Aging-induced type I interferon response at the choroid plexus negatively affects brain function

I'm sure you want decent cognitive functioning post-stroke. So ask your doctors how they are  blocking type I interferon (IFN-I)–dependent gene expression
http://www.sciencemag.org/content/346/6205/89

1. Kuti Baruch¹,*,
2. Aleksandra Deczkowska¹,*,
3. Eyal David²,
4. Joseph M. Castellano³,
5. Omer Miller¹,
6. Alexander Kertser¹,
7. Tamara Berkutzki¹,
8. Zohar Barnett-Itzhaki²,
9. Dana Bezalel²,
10. Tony Wyss-Coray³,
11. Ido Amit²,†,
12. Michal Schwartz¹,†

+ Author Affiliations

1. ¹Department of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.
2. ²Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.
3. ³Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.

1. ↵†These authors contributed equally to this work and are corresponding authors. E-mail: michal.schwartz@weizmann.ac.il (M.S.); ido.amit@weizmann.ac.il (I.A.)

1. ↵* These authors contributed equally to this work.

• Abstract
• Editor's Summary

Aging-associated cognitive decline is affected by factors produced inside and outside the brain. By using multiorgan genome-wide analysis of aged mice, we found that the choroid plexus, an interface between the brain and the circulation, shows a type I interferon (IFN-I)–dependent gene expression profile that was also found in aged human brains. In aged mice, this response was induced by brain-derived signals, present in the cerebrospinal fluid. Blocking IFN-I signaling within the aged brain partially restored cognitive function and hippocampal neurogenesis and reestablished IFN-II–dependent choroid plexus activity, which is lost in aging. Our data identify a chronic aging-induced IFN-I signature, often associated with antiviral response, at the brain’s choroid plexus and demonstrate its negative influence on brain function, thereby suggesting a target for ameliorating cognitive decline in aging.

Neurons in human muscles emphasize stimulation from the outside world

Your doctor should be able to incorporate this knowledge into your stroke protocol for spasticity.
So demand that spasticity protocol. Your doctor better have one.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=145983&CultureCode=en
Stretch sensors in our muscles participate in reflexes that serve the subconscious control of posture and movement. According to a new study published in the Journal of Neuroscience, these sensors respond weakly to muscle stretch caused by one's voluntary action, and most strongly to stretch that is imposed by external forces. The ability to reflect causality in this manner can facilitate appropriate reflex control and accurate self-perception.
“The results of the study show that stretch receptors in our muscles indicate more than which limb is moving or how fast; these sensors also adjust their signals according to who caused the movement,” says Michael Dimitriou, who conducted this study and is currently a post doc at the Department of Integrative Medical Biology, Umeå University, Sweden.
Normally, we can easily distinguish between movements we make ourselves and movements that are imposed on our body by external forces. The ability to discriminate between self-generated and externally generated sensory events is crucial for accurate perception and the control of posture and movement. This ability is also believed to form the foundation on which conscious self-awareness is built.
Such discrimination between self and other has previously been thought to arise as a result of complex computations performed in the brain, that use prior knowledge or memories of the consequences of own actions. But the study by Michael Dimitriou shows that information on the cause of a sensory effect can be provided in real-time by so-called ‘muscle spindles’, a class of stretch receptors found in most of our skeletal muscles.
Muscle spindles differ from other sensory receptors, such as stretch receptors in the skin, because their sensitivity can be controlled by the nervous system via specialized motor neurons. The purpose of this control has been unclear. The neural data presented by Michael Dimitriou indicates that these specialized motor neurons increase the sensitivity of stretch receptors when the body is exposed to an externally imposed stretch stimulus, such as when a falling ball is caught in the hand. Because amplified spindle responses mean stronger stretch reflexes, the resulting muscle activity instantly counteracts movement of the hand. When making a voluntary movement, however, the nervous system ‘automatically’ reduces the sensitivity of spindles in the stretching muscles, thereby making it possible for us to move without setting off strong stretch reflexes that would otherwise counteract movement. Uncontrollably strong stretch reflexes are commonly referred to as ‘spasticity’.
“These results provide an explanation of how reflexes can be functionally adjusted to help us achieve our everyday tasks, without requiring conscious control of reflex sensitivity or complex computations in the brain for predicting the sensory consequences of our actions,” says Michael Dimitriou.
He believes that these new findings are important both for understanding the neural mechanisms that underlie movement control and self-perception, but also for understanding pathological states where these mechanisms are disturbed.
“With these findings, we also get new insights into mechanisms whose malfunction may contribute to neuromuscular problems such as spasticity or alien hand syndrome (also known as ‘Dr. Strangelove syndrome’), and help identify potential treatment targets for these conditions,” says Michael Dimitriou.

