluded that "more is not necessarily better."
"The bottom line is that more than a 2-fold increase of arm and hand therapy did not improve motor performance or patient-reported outcomes at 1 year. We were very surprised at this result, which flies in face of 'more is better' in terms of neuroplasticity responding to repetitive task training, but it is consistent with other studies," she added.
Commenting on the finding that the intensive therapy did appear to accelerate some patient-reported outcomes by the end of the therapy period, she said, "It does seem to get patients to the same point more quickly. We now need to focus on how we maintain that accelerated benefit."
Dr Winstein noted that better neurorehabilitation is needed for stroke because after 6 months 65% of patients cannot effectively incorporate their affected arm and hand into daily activities.
Although task-based, intense motor therapy training approaches are well accepted, the effect of the dose and contents of such therapy on motor recovery is unknown.
The ICARE trial is only the fourth randomized study of stroke rehabilitation and is the first such trial to be conducted in the first weeks after stroke, when the opportunity for learning-dependent plasticity is high and the recovery trajectory is positive, she added.
Patient-Perceived Improvements
The study tested a behavioral task-based therapy known as the Accelerated Skill Acquisition Program (ASAP), a patient-centered intervention focused on meaningful task practice, capacity building, and motivational enhancements. Therapy was initiated between 14 and 106 days after stroke in the outpatient setting.
For the study, 361 patients were assigned to 1 of 3 groups:

• Intensive therapy with the ASAP program, delivered as three 1-hour sessions each week for 10 weeks
• Dose-equivalent therapy, consisting of the same number of sessions of usual occupational therapy
• Usual occupational therapy provided as whatever the treating physician prescribed, with a specific number of sessions not specified

Study participants had pure motor hemiparesis without substantial cognitive or sensory impairments, with an average National Institutes of Health Stroke Scale score of 3.6. Dr Winstein said the patients could be described as "moderately impaired with some function in their affected arm but slow speed of movement and impaired ability to open and close the hand and manipulate objects."
Patients had a mean age was 60 years and were an average of 45 days post-stroke. In 49% of patients, the stroke affected the dominant arm and hand, and 29% had received 6 hours of outpatient occupational therapy or less before randomization; this did not differ across groups.
All three groups improved with regard to motor function and hand movements, with 70% of patients meeting the endpoint for hand function improvement.
The mean improvement in motor performance score was substantial (46%), but there was no difference among the three groups at the 1-year post-stroke primary endpoint.
However, compared with the two control groups, the group receiving the intensive therapy did show early improvements in secondary patient-perceived outcomes (on the Stroke Impact Scale), including physical function and quality of life.
These improvements were seen at the end of therapy, approximately 4 months after randomization and 6 months after stroke, but the differences were not present at 12 months.
"Building on end-of-therapy group differences in the context of the continuum of care is an important challenge for future research," Dr Winstein concluded.
She pointed out that the current study did not have a "no therapy" group. This differs from the EXCITE trial, which did have a "no therapy" control and did show a difference.
The ICARE study was funded jointly by the National Institute of Neurological Disorders and Stroke and National Center for Medical Rehabilitation Research of the National Institutes of Health.
International Stroke Conference (ISC) 2015. Presented February 13, 2015. Abstract LB15.

First full body transplant is two years away, surgeon claims

First full body transplant is two years away, surgeon claims
Or you could listen to a biologist;

The talk of head transplants is completely nuts

Sleep a lot? You might have a heightened risk of stroke, study says

I can't see a cause and effect here at all. But post-stroke I don't think I really have ever slept more than 8 hours straight although I would sleep during the day whenever possible.
What a waste of time, so instead of actually solving some of the problems in stroke they went for this fairly useless research that doesn't help survivors at all.
The article here:
Sleep a lot? You might have a heightened risk of stroke, study says
Older adults who said they slept more than eight hours were 46% more likely to suffer strokes in the next decade than adults who slept for six to eight hours, according to an analysis published Wednesday in the journal Neurology. Even worse, the stroke risk for people who went from sleeping less than six hours to sleeping more than eight hours was nearly four times greater than for people who consistently got six to eight hours of ZZZZs.
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The abstract this is based upon here:
Sleep duration and risk of fatal and nonfatal stroke A prospective study and meta-analysis

1. Yue Leng, MPhil,
2. Francesco P. Cappuccio, MD,
3. Nick W.J. Wainwright, PhD,
4. Paul G. Surtees, PhD,
5. Robert Luben, MSc,
6. Carol Brayne, MD and
7. Kay-Tee Khaw, MD

+Show Affiliations

| + Show Full Disclosures

1. Correspondence to Dr. Leng: yl411@medschl.cam.ac.uk

1. Published online before print February 25, 2015, doi: 10.1212/WNL.0000000000001371 Neurology 10.1212/WNL.0000000000001371

• Free via Open Access: OA
• Abstract
• Full Text (PDF)

1. Also available:
2. Data Supplement
3. Accompanying Editorial

Abstract

Objective: To study the association between sleep duration and stroke incidence in a British population and to synthesize our findings with published results through a meta-analysis.