Coconut oil supplementation reduces blood pressure and oxidative stress in spontaneously hypertensive rats

I'm already using coconut oil as a dementia preventer. But never listen to me, your doctor knows everything even if you have to train them in their job.
http://www.biomedcentral.com/content/pdf/1753-6561-8-S4-P68.pdf
Background
Oxidative stress has been implicated in the pathogenesis
of hypertension and antioxidant compounds have been
used in the prevention and treatment of this disease. In
this context, coconut oil (CO) was found to have antioxidant
property due to its high polyphenol content. In
this study, we investigated the effects caused by chronic
treatment with CO on mean arterial pressure (MAP),
heart rate (HR), and lipid peroxidation in spontaneously
hypertensive rats (SHR).
Methods
SHR and their controls (Wistar Kyoto, WKY) were orally
treated with coconut oil (2 ml/day) or saline for thirty
days. Cardiovascular parameters were evaluated 24 hours
after the end of the thirtieth day. Serum oxidative stress
was measured by tiobarbituric acid reactive species assay
(TBARS).
Results and conclusions
The administration of CO was able to reduced the MAP
of SHR compared to SHR treated with saline (146 ± 11
n = 5 vs. 174 ± 6 n = 8 mmHg, respectively, p < 0.05).
On the other hand, treatment with CO had no effect on
MAP of WKY compared with WKY treated with saline
(136 ± 3 n = 6 vs. 113 ± 1 mmHg n = 8, respectively,
p < 0.05). In addition, CO supplementation reduced lipid
peroxidation in the SHR group compared to SHR + saline
(13.7 ± 2 vs. 27.5 ± 5 nmol/g n = 7, respectively, p < 0.05)
and also reduced in WKY compared with WKY treated
with saline (11.5 ± 1 vs. 21.9 ± 2 nmol/g n = 7 respectively,
p < 0.05). We concluded that treatment with coconut oil
(2 ml/day) for thirty days reduces the blood pressure and
oxidative stress in hypertensive rats.

Tooth loss inhibits neurogenesis in the dentate gyrus of adult mice

Just for grins, ask your doctor how badly your neurogenesis is affected by the teeth you've lost. What stroke protocol is your doctor using to get around that problem? Would that include removed wisdom teeth? 

Tooth loss inhibits neurogenesis in the dentate gyrus of adult mice

Shaochen Su¹, Tao Qi², Baoli Su³, Huibin Gu³, Jianlin Wang¹, Lan Yang^1
1 School of Life Sciences, Lanzhou University; Second Hospital, Lanzhou University, Lanzhou, Gansu Province, China
² First Hospital, Lanzhou University, Lanzhou, Gansu Province, China
³ Changzhou Institute of Mechatronic and Technology, Changzhou, Jiangsu Province, China

Date of Acceptance	30-Jul-2014
Date of Web Publication	4-Oct-2014

Correspondence Address:
Jianlin Wang
School of Life Sciences, Lanzhou University; Second Hospital, Lanzhou University, Lanzhou 730030, Gansu Province
China
Lan Yang
School of Life Sciences, Lanzhou University; Second Hospital, Lanzhou University, Lanzhou 730030, Gansu Province
China

DOI: 10.4103/1673-5374.141786

Abstract

Tooth loss has been shown to affect learning and memory in mice and increases the risk of Alzheimer's disease. The dentate gyrus is strongly associated with cognitive function. This study hypothesized that tooth loss affects neurons in the dentate gyrus. Adult male mice were randomly assigned to either the tooth loss group or normal control group. In the tooth loss group, the left maxillary and mandibular molars were extracted. Normal control mice did not receive any intervention. Immunofluorescence staining revealed that the density and absorbance of doublecortin- and neuronal nuclear antigen-positive cells were lower in the tooth loss group than in the normal control group. These data suggest that tooth loss may inhibit neurogenesis in the dentate gyrus of adult mice.

Keywords: nerve regeneration; neurogenesis; neurons; tooth loss; hippocampus; dentate gyrus; doublecortin; neuronal nuclear antigen; neural regeneration

How to cite this article: Su S, Qi T, Su B, Gu H, Wang J, Yang L. Tooth loss inhibits neurogenesis in the dentate gyrus of adult mice. Neural Regen Res 2014;9:1606-9

WorldStrokeDay - can you help?

An email from the American Stroke Association. My response back at the end.

Hello, Dean!

I'm the social media manager for the American Stroke Association and I am hoping that you will be able to help us with our #WorldStrokeDay campaign.

World Stroke Day is October 29 and we need you to help us end this leading killer of Americans. We want to educate all Americans how to recognize and react in a stroke emergency. You can help us by sharing these messages in social media throughout October.

Here are some posts you can use:

#WorldStrokeDay is October 29 and 1 in 3 Americans don’t know how to recognize a stroke. When you don’t know what to look for, you can’t save a life. I want to change that and you can help us! Download and share @American Stroke Association’s stroke warning signs app. http://bit.ly/1nNG8cx

Survival is why I want to end stroke. #LifeIsWhy the American Stroke Association is working to end stroke every day of the year. On October 29, #WorldStrokeDay, they are doing more than ever. Take this pledge and help us end stroke for good. http://bit.ly/1rIxGBp

Ending stroke is a big job, but we can all play a part. Pledge to help on #WorldStrokeDay http://bit.ly/1rIxGBp

When strokes strike, minutes matter. Share the signs and be prepared. #WorldStrokeDay http://bit.ly/1rXzPrl

Survival is why I want everyone to know what to do in a stroke emergency. #LifeisWhy #WorldStrokeDay http://bit.ly/1rXzPrl

(ON OCT 29) Today, the world comes together to end stroke. Do you know what to do in a stroke emergency? #WorldStrokeDay http://bit.ly/1rXzPrl

Please let me know if you have any questions! We appreciate your support!

Best,

Alexson

Alexson Calahan
Manager, Engagement Marketing

7272 Greenville Avenue  I  Dallas, Texas 75231
alexson.calahan@heart.org  I  www.heart.org I  www.strokeassociation.org
P 515-994-0772

Dear M. Calahan,
I consider your organization a huge part of the problem. You put out press releases but never solve any of the problems in stroke.You keep pushing the F.A.S.T. paradigm and tPA which is a 12% efficacy failure. You are solving the wrong problem by assuming that total stroke prevention is the way to go. I'd be willing to bet you could save more neurons in total by stopping the neuronal cascade of death in the first week. You can never prevent all strokes and TBIs would be able to be helped by this approach also. Even if you could prevent all 80% of preventable strokes that would still leave 3 million persons yearly needing intervention worldwide.  If you want to be useful you will publicize the existing problems in stroke and what exactly you are doing to solve those problems. 

Read my blog Deans' Stroke Musings -  www.oc1dean.blogspot.com and come back in 10 months after reading it all and tell me what your association has that is useful for survivors.

0. There is no fast, easy and objective way to diagnose a stroke.
1. tPA may save your life but only has a 12% efficacy for full recovery.
2. Your neurologist doesn't have any concrete stroke protocols to save all the neurons that are dying in the first week.
3. Your neurologist or physiatrist doesn't have any clue about how to get you to full recovery. (Ask them exactly how to do it), you'll get excuses.
4. Only 10% get to full recovery.
5. No protocols to prevent your 33% chance of getting dementia post-stroke.
6. Nothing to alleviate your fatigue.
7. Nothing that will cure your spasticity.
8. Nothing on cognitive training unless you find this yourself.
9. No published stroke protocols.
10. No way to compare your stroke hospital results vs. other stroke hospitals. Results not processes!
11.  No Specific post-stroke stroke and dementia prevention diet. 

Picturing Inflammation in Blood Vessels

Have your doctor get this and explain how the protocols given you are preventing atherosclerosis.
http://stm.sciencemag.org/content/6/255/255ec166.short

1. Eric C. Stecker

+ Author Affiliations

1. Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR 97239, USA. E-mail: steckere@ohsu.edu

Atherosclerosis—a build-up of fatty material, called plaques, in the arteries—is responsible for a majority of cardiovascular morbidity and mortality. Local vascular inflammation is well established as the critical driver of many atherogenic processes, including cholesterol accumulation and plaque instability. It would therefore be useful to picture all aspects of this inflammation so as to better understand disease progression and its mechanisms. In a new study, van der Valk et al. successfully imaged the involvement of white blood cells early in the process of vascular inflammation in humans.

The investigators first used a clinically approved imaging modality, single-photon emission computed tomography with transmission computed tomography (SPECT/CT), to prove the feasibility of SPECT/CT for visualizing the trafficking of peripheral blood monocytes into atherosclerotic plaques in humans. Among 10 patients with known vascular disease and five healthy volunteers, monocytes were isolated from venous blood samples, labeled with a radioactive isotope, and reinfused. SPECT/CT was used to image the migration of the monocytes into the vascular wall over time. Vascular infiltration by monocytes corresponded to areas of atherosclerosis by means of magnetic resonance imaging and correlated with the degree of vascular wall inflammation by means of positron emission tomography. The kinetics of monocyte trafficking were evaluated, although not fully characterized.

The technique used by van der Valk et al. will allow longitudinal study of the phases of plaque infiltration by monocytes. Different aspects of plaque inflammation have been evaluated in snapshots, but not dynamically, to see leukocyte trafficking characteristics. This new SPECT/CT approach could evaluate the mechanisms of vascular inflammation in a variety of disease states—such as acute myocardial infarction, acute stroke, chronic atherosclerotic vascular disease, and chronic aneurysmal vascular disease—providing not only mechanistic insights, but also the ability to evaluate new therapies.

F. M. van der Valk et al., In vivo imaging of enhanced leukocyte accumulation in atherosclerotic lesions in humans. J. Am. Coll. Cardiol. 64, 1019–1029 (2014). [Abstract]

• Copyright © 2014, American Association for the Advancement of Science

Citation: E. C. Stecker, Picturing Inflammation in Blood Vessels. Sci. Transl. Med. 6, 255ec166 (2014).

You will have to ask your doctor if this video is better.

You can see a video of how plaque forms here:
Inflammation In Atherosclerotic Plaque Formation

Noninvasive brain-computer interface enables communication after brainstem stroke

How many decades before this gets rolled out to your hospital? A great stroke association would be personally contacting every single stroke department head and getting commitments to stay up-to-date on all stroke rehab. This is absolutely necessary since the hospital is waiting on somebody else to solve the problem.   Depending on the response is whether the good cop or the bad cop would show up.
http://stm.sciencemag.org/content/6/257/257re7

1. Eric W. Sellers¹,*,
2. David B. Ryan¹ and
3. Christopher K. Hauser¹,²

+ Author Affiliations

1. ¹Department of Psychology, East Tennessee State University, Johnson City, TN 37614, USA.
2. ²Department of Neurobiology and Anatomy, Wake Forest University, Winston Salem, NC 27106, USA.