Methods: The prospective study included 9,692 stroke-free participants aged 42–81 years from the European Prospective Investigation into Cancer–Norfolk cohort. Participants reported sleep duration in 1998–2000 and 2002–2004, and all stroke cases were recorded until March 31, 2009. For the meta-analysis, we searched Ovid Medline, EMBASE, and the Cochrane Library for prospective studies published until May 2014, and pooled effect estimates using a weighted random-effect model.

Results: After 9.5 years of follow-up, 346 cases of stroke occurred. Long sleep was significantly associated with an increased risk of stroke (hazard ratio [HR] = 1.46 [95% confidence interval (CI) 1.08, 1.98]) after adjustment for all covariates. The association remained robust among those without preexisting diseases and those who reported sleeping well. The association for short sleep was smaller (and not statistically significant) (HR = 1.18 [95% CI 0.91, 1.53]). There was a higher stroke risk among those who reported persistently long sleep or a substantial increase in sleep duration over time, compared to those reporting persistently average sleep. These were compatible with the pooled HRs from an updated meta-analysis, which were 1.15 (1.07, 1.24) and 1.45 (1.30, 1.62) for short and long sleep duration, respectively.

Conclusions: This prospective study and meta-analysis identified prolonged sleep as a potentially useful marker of increased future stroke risk in an apparently healthy aging population.

The formal advance of the research on beer-vs-coffee spilling - stroke rehab possibilities

This seems like it would be a good test to determine your advancements in carrying liquids in your affected hand. I have never even tried to carry any liquid in my affected hand for the past 8.7 years. The spasticity doesn't even allow the hand to be in a straight line with the forearm.The bubbles in beer make it more likely you would succeed with that and you could reward yourself by drinking it.
http://www.improbable.com/2015/02/25/the-formal-advance-of-the-research-on-beer-vs-coffee-spilling/?

New Neurons: Who Needs Em Anyway?

This blog writer has really pointed out the Catch-22 situation in stroke rehab with neurogenesis. Stress reduces the ability to create neurons and our doctors are responsible for massive amounts of our stress because they know absolutely nothing about how to get you 100% recovered. They don't even have any stroke rehab protocols that can get you back to some semblance of normality.
So you know you are totally screwed and because you know that, the neurogenesis that might help you recover won't occur.
https://psychneuro.wordpress.com/2015/02/25/new-neurons-who-needs-em-anyway/

NSAIDs: A Risky Addition to Post-MI Antithrombotics

Ok, a very very serious question for your doctor. What should be done about NSAIDs post stroke? Since they might be helpful for recovery.
Common Medicine Helps Repair Brain After Stroke, Study in Rats Suggests - Ibuprofen

NSAIDs: A Risky Addition to Post-MI Antithrombotics

Neurons cool off - Synaptic reestablishment

This seems like a useful occurrence post-stroke. What will it take for your doctor to follow up with a clinical trial to prove it one way or another? Or does your doctor not have any goals around solving problems in stroke because your hospital president has failed at leading?

"You can judge a leader by the size of the problems they tackle."

http://stm.sciencemag.org/content/7/276/276ec33.full? 

1. Anne Schaefer

+ Author Affiliations

1. Friedman Brain Institute, Department of Neuroscience and Department of Psychiatry, Mount Sinai School of Medicine, New York, NY 10029, USA. E-mail: anne.schaefer@mssm.edu

It’s common wisdom that a cold shower is good for your health. Now, Peretti et al. show that Rbm3, a protein induced by cold shock, triggers neurons to form new synapses.

Low body temperature in hibernating mammals leads to a reversible loss of synaptic contacts that are efficiently re-established upon rewarming. Using electron microscopy, Peretti et al. report that the induction of a hibernation-like body temperature in mice for as little as 45 minutes caused a similar loss of synaptic connections that were regained upon rewarming the animals. This capacity for synaptic regeneration after cold trauma was lost in mice suffering from two neurodegenerative diseases. The impaired cooling-induced regeneration of synapses in mice suffering from either prion-like disease or Alzheimer’s disease was associated with a decrease in one of the known cold-shock proteins, the RNA-binding motif protein RBM3. The authors show that RNAi-based knockdown of RBM3 exacerbated the loss of synapses in both disease models and accelerated disease progression. Conversely, the enhanced ectopic expression of RBM3 using lentiviral-based delivery to the hippocampus, the brain region that is important for memory formation, restored cold-induced synaptic regeneration in the two mouse models of neurodegenerative disease. Moreover, RBM3 overexpression reduced prion neuropathology, prevented neuronal loss, and significantly enhanced the survival of prion-diseased animals. Ectopic RBM3 expression before exposure of young mice with neurodegenerative disease to two consecutive cold-shocks one week apart was sufficient to boost endogenous RBM3 expression in the brain and to achieve synaptic protection.

Although the RBM3-based mechanism of synaptic regeneration remains unknown, these data suggest that RBM3 might have long-term neuroprotective effects. The results of this study could have far-reaching consequences for enhancing cold-shock pathways as a new therapeutic approach for treating neurodegenerative disease.