1. ↵*Corresponding author. E-mail: sellers@etsu.edu

AbstractBack to Top

Brain-computer interfaces (BCIs) provide communication that is independent of muscle control, and can be especially important for individuals with severe neuromuscular disease who cannot use standard communication pathways or other assistive technology. It has previously been shown that people with amyotrophic lateral sclerosis (ALS) can successfully use BCI after all other means of independent communication have failed. The BCI literature has asserted that brainstem stroke survivors can also benefit from BCI use. This study used a P300-based event-related potential spelling system. This case study demonstrates that an individual locked-in owing to brainstem stroke was able to use a noninvasive BCI to communicate volitional messages. Over a period of 13 months, the participant was able to successfully operate the system during 40 of 62 recording sessions. He was able to accurately spell words provided by the experimenter and to initiate dialogues with his family. The results broadly suggest that, regardless of the precipitating event, BCI use may be of benefit to those with locked-in syndrome.

• Copyright © 2014, American Association for the Advancement of Science

Citation: E. W. Sellers, D. B. Ryan, C. K. Hauser, Noninvasive brain-computer interface enables communication after brainstem stroke. Sci. Transl. Med. 6, 257re7 (2014).

Read the Full Text

Sidehill walking

My latest challenges, straight and level walking doesn't do anything useful anymore. This is great for strengthening the muscles that prevent rolling the ankle. Don't do this! Someday I'll push myself to try running. That will probably be downhill running because it would force you to get your feet in front of you very quickly.

Health Risks After Stroke May Linger for at Least 5 Years: Study

I quit seeing a doctor 2 years after my stroke because he knew absolutely nothing about stroke rehab. But your doctor might be better. Did your doctor manage to get you into the 10% get to almost full recovery? Mine obviously didn't. I look at this as mainly a way to try to get payable visits from survivors. I still wait for pay for performance for recovery goals.
http://consumer.healthday.com/cognitive-health-information-26/neurology-news-496/health-risks-after-stroke-linger-for-at-least-5-years-study-692375.html
Stroke survivors remain at high risk for another stroke or other serious medical problems and death for at least five years, a new study suggests.
The findings may mean that stroke survivors require closer follow-up to prevent these health problems, the Canadian researchers said.
"This high long-term risk was surprising and shows that we need to develop better strategies and interventions for these patients to prevent as many of these serious problems as we can," study leader Dr. Richard Swartz, director of the University of Toronto stroke program, said in a Heart and Stroke Foundation of Canada news release.
In the study, Swartz's team analyzed data from about 24,000 patients in Canada who suffered a stroke or mini-stroke, clinically known as a "transient ischemic attack" (TIA).
All of the patients had already survived the "high-danger" period, which is typically thought to be the 90 days after hospital discharge.
However, within the first year after this high-risk period, 9.3 percent of the patients died, had a repeat stroke, mini-stroke, heart attack or were admitted to long-term care. Death was the most common of these events, affecting more than 5 percent of patients in the first year.
Among patients who were still alive after a year, the rate of these events remained at 5 percent in each of the following four years, according to the study to be presented Tuesday at the Canadian Stroke Congress in Vancouver.
"We now need to identify ways to determine which people, among those who have made it through the riskiest period, remain most at risk for serious events so we can develop appropriate preventive interventions," Swartz said.

More at link.

The great stroke divide: Both these fathers had strokes. Matt was back at work two weeks later but Chris is still in a wheelchair five years on. The difference? Their first few hours of care

Matt is the new CEO of the National Stroke Association. I hope his experience doesn't bias the focus on F.A.S.T. and tPA delivery. That would be the wrong takeaway from his experience.
http://www.dailymail.co.uk/health/article-2273468/Stoke-divide-Both-fathers-strokes-Matt-work-weeks-later-Chris-wheelchair-years-The-difference-Their-hours-care.html

Call for Entries: 6th Annual Neuro Film Festival Online Video Competition

Fire up those cameras.

Thank you for your past submission to the Neuro Film Festival®! Do you have another compelling story to tell about the impact of brain disease, such as Alzheimer's disease, stroke, concussion, and Parkinson's disease? Could your story once again inspire others and raise awareness for why more research is needed into causes, treatments, and cures for brain disease? If so, we want to hear from you again! Submit a short video to the 2015 Neuro Film Festival that is no more than five minutes in length, and you could win up to $1,000 and a trip to Washington, DC, to see your video premiered during the American Academy of Neurology's 2015 Annual Meeting, the world's largest gathering of neurologists.

SUBMIT VIDEO NOW

Video submissions are due by February 25, 2015. See complete contest rules and submission guidelines.

'You cannot mange what you cannot measure'

Possibly from management thinker Peter Drucker. Correction - Quote from William Edwards Deming. And our stroke hospitals, doctors and therapists are completely failing at this. Our hospitals don't seem to measure anything to do with stroke results, just the stupid processes they are following.  Thus every stroke department head should be fired if they have no clue what they aren't measuring.  With no measurements or starting point we will never know what stroke protocols work best. But our stroke medical providers are great at deflecting questions by parroting the insanely stupid comment, 'All strokes are different, all stroke recoveries are different'. 


That's my rant for the day.

Coffee-drinking Genes Identified

So do those with these genes have a lower chance of dementia because of this?
Coffee May Lower Your Risk of Dementia

http://www.biosciencetechnology.com/news/2014/10/coffee-drinking-genes-identified?et_cid=4195077&et_rid=648870051&type=headline

Meditation Benefits: 10 Ways It Helps Your Mind

With all these benefits and the cheapness of it, why hasn't your doctor set up a stroke protocol on meditation? More ammunition for you Amy.

The latest here:

Meditation Benefits: 10 Ways It Helps Your Mind

Full information at the link.

1. Lasting emotional control

2. Cultivate compassion

3. Change brain structures

4. Reduce pain

5. Accelerate cognition

6. Meditate to create

7. Sharpen concentration

8. Improve multitasking at work

9. Reduce anxiety

10 Fight depression

Abnormal yawning in stroke patients: the role of brain thermoregulation

I want to know why when I yawn my spastic arm starts wandering on its own. I usually have to hold it down. Not quite as bad as sneezing but still.
http://journal.frontiersin.org/Journal/10.3389/fnins.2014.00300/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w41-2014
Andrew C. Gallup^*

• Psychology Department, State University of New York at Oneonta, Oneonta, NY, USA

A commentary on
Insular and caudate lesions release abnormal yawning in stroke patients

by Krestel, H., Weisstanner, C., Hess, C. W., Bassetti, C. L., Nirkko, A., and Wiest, R. (2013). Brain Struct. Funct. doi: 10.1007/s00429-013-0684-6. [Epub ahead of print].

Krestel et al. (2013) recently investigated the potential contributing factors associated with abnormal yawning (defined as ≥3 yawns/15 min) in 10 patients with acute anterior circulation stroke. Though frequent yawning had previously been observed in stroke patients (Cattaneo et al., 2006; Singer et al., 2007), this study attempted to assess the influence of specific physiologic and lesion topographic variables contributing to this association. All patient parameters were taken within 1 h after admission and emergency nurses recorded a single axillary body temperature with a digital thermometer (Krestel, personal communication). Using MRI lesion maps, and reportedly finding no associations between various physiologic measures, including blood oxygen saturation, glucose, body temperature, blood pressure, and heart rate, the authors concluded that ischemic lesions in the posterior insula and caudate nucleus might facilitate high frequency yawning in stroke patients. While this report improves our neurological understanding regarding the association between frequent yawning in stroke patients, limitations in the analysis and interplay of temperature need to be addressed.

Yawning is characterized by a powerful gaping of the jaw with inspiration, a brief period of peak muscle contraction, and a passive closure of the jaw with shorter expiration (Barbizet, 1958). The localized circulatory changes resulting from this action pattern have led researchers to hypothesize that yawns may function to cool the brain (Gallup and Gallup, 2007). For example, yawns produce increases in blood flow to the skull and enhanced venous return (Bhangoo, 1974), while the deep inhalation during yawning can modify the temperature of venous blood draining from the nasal and oral orifices into the cavernous sinus, which surrounds the internal carotid artery (Zenker and Kubik, 1996). Together, these processes act like a radiator removing hyperthermic blood from brain while introducing cooler arterial blood to the brain. Moreover, the flexing of the musculature during yawning may encourage the evaporation of the sinus mucosa (see Gallup and Hack, 2011). Research supporting the brain cooling hypothesis has accumulated over the past 5 years, including evidence for predicted brain and body temperature fluctuations surrounding yawning events, indirect manipulations of brain temperature causing a reduction in yawn frequency, and an altered expression of yawning which appears to be driven by ambient temperature manipulation/variation (reviewed by Gallup and Eldakar, 2013). For example, by directly monitoring continuous changes in prelimbic cortex temperature of rats it was shown that yawning is preceded by intermittent and rapid increases in brain temperature (i.e., ~0.1°C/min), and that following the completion of a yawn the slope of the temperature change reverses and quickly returns to baseline (Shoup-Knox et al., 2010).

While the breadth of physiologic measures taken by Krestel et al. (2013) is laudable, a single measure of axillary temperature taken long after the onset of the yawning episode is inadequate for assessing this relationship. Since distinct brain temperature changes in rats occur before and after single yawns on a rather short temporal scale; i.e., 60–90 s (Shoup-Knox et al., 2010), and isolated bouts of excessive yawning in humans have been shown to reduce skull temperature by as much as 0.4°C (Gallup and Gallup, 2010), it remains possible that the pathological yawning experienced by these patients was accompanied by recurrent changes in temperature that were never recorded. Furthermore, temperature measures taken from the skull (e.g., oral, tympanic, forehead) would be more informative since the motor pattern of yawning and the associated circulatory changes are localized to this area. That said, even these measurements could miss important temperature fluctuations confined to particular brain regions.