D. Peretti et al., RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration. Nature 518, 236–239 (2015). [PubMed]

 

Live Jazz at Moriarty's Pub - stroke rehab

A night full of stroke rehab. Is your stroke department so incompetent that they don't take you to live music? Do they know of ANY of this research?
Action observation; your choice of finger movements, drummer, guitarist, violinist, keyboardist.
Music listening.
Balance challenges; walking in the dark amongst the narrow spaces between chairs and tables.
Drinking alcohol helps challenge your balance.
https://www.facebook.com/moriartyspub
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Action observation

New research supporting stroke rehabilitation   Nov. 2014.

Plasticity and Response to Action Observation   Oct. 2014.

Motor imagery during action observation modulates automatic imitation effects in rhythmical actions   Mar. 2014.

Clinical feasibility of action observation training for walking function of patients with post-stroke hemiparesis: a randomized controlled trial   Mar. 2014.

Training Videos Help Restore Motor Function, May Aid in Stroke Rehabilitation Mar. 2014.

 Using action observation to study superior motor performance: a pilot fMRI study  Jan. 2014.

Multiple roles of motor imagery during action observation  Jan. 2014.

Motor imagery ability in stroke patients: the relationship between implicit and explicit motor imagery measures  Dec. 2013.

From action representation to action execution: exploring the links between cognitive and biomechanical levels of motor control  Oct. 2013.

Action observation as a stroke therapy  June 2013.

Action-Observation In Stroke Rehabilitation  June 2013.

Exercise for stroke patients' brains  June 2013.

Watching object related movements modulates mirror-like activity in parietal brain regions  March 2013.

Watching object related movements modulates mirror-like activity in parietal brain regions  May 2012.

Action observation and mirror neuron network: a tool for motor stroke rehabilitation.  April 2012.

Modulating the motor system by action observation: Implications for stroke rehabilitation  Feb. 2012.

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Music rehabilitation

Exploring a Neuroplasticity Model of Music Therapy  

11 Problems Music Can Solve

Why does music therapy work? The Science Behind the Music.

Musical Training Can Increase Blood Flow in Brain

Listening to classical music ameliorates unilateral neglect after stroke

Music brings memories back to the brain injured 

Moderating variables of music training-induced neuroplasticity: a review and discussion

Plasticity in the sensorimotor cortex induced by Music-supported therapy in stroke patients: a TMS study

Hand-Clapping Songs Improve Motor and Cognitive Skills, Research Shows

 Music listening enhances cognitive recovery and mood after middle cerebral artery stroke

Intensive musical therapy may help improve speech in stroke patients 

The Creative Therapy Which Reduces Depression in Young and Old Alike - Music

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Balance

Easy exercises to improve stability and prevent falls

Simple, everyday activities can strengthen balance

Longitudinal Analysis of Balance Confidence in Individuals With Stroke Using a Multilevel Model for Change

Clinical Correlates of Between-Limb Synchronization of Standing Balance Control and Falls During Inpatient Stroke Rehabilitation

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How badly is your stoke hospital failing by not providing any of these as stroke protocols?

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Wearable Soft Robotics for Independent Living (EP/M026388/1)

This sounds like it would easily meet up with survivor needs. What is your doctor doing to facilitate this?
http://phys.org/wire-news/186233091/prosthetic-hands-robotic-trousers-and-biosensors-amppound53-m.html
Wearable Soft Robotics for Independent Living (EP/M026388/1) Research at the University of Bristol, University of the West of England, University of Nottingham, University of Leeds, University of Strathclyde, University of Southampton and Loughborough University. Awarded £2 million
The research team will develop soft robotic clothing to enable those with mobility impairments, disabilities and age-related weakness to move easily and unaided and to live independently and with dignity. The end results will be easy to use, comfortable, adaptable and meet the user's individual mobility needs.
Smart trousers could help vulnerable people avoid falls by supporting them whilst walking, give people added bionic strength to move between sitting and standing positions, and help people climb stairs which were previously insurmountable. They could replace the stair lift in the home and other bulky and uncomfortable mobility and stability aids. Ultimately they have the potential to free many wheelchair users from their wheelchairs.
This intelligent clothing or 'second skin' will use artificial 'muscles' made from smart materials and reactive polymers which are capable of exerting great forces. This will be developed using the latest wearable soft robotic, nanoscience, 3D fabrication, functional electrical stimulation and full-body monitoring technologies, all driven by the need of the end users, who will also be directly involved in the project. They will include control systems that monitor the wearer and adapt to give the most suitable assistance, working with the body's own muscles. For patients needing rehabilitation the smart clothing can initially provide strong support and subsequently reduce assistance as the patient recovers mobility and strength.
Many existing devices used by people with mobility problems can cause or aggravate conditions such as poor circulation, skin pressure damage or susceptibility to falls, each of which is a drain on health resources. Wearable Soft Robotics has the potential to alleviate many of these patients problems and reduce healthcare costs.

Skin may helps spot Alzheimer's and Parkinson's disease

And with this early detection our doctors will have to come up with some prevention protocols. But they won't, you'll have to figure this out on your own. Do not follow my ideas, they are not clinically proven.

My complete list here: Don't listen to me, your doctor obviously knows more than I do. Have him/her prove that knowledge or fire them.
Dementia prevention 19 ways

Skin may helps spot Alzheimer's and Parkinson's disease 

Tracking Early Decline in Cognitive Function in Older Individuals at Risk for Alzheimer Disease Dementia

What testing is your doctor doing to identify whether you are susceptible to your 33% dementia chance post-stroke from an Australian study?
What protocols are setup to prevent that problem from occurring?
 Tracking Early Decline in Cognitive Function in Older Individuals at Risk for Alzheimer Disease Dementia

Rebecca E. Amariglio, PhD^1,2,3; Michael C. Donohue, PhD^4,5; Gad A. Marshall, MD¹; Dorene M. Rentz, PsyD¹; David P. Salmon, PhD⁵; Steven H. Ferris, PhD⁶; Stella Karantzoulis, PhD⁶; Paul S. Aisen, MD⁵; Reisa A. Sperling, MD¹; for the Alzheimer’s Disease Cooperative Study

[+] Author Affiliations

JAMA Neurol. Published online February 23, 2015. doi:10.1001/jamaneurol.2014.3375

Text Size: A A A

Article

Figures

Tables

References

Comments

ABSTRACT

ABSTRACT | INTRODUCTION | METHODS | RESULTS | DISCUSSION | CONCLUSIONS | ARTICLE INFORMATION | REFERENCES

Importance  Several large-scale Alzheimer disease (AD) secondary prevention trials have begun to target individuals at the preclinical stage. The success of these trials depends on validated outcome measures that are sensitive to early clinical progression in individuals who are initially asymptomatic.
Objective  To investigate the utility of the Cognitive Function Instrument (CFI) to track early changes in cognitive function in older individuals without clinical impairment at baseline.
Design, Setting, and Participants  Longitudinal study from February 2002 through February 2007 at participating Alzheimer’s Disease Cooperative Study sites. Individuals were followed up annually for 48 months after the baseline visit. The study included 468 healthy older individuals (Clinical Dementia Rating scale [CDR] global scores of 0, above cutoff on the modified Mini-Mental State Examination and Free and Cued Selective Reminding Test) (mean [SD] age, 79.4 [3.6] years; age range, 75.0-93.8 years). All study participants and their study partners completed the self and partner CFIs annually. Individuals also underwent concurrent annual neuropsychological assessment and APOE genotyping.
Main Outcomes and Measures  The CFI scores between clinical progressors (CDR score, ≥0.5) and nonprogressors (CDR score, 0) and between APOE ε4 carriers and noncarriers were compared. Correlations of change between the CFI scores and neuropsychological performance were assessed longitudinally.
Results  At 48 months, group differences between clinical progressors and non-progressors were significant for self (2.13, SE=0.45, P < .001), partner (5.08, SE=0.59, P < .001), and self plus partner (7.04, SE=0.83, P < .001) CFI total scores. At month 48, APOE ε4 carriers had greater progression than noncarriers on the partner (1.10, SE=0.44, P < .012) and self plus partner (1.56, SE=0.63, P  < .014) CFI scores. Both self and partner CFI change were associated with longitudinal cognitive decline (self, ρ=0.32, 95% CI, 0.13 to 0.46; partner, ρ=0.56, 95% CI, 0.42 to 0.68), although findings suggest self-report may be more accurate early in the process, whereas accuracy of partner report improves when there is progression to cognitive impairment.
Conclusions and Relevance  Demonstrating long-term clinical benefit will be critical for the success of recently launched secondary prevention trials. The CFI appears to be a brief, but informative potential outcome measure that provides insight into functional abilities at the earliest stages of disease.

New Assistive Equipment to Maximize Human Sensorimotor Function

This seems quite useable for stroke rehab. What is your doctor doing about it?
News release here:
http://www.alphagalileo.org/ViewItem.aspx?ItemId=149993&CultureCode=en
Images here:
http://www.engadget.com/2015/02/24/sensorimotor-enhancing-suit/

Frequent saunas may boost survival, Finnish study suggests

How long before your hospital installs a sauna? Find out from your doctor what the frequency and heat protocol is. Do not attempt this on your own.
The readable article here:
http://news.yahoo.com/frequent-saunas-may-boost-survival-finnish-study-suggests-173148012.html
The abstract here:
http://archinte.jamanetwork.com/article.aspx?articleid=2130724

Conclusions and Relevance  Increased frequency of sauna bathing is associated with a reduced risk of SCD, CHD, CVD, and all-cause mortality. Further studies are warranted to establish the potential mechanism that links sauna bathing and cardiovascular health.

Have your doctor reconcile sauna use with this research;

Mortality rates increase due to extreme heat and cold

Up to now it has been known that high temperatures, amongst other things, can affect the blood-clotting mechanism (haemostasis) and make the blood more viscous, thereby increasing the risk of thrombosis. Furthermore, as decreasing temperatures have an impact on blood pressure, it can be assumed that there is a link between cold temperatures and the increase in cardiovascular events and stroke.