The use of MRI lesion maps to establish a relationship between ischemic lesions in the posterior insula and caudate nucleus and the duration of abnormal yawning is certainly of great importance (Krestel et al., 2013). At this point, however, it is premature to declare that there was “no evidence of other potential causes” related to abnormal yawning in these patients. To the contrary, frequent or abnormal yawning in stroke patients may be a consequence of thermoregulatory dysfunction associated with the brain injury (Gallup and Gallup, 2008). Given the close temporal association between yawning and changes in brain/skull temperature, future research monitoring patients with abnormal or excessive yawning bouts should take continuous temperature measures from areas proximate to the cranium in order to properly assess this relationship.

Neural precursor cells in the ischemic brain – integration, cellular crosstalk, and consequences for stroke recovery

We need to know how to use this in our recovery. Ask about the stroke protocol that will be coming in 50 years.
http://journal.frontiersin.org/Journal/10.3389/fncel.2014.00291/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w41-2014
Dirk M. Hermann^1*, Luca Peruzzotti-Jametti², Jana Schlechter¹, Joshua D. Bernstock², Thorsten R. Doeppner¹ and Stefano Pluchino^2*

• ¹Chair of Vascular Neurology, Dementia and Cognitive Health of the Elderly, Department of Neurology, University Hospital Essen, Essen, Germany
• ²John van Geest Centre for Brain Repair, Department of Clinical Neurosciences, NIHR Biomedical Research Centre, and Wellcome Trust-Medical Research Council Stem Cell Institute, University of Cambridge, Cambridge, UK

After an ischemic stroke, neural precursor cells (NPCs) proliferate within major germinal niches of the brain. Endogenous NPCs subsequently migrate toward the ischemic lesion where they promote tissue remodeling and neural repair. Unfortunately, this restorative process is generally insufficient and thus unable to support a full recovery of lost neurological functions. Supported by solid experimental and preclinical data, the transplantation of exogenous NPCs has emerged as a potential tool for stroke treatment. Transplanted NPCs are thought to act mainly via trophic and immune modulatory effects, thereby complementing the restorative responses initially executed by the endogenous NPC population. Recent studies have attempted to elucidate how the therapeutic properties of transplanted NPCs vary depending on the route of transplantation. Systemic NPC delivery leads to potent immune modulatory actions, which prevent secondary neuronal degeneration, reduces glial scar formation, diminishes oxidative stress and stabilizes blood–brain barrier integrity. On the contrary, local stem cell delivery allows for the accumulation of large numbers of transplanted NPCs in the brain, thus achieving high levels of locally available tissue trophic factors, which may better induce a strong endogenous NPC proliferative response. Herein we describe the diverse capabilities of exogenous (systemically vs. locally transplanted) NPCs in enhancing the endogenous neurogenic response after stroke, and how the route of transplantation may affect migration, survival, bystander effects and integration of the cellular graft. It is the authors’ claim that understanding these aspects will be of pivotal importance in discerning how transplanted NPCs exert their therapeutic effects in stroke.

Antigen-specific immune reactions to ischemic stroke

I'm not sure how this will help us so ask your doctors what they will do with this information. Hopefully not scoff at you. Mine pretty much did when I asked about specific research articles. I doubt he had read anything new since medical school. That lack of acquiring knowledge needs to be brought up to the hospital president because that means the stroke department head is not setting proper goals and expectations. 

Antigen-specific immune reactions to ischemic stroke

http://journal.frontiersin.org/Journal/10.3389/fncel.2014.00278/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w41-2014
Xabier Urra^1,2, Francesc Miró², Angel Chamorro^1,2 and Anna M. Planas^2,3*

• ¹Functional Unit of Cerebrovascular Diseases, Hospital Clínic, Barcelona, Spain
• ²August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain
• ³Department of Brain Ischemia and Neurodegeneration, Instituto de Investigaciones Biomédicas de Barcelona (IIBB), Consejo Superior de Investigaciones Científicas (CSIC), Barcelona, Spain

Brain proteins are detected in the cerebrospinal fluid (CSF) and blood of stroke patients and their concentration is related to the extent of brain damage. Antibodies against brain antigens develop after stroke, suggesting a humoral immune response to the brain injury. Furthermore, induced immune tolerance is beneficial in animal models of cerebral ischemia. The presence of circulating T cells sensitized against brain antigens, and antigen presenting cells (APCs) carrying brain antigens in draining lymphoid tissue of stroke patients support the notion that stroke might induce antigen-specific immune responses. After stroke, brain proteins that are normally hidden from the periphery, inflammatory mediators, and danger signals can exit the brain through several efflux routes. They can reach the blood after leaking out of the damaged blood-brain barrier (BBB) or following the drainage of interstitial fluid to the dural venous sinus, or reach the cervical lymph nodes through the nasal lymphatics following CSF drainage along the arachnoid sheaths of nerves across the nasal submucosa. The route and mode of access of brain antigens to lymphoid tissue could influence the type of response. Central and peripheral tolerance prevents autoimmunity, but the actual mechanisms of tolerance to brain antigens released into the periphery in the presence of inflammation, danger signals, and APCs, are not fully characterized. Stroke does not systematically trigger autoimmunity, but under certain circumstances, such as pronounced systemic inflammation or infection, autoreactive T cells could escape the tolerance controls. Further investigation is needed to elucidate whether antigen-specific immune events could underlie neurological complications impairing recovery from stroke.