Ruckusmaker day

Steve Jobs' 60th birthday. So make a ruckus because unless we do, nothing is going to change in the stroke world. There are 10 million survivors a year, We could be deafening enough that even doctors listen to us.
1. Call your stroke hospital president and ask when the hell they will start providing detailed statistics of how good their stroke department is; 30 day deaths, 100% recovery, tPA efficacy, number of updated stroke protocols with efficacy ratings. Who will be fired if those goals are not achieved?
2. Call/email the presidents of the ASA, NSA, WSO.
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 
Ask them point blank when they are going to define a strategy with dates to solve the problems in stroke.
And whom is assigned the goal of solving those problems? Specifics only, NO bland appeasement statements allowed.  

Ruckusmaker day by Seth Godin

 

Seeing a pattern - stroke deaths reduction

Our stroke leaders have no clue as to why stroke has fallen in the US from 3rd to 4th to 5th most deadly disease. This would be an excellent way to find out if we had anybody in our stroke associations that have two neurons to rub together. But I can guarantee that our stroke associations will fail miserably once again. And their boards of directors must be ok with such f*cking failure because they allow it to continue.

Stroke Deaths Drop in 2013

Possible Explanations

While it’s too early to know exactly why the stroke numbers went down, interventions like the clot-buster tPA likely are a factor, Lackland said.
“We know that management of blood pressure has a major impact here yet only 50 percent of people with high blood pressure have it under control,” he said.
According to Lackland, stroke deaths, stroke incidence, and recurrent strokes are all on the decline.
So they really know nothing.

 

Seeing a pattern

Joseph Budner Elad has sought patterns in roadside bombings in war, and the path of deadly pathogens.
Now, Elad, president and CEO of Quantum Leap Innovations of Newark, has begun putting his company’s pattern-seeking technology to more everyday use for business.
For instance, the software can examine whether patients who get readmitted to a hospital share certain traits, or which other products a bank customer might be likely to buy.
Elad, originally of Israel, uses technology he calls “pattern-based analytics.”
“We’re just scratching the surface of what can be done,” he said.
Predictive analytics, also known as data mining, is widespread in the field of business intelligence. But Elad has managed to find a new twist, said Tom Davenport, professor of information technology and management at Babson College in Massachusetts.
Most analytics use regression, a statistical technique that’s been around for a century, which helps explain the relationship between variables, he said.
What Elad is doing is pattern matching, which is more complicated and relies on artificial intelligence, Davenport said. By establishing that something has taken place in the past, it predicts what will happen in the future, he said.
- See more at: http://deltechpark.org/2011/12/seeing-a-pattern/#sthash.ufX9Zjfg.dpuf

Joseph Budner Elad has sought patterns in roadside bombings in war, and the path of deadly pathogens.
Now, Elad, president and CEO of Quantum Leap Innovations of Newark, has begun putting his company’s pattern-seeking technology to more everyday use for business.
For instance, the software can examine whether patients who get readmitted to a hospital share certain traits, or which other products a bank customer might be likely to buy.
Elad, originally of Israel, uses technology he calls “pattern-based analytics.”
“We’re just scratching the surface of what can be done,” he said.
Predictive analytics, also known as data mining, is widespread in the field of business intelligence. But Elad has managed to find a new twist, said Tom Davenport, professor of information technology and management at Babson College in Massachusetts.
Most analytics use regression, a statistical technique that’s been around for a century, which helps explain the relationship between variables, he said.
What Elad is doing is pattern matching, which is more complicated and relies on artificial intelligence, Davenport said. By establishing that something has taken place in the past, it predicts what will happen in the future, he said.
- See more at: http://deltechpark.org/2011/12/seeing-a-pattern/#sthash.ufX9Zjfg.dpuf

Joseph Budner Elad has sought patterns in roadside bombings in war, and the path of deadly pathogens.

Now, Elad, president and CEO of Quantum Leap Innovations of Newark, has begun putting his company’s pattern-seeking technology to more everyday use for business.

For instance, the software can examine whether patients who get readmitted to a hospital share certain traits, or which other products a bank customer might be likely to buy.

Elad, originally of Israel, uses technology he calls “pattern-based analytics.”

“We’re just scratching the surface of what can be done,” he said.

Predictive analytics, also known as data mining, is widespread in the field of business intelligence. But Elad has managed to find a new twist, said Tom Davenport, professor of information technology and management at Babson College in Massachusetts.

Most analytics use regression, a statistical technique that’s been around for a century, which helps explain the relationship between variables, he said.

What Elad is doing is pattern matching, which is more complicated and relies on artificial intelligence, Davenport said. By establishing that something has taken place in the past, it predicts what will happen in the future, he said.

BrainBrowser: distributed, web-based neurological data visualization

Ask your doctor if this is enough to get 3d images of damaged parts of your brain and then correlate stroke protocols that fix such damage. This would be the holy grail of stroke rehab. We just need our doctors to implement this. It is so goddammed simple even I can see the possibilities.
http://journal.frontiersin.org/article/10.3389/fninf.2014.00089/full?
Tarek Sherif, Nicolas Kassis, Marc-Étienne Rousseau, Reza Adalat and Alan C. Evans^*

• McGill Centre for Integrative Neuroscience, McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, QC, Canada

Recent years have seen massive, distributed datasets become the norm in neuroimaging research, and the methodologies used to analyze them have, in response, become more collaborative and exploratory. Tools and infrastructure are continuously being developed and deployed to facilitate research in this context: grid computation platforms to process the data, distributed data stores to house and share them, high-speed networks to move them around and collaborative, often web-based, platforms to provide access to and sometimes manage the entire system. BrainBrowser is a lightweight, high-performance JavaScript visualization library built to provide easy-to-use, powerful, on-demand visualization of remote datasets in this new research environment. BrainBrowser leverages modern web technologies, such as WebGL, HTML5 and Web Workers, to visualize 3D surface and volumetric neuroimaging data in any modern web browser without requiring any browser plugins. It is thus trivial to integrate BrainBrowser into any web-based platform. BrainBrowser is simple enough to produce a basic web-based visualization in a few lines of code, while at the same time being robust enough to create full-featured visualization applications. BrainBrowser can dynamically load the data required for a given visualization, so no network bandwidth needs to be waisted on data that will not be used. BrainBrowser's integration into the standardized web platform also allows users to consider using 3D data visualization in novel ways, such as for data distribution, data sharing and dynamic online publications. BrainBrowser is already being used in two major online platforms, CBRAIN and LORIS, and has been used to make the 1TB MACACC dataset openly accessible.

1. Introduction

BrainBrowser is an open source JavaScript library exposing a set of web-based 3D visualization tools primarily targeting neuroimaging. Using open web technologies, such as WebGL and HTML5, it allows for real-time manipulation and analysis of 3D imaging data through any modern web browser. BrainBrowser includes two major components. The BrainBrowser Surface Viewer (Figure 1) is a WebGL-based 3D viewer capable of displaying 3D surfaces in real time and mapping various sorts of data to them. The BrainBrowser Volume Viewer (Figure 2) is an HTML5 Canvas-based viewer allowing slice-by-slice traversal of 3D or 4D MINC volumetric data (Vincent et al., 2004).

FIGURE 1

Figure 1. The BrainBrowser Surface Viewer.

FIGURE 2

Figure 2. The BrainBrowser Volume Viewer.

In recent years, neuroimaging research has seen itself inundated by large, distributed datasets that have necessitated a shift in how scientists approach their research: guiding hypotheses are often articulated after analyzing the mass of available data (Margulies et al., 2013), and data sharing has become a necessity for scientific discovery (Jomier et al., 2011). Several large-scale, distributed, collaborative platforms have been developed to facilitate this new approach, and they tend to integrate poorly with traditional visualization tools requiring a local installation and local data. These tools and their dependencies would have to be installed locally, and data would generally have to be exported from the platform in order to be visualized in the local environment. Web-based visualization tools, on the other hand, present significant benefits in the context of distributed research platforms:

Sen. Kirk launches 'Battle Buddies' to help people with disabilities

If Senator Kirk really wants to help stroke survivors, future and current, he would be pushing for a National Stroke Plan, similar to the  National Alzheimer’s Project Act (Public Law 111-375)
If you are one of his constituents push that idea to him.
http://chicago.suntimes.com/chicago-politics/7/71/387100/mark-kirk-battle-buddies-support-group

A bidirectional relationship between physical activity and executive function in older adults

This sounds extremely important for survivors. What stroke protocol does your doctor have for this?
http://journal.frontiersin.org/article/10.3389/fnhum.2014.01044/full?
Michael Daly^1*, David McMinn² and Julia L. Allan³

• ¹Behavioural Science Centre, Stirling Management School, University of Stirling, Stirling, UK
• ²School of Medicine and Dentistry, Rowett Institute of Nutrition and Health, University of Aberdeen, Aberdeen, UK
• ³Health Psychology, Institute of Applied Health Sciences, University of Aberdeen, Aberdeen, UK

Physically active lifestyles contribute to better executive function. However, it is unclear whether high levels of executive function lead people to be more active. This study uses a large sample and multi-wave data to identify whether a reciprocal association exists between physical activity and executive function. Participants were 4555 older adults tracked across four waves of the English Longitudinal Study of Aging. In each wave executive function was assessed using a verbal fluency test and a letter cancelation task and participants reported their physical activity levels. Fixed effects regressions showed that changes in executive function corresponded with changes in physical activity. In longitudinal multilevel models low levels of physical activity led to subsequent declines in executive function. Importantly, poor executive function predicted reductions in physical activity over time. This association was found to be over 50% larger in magnitude than the contribution of physical activity to changes in executive function. This is the first study to identify evidence for a robust bidirectional link between executive function and physical activity in a large sample of older adults tracked over time.

Introduction

Advancements in medical science in the past century have markedly increased life expectancy but have also heralded a broad set of challenges that accompany an aging population (United Nations, 2011). Age-related cognitive decline is one such challenge, producing wide ranging psychological, social, and economic consequences at both the individual and population level (Frank et al., 2006; Olesen et al., 2012). Emerging evidence suggests that age-related neurocognitive-decline should not be seen as fixed or immutable (Hamer and Chida, 2009). Rather, cognitive function seems to benefit from a healthy lifestyle, most notably from regular physical activity (Hertzog et al., 2009; Ku et al., 2012; Gow, 2013).