National Stroke Association - Announcing our best e-newsletter yet

I don't think I have gotten any useful information yet from the NSA.

Ms. Clair Diones, How many survivors have you personally asked about the usefulness of your work? Any at all? Try calling their 1-800 number and see how bad it is. 1-800-787-6537 or 1-800-STROKES
You first would have a great outreach to survivors, which you could directly copy from the British Stroke Association.

Mr. Matt Lopez as Next CEO,  you have your work cut out for you. Lots to fix in your organization if you are to fulfill your mission statement.

http://www.stroke.org/site/R?i=SOnLnlOfaGc5mgeF1Utuuw

Dear dean,

To keep you better informed about all of our work, we’re giving our signature e-newsletter a fresh, new design. Moving forward Brain Alert will be called the National Stroke Association Monthly E-newsletter. You will receive the first issue in November. Here are a few of the exciting new features:

• Mobile-friendly - Now you can stay informed about our latest projects in a format that’s easy-to-read on your smartphone or tablet.
• Content by category - Each article will be clearly marked with a category. This will help you find the information you value most at a glance.
• More exclusive info - The monthly e-newsletter will focus solely on the educational programs and resources developed by National Stroke Association. We have a lot to offer the stroke community(I really doubt it), and we want to make sure you know about everything.

You can still stay informed about the latest stroke news and research. Subscribe to our StrokeSmart^® e-newsletter, which goes out twice a month.

To see what we’re working on in October, visit www.stroke.org.

Sincerely,

Clair Diones
Director, Marketing and Communications

Swear Your Pain Away

I've noticed anecdotally that some aphasia patients are able to fluently swear. Whom is going to research the reason for that? And can decent research be done to see if this helps those patients regain regular speech?
http://brainblogger.com/2014/10/06/swear-your-pain-away/

System Integration and Control of Finger Orthosis for Post Stroke Rehabilitation

What does your clinic have for hand rehab and what is the success rate?
The other ones I've written on are here:
http://oc1dean.blogspot.com/2011/04/arm-hand-stroke-exercises-by-madfit.html

novel design of a robotic hand exoskeleton device (PMHand) for the purpose of aiding post stroke rehabilitation

Music Glove Presentation - Hand stroke rehab

Kinematic Analysis of a Novel Exoskeleton Finger Rehabilitation Robot for Stroke Patients 

Assessment of hand kinematics using inertial and magnetic sensors

Multisensory Representation of the Space Near the Hand From Perception to Action and Interindividual Interactions

Functional Electrical Stimulation to Augment Poststroke Reach and Hand Opening in the Presence of Voluntary Effort

Australia - first hand therapy aims to close gap 

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

Haptic-based neurorehabilitation in post-stroke patients: a feasibility prospective multicentre trial for robotics hand rehabilitation.

Clinical Effects of Using HEXORR (Hand Exoskeleton Rehabilitation Robot) for Movement Therapy in Stroke Rehabilitation

Mechatronic Design and Characterization of the Index Finger Module of a Hand Exoskeleton for Post-Stroke Rehabilitation 

Wireless Electronic Glove Helps Improve Motor Skills of Spinal Cord Injury Victims

Stroke rehab hand exercises

5 exercises to improve hand mobility and reduce pain

Development of a haptic keypad for training finger individuation after stroke

Rome doctors use robotic glove, videogame on stroke patients

Hand dryer stroke rehab

OT Review of iPad App Dexteria for Fine Motor Skills

Hand Robotics Rehabilitation: Feasibility and Preliminary Results of a Robotic Treatment in Patients with Hemiparesis

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

Cable Actuated Exomusculature Glove for Stroke Rehabilitation and Assistance

Robo-Gloves to Aid Stroke Victims

Association of Activity Changes in the Primary Sensory Cortex With Successful Motor Rehabilitation of the Hand Following Stroke

Exoskeleton hand gives you robo-powered fingers

I have another 21 on fingers that you will need to look at also.

   And the latest here;

http://www.sciencedirect.com/science/article/pii/S2212017314001637

• Mohd Nor Azmi Ab Patar^{a, b, ,} ,
• Takashi Komeda^a,
• Cheng Yee Low^{b, c},
• Jamaluddin Mahmud^b

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DOI: 10.1016/j.protcy.2014.09.048

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Abstract

Stroke is a major cause of long-term disability among adults in many countries. Post stroke rehabilitation consumes a huge amount of health care resources in terms of costs related to hospital and home assistance. Recently, robot-assisted rehabilitation has been introduced to support physiotherapists in providing high-intensity and repetitive rehabilitation sessions. It has been observed that robotics offers an objective and reliable tool to monitor patient's progress and to accurately assess their motor function. This paper presents a novel finger rehabilitation approach for acute paralyzed stroke survivors using a wearable device for hand motor function restoration. After analyzing four main working mechanisms for hand assistance and rehabilitation, i.e. pneumatic cylinders, artificial rubber muscles, linkage mechanism and cable-driven mechanism, a new device called Pneumatic Actuated Finger Exoskeleton (PAFEx) has been designed. The prototype development was carried out in four stages involving simulation of the assisted structure of the MCP joint and the PIP joint, algorithm development, design and fabrication of prototype as well as product function evaluation. Offering ease of use and affordability, the device has great potential to be deployed for individualized rehabilitation session for patients who have to undergo therapy in their home.