This study examines whether engaging in physical activity attenuates declines in higher level cognitive function (executive functioning) over a period of 6 years in older English adults. In addition, the current study investigates the more novel prediction that the relationship between physical activity and cognitive performance is bidirectional, and that executive function will also play a predictive role in shaping activity levels over time (Batty et al., 2007; Sabia et al., 2010). The executive functions, in particular, may enable people to consistently engage in effortful behaviors like physical activity in order to achieve long-term health benefits (Hall and Fong, 2007). As the contribution of executive functioning to physical activity has not yet been established in large scale prospective studies, this study also aimed to test this pathway in a sample of more than four thousand older English adults.

Beneficial effects of nicotine, cotinine and its metabolites as potential agents for Parkinson’s disease

What is your doctors' take on beneficial effects for stroke? I've only written 18 posts on it.
http://journal.frontiersin.org/article/10.3389/fnagi.2014.00340/full?
Don't prescribe smoking for yourself.
George E. Barreto^1*, Alexander Iarkov^2,3 and Valentina Echeverria Moran^2,3,4,5*

• ¹Department of Nutrition and Biochemistry, Pontificia Universidad Javeriana, Bogotá, D. C., Colombia
• ²Center of Research in Biomedical Sciences, Universidad Autónoma de Chile, Santiago, Chile
• ³Research & Development Service, Bay Pines VA Healthcare System, Bay Pines, FL, USA
• ⁴Research Service, James A Haley Veterans’ Hospital, Tampa, FL, USA
• ⁵Department of Molecular Medicine, Morsani College of Medicine, University of South, Tampa, FL, USA

Parkinson’s disease (PD) is a progressive neurodegenerative disorder, which is characterized by neuroinflammation, dopaminergic neuronal cell death and motor dysfunction, and for which there are no proven effective treatments. The negative correlation between tobacco consumption and PD suggests that tobacco-derived compounds can be beneficial against PD. Nicotine, the more studied alkaloid derived from tobacco, is considered to be responsible for the beneficial behavioral and neurological effects of tobacco use in PD. However, several metabolites of nicotine, such as cotinine, also increase in the brain after nicotine administration. The effect of nicotine and some of its derivatives on dopaminergic neurons viability, neuroinflammation, and motor and memory functions, have been investigated using cellular and rodent models of PD. Current evidence shows that nicotine, and some of its derivatives diminish oxidative stress and neuroinflammation in the brain and improve synaptic plasticity and neuronal survival of dopaminergic neurons. In vivo these effects resulted in improvements in mood, motor skills and memory in subjects suffering from PD pathology. In this review, we discuss the potential benefits of nicotine and its derivatives for treating PD.

Introduction

Parkinson’s disease (PD) is the second most common neurodegenerative illness after Alzheimer’s disease (AD), and reaches a prevalence of 3% after 65 years of age (Jellinger, 2003). Parkinson’s disease is predominantly sporadic, and rarely familial. The familial form of the disease can develop due to single genetic mutations (Dexter and Jenner, 2013). Parkinson’s disease is characterized by the presence of Lewy bodies, mainly composed of alpha-synuclein fibrils, a depletion of dopamine (DA)-generating neurons in substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) regions of the brain (Wirths and Bayer, 2003; Dexter and Jenner, 2013), that results in a decrease of DA levels in the striatum and frontal cortex regions of the brain (Thompson et al., 2005). Parkinson’s disease affects cognitive and motor abilities (Riedel et al., 2014), and progressively impairs sleep (Dos Santos et al., 2014), attention, and short-term memory, as well as visuospatial and executive functions (Liu et al., 2012; Conte et al., 2013; Rottschy et al., 2013; Zokaei et al., 2014). The dopaminergic deficit observed in PD patients seems to underlie the motor impairment symptoms such as hypokinesia, tremor and rigidity (Murer and Moratalla, 2011).

The cause of death of dopaminergic neurons is still a mystery; however, actual evidence is consistent with the idea that oxidative stress, mitochondrial dysfunction and neuroinflammation are the main factors involved in the etiology of PD (Büeler, 2010; Zuo and Motherwell, 2013; Camilleri and Vassallo, 2014; Celardo et al., 2014). It has been proposed that various genetic and environmental factors causing mitochondrial dysfunction result in abnormal accumulation of miscoded proteins and the generation of oxidative stress in the brain of subjects with PD (Bové and Perier, 2012; Cabezas et al., 2012, 2014; Perier and Vila, 2012; Dexter and Jenner, 2013; Trinh and Farrer, 2013; Zuo and Motherwell, 2013; Figure 1).

How brain waves guide memory formation

What EXACT stroke protocol is your doctor having you do to make sure your brain waves are doing the correct thing and not giving you memory problems as a result of your stroke? This is an extremely serious question for your doctor, don't let them pooh-pooh it. Do these waves still form post-stroke?
http://www.rdmag.com/news/2015/02/how-brain-waves-guide-memory-formation?
Our brains generate a constant hum of activity: As neurons fire, they produce brain waves that oscillate at different frequencies. Long thought to be merely a byproduct of neuron activity, recent studies suggest that these waves may play a critical role in communication between different parts of the brain.
A new study from Massachusetts Institute of Technology (MIT) neuroscientists adds to that evidence. The researchers found that two brain regions that are key to learning—the hippocampus and the prefrontal cortex—use two different brain-wave frequencies to communicate as the brain learns to associate unrelated objects. Whenever the brain correctly links the objects, the waves oscillate at a higher frequency, called “beta,” and when the guess is incorrect, the waves oscillate at a lower “theta” frequency.
“It’s like you’re playing a computer game and you get a ding when you get it right, and a buzz when you get it wrong. These two areas of the brain are playing two different ‘notes’ for correct guesses and wrong guesses,” says Earl Miller, the Picower Professor of Neuroscience, a member of MIT’s Picower Institute for Learning and Memory, and senior author of a paper describing the findings in Nature Neuroscience.
Furthermore, these oscillations may reinforce the correct guesses while repressing the incorrect guesses, helping the brain learn new information, the researchers say.
Signaling right and wrong
Miller and lead author Scott Brincat, a research scientist at the Picower Institute, examined activity in the brain as it forms a type of memory called explicit memory—memory for facts and events. This includes linkages between items such as names and faces, or between a location and an event that took place there.
During the learning task, animals were shown pairs of images and gradually learned, through trial and error, which pairs went together. Each correct response was signaled with a reward.
As the researchers recorded brain waves in the hippocampus and the prefrontal cortex during this task, they noticed that the waves occurred at different frequencies depending on whether the correct or incorrect response was given. When the guess was correct, the waves occurred in the beta frequency, about 9 to 16 hertz (cycles per second). When incorrect, the waves oscillated in the theta frequency, about 2 to 6 hertz.
Previous studies by MIT’s Mark Bear, also a member of the Picower Institute, have found that stimulating neurons in brain slices at beta frequencies strengthens the connections between the neurons, while stimulating the neurons at theta frequencies weakens the connections.
Miller believes the same thing is happening during this learning task.
“When the animal guesses correctly, the brain hums at the correct answer note, and that frequency reinforces the strengthening of connections,” he says. “When the animal guesses incorrectly, the ‘wrong’ buzzer buzzes, and that frequency is what weakens connections, so it’s basically telling the brain to forget about what it just did.”
The findings represent a major step in revealing how memories are formed, says Howard Eichenbaum, director of the Center for Memory and Brain at Boston Univ.
“This study offers a very specific, detailed story about the role of different directions of flow, who’s sending information to whom, at what frequencies, and how that feedback contributes to memory formation,” says Eichenbaum, who was not part of the research team.
The study also highlights the significance of brain waves in cognitive function, which has only recently been discovered by Miller and others.
“Brain waves had been ignored for decades in neuroscience. It’s been thought of as the humming of a car engine,” Miller says. “What we’re discovering through this experiment and others is that these brain waves may be the infrastructure that supports neural communication.”
Enhancing memory
The researchers are now investigating whether they can speed up learning by delivering noninvasive electrical stimulation that oscillates at beta frequencies when the correct answer is given and at theta frequencies when the incorrect answer is given. “The idea is that you make the correct guesses feel more correct to the brain, and the incorrect guesses feel more incorrect,” Miller says.
This form of very low voltage electrical stimulation has already been approved for use in humans.
“This is a technique that people have used in humans, so if it works, it could potentially have clinical relevance for enhancing memory or treating neurological disorders,” Brincat says.
Source: Massachusetts Institute of Technology

Sleep hygiene - 6 Easy Steps to Falling Asleep Fast

What protocol did your doctor give you on sleeping? None? In the hospital I was at, Ambiens were handed out like candy at bedtime. You'll have to ask your doctor if sleeping pill sleep actually counts as sleep and does the nightly brain cleanup task.
http://www.spring.org.uk/2011/05/6-easy-steps-to-falling-asleep-fast.php

Does High IQ Increase the Risk of Depression and Mental Disorders?

Does this match up earlier research that had those with a high IQ were more likely to get depressed following a brain injury because they knew how much intelligence they lost? I can't find that research right now. Damn my 7100 posts, it's too much to juggle at one time in my brain.
Or is depression an advantage?

4 Surprising Advantages of Being Depressed

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Or maybe you want  alcohol to reduce your chances of depression;

RESULTS:

Moderate alcohol intake within the range of 5 to 15 g/day was significantly associated with lower risk of incident depression (hazard ratio (HR) and 95% confidence interval (95% CI) = 0.72 (0.53 to 0.98) versus abstainers). Specifically, wine consumption in the range of two to seven drinks/week was significantly associated with lower rates of depression (HR (95% CI) = 0.68 (0.47 to 0.98)).
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I'm sure your doctor won't be doing this;

Psilocybin inhibits the processing of negative emotions in the brain

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This from the 1920s might be hard to find.

It brings mental sunshine (1920): 'Sa-tan-ic' liniment

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Does High IQ Increase the Risk of Depression and Mental Disorders? 

These lines are entertaining to me.

The super-brainy computer programmer, the scientist, or the nerdy professor is supposed to be a social misfit. He turns up at parties with unkempt hair and disheveled attire and spends the evening hunched up in a corner.