Stroke rehabilitation in Fiji: are patients receiving services?

At least their country is trying to look out for survivors. I know in the US this followup isn't occurring.
http://www.ingentaconnect.com/content/iuatld/pha/2014/00000004/00000003/art00007?crawler=true&mimetype=application/pdf

Authors: Waloki, M.¹; Roseveare, C.²; Tikolevu, L.³; Ram, S.¹; Bissell, K.⁴

Source: Public Health Action, Volume 4, Number 3, 21 September 2014, pp. 150-154(5)
Publisher: International Union Against Tuberculosis and Lung Disease

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Abstract:

Setting: The national hospital and stroke rehabilitation services of the Fiji Ministry of Health.

Objective: To describe patients admitted with stroke to the Fiji Colonial War Memorial Hospital (CWMH) from January 2010 to December 2012, and to report on rehabilitation services accessed during and after admission.

Design: Retrospective descriptive study using patient records.

Result: Of the 328 patients admitted with stroke, 54% were male, 55% i-Taukei and 16% aged ?50 years; 75% had hypertension, 41% diabetes and 37% both; 23% (n = 76) died. Of the survivors, 58% (146) received rehabilitation therapy during admission at the CWMH. After discharge, 10% (n = 26) received therapy at the National Rehabilitation Hospital; six accessed the services of the community rehabilitation assistants. Just over half of stroke survivors (52%) remained in CWMH for <1 week (median stay 6 days, IQR 4-11).

Conclusion: The length of stay and access to rehabilitation was inadequate for over half of the stroke survivors. After discharge, very few accessed the available ehabilitation services of the Ministry of Health. It will be crucial to review procedures for tracking patient use of rehabilitation services and to explore why patients are not accessing these services, which are vital to recovery and restoration of function.

A proprioceptive neuromuscular facilitation integrated robotic ankle-foot system for post stroke rehabilitation

Your doctor and therapist are going to have to get the article and possibly contact the author in order to create a stroke protocol from this. Thousands of clinics and hospitals will need to do this. You will have to hope yours does it correctly. A much better option would be to contact that great stroke association and have them use their experts to do it once and distribute around the world.

Or does your clinic think what they are doing is already better than this?

http://www.sciencedirect.com/science/article/pii/S0921889014002085

• Zhihao Zhou^a,
• Yuan Zhou^b,
• Ninghua Wang^b,
• Fan Gao^c,
• Kunlin Wei^d,
• Qining Wang^{a, ,}

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DOI: 10.1016/j.robot.2014.09.023

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Highlights

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We developed a proprioceptive neuromuscular facilitation (PNF) integrated robotic ankle-foot system for post stroke rehabilitation.

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It is the first time that PNF method has been used in ankle spasticity/contracture rehabilitation.

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Five able-bodied subjects participated in the experiments and five stroke patients were recruited with a six-week PNF treatment.

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The proposed system can offer more effective treatment than passive stretching in improvement of both passive and active joint properties.

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Abstract

Ankle joint with spasticity and/or contracture can severely disable the mobility and the independence of stroke survivors. In this paper, we developed a proprioceptive neuromuscular facilitation (PNF) integrated robotic ankle-foot system for post stroke rehabilitation. The system consists of a robotic platform and a control system with graphic user interface. We employ five normal subjects to test the reliability and feasibility of the proposed system. To validate the effectiveness of the PNF integrated robotic system, we recruit five stroke patients and carry out a six-week PNF treatment. Treatment outcome was evaluated quantitatively in passive and active joint properties. The passive hysteresis loop shows that the maximum dorsiflexion angle increases from 32.9°±1.5°$32.9°\pm 1.5°$ to 42.0°±3.2°$42.0°\pm 3.2°$ (p=0.014$p=0.014$) while the resistance torque decreases from 45.6 Nm±5.8 Nm to 29.8 Nm±4.4 Nm (p=0.019$p=0.019$). The active joint properties are improved significantly with the training score increasing from 5.7±0.9$5.7\pm 0.9$ to 8.1±0.6$8.1\pm 0.6$, and getting close to that of normal subjects (9.5±0.3$9.5\pm 0.3$). In addition, muscle strength has a rising trend as time goes on. The results demonstrate that the proposed PNF integrated robotic ankle-foot rehabilitation system is effective in improving ankle spasticity and/or contracture and is a promising solution in clinical rehabilitation.

Sonification as a possible stroke rehabilitation strategy

The possibility of using auditory information supplementary to visual feedback in order to inform patients about movements of their impaired arms is a promising new method, referred to as “sonification”.  This is way too new and novel to get to your rehab center for another 100 years.

Sonification as a possible stroke rehabilitation strategy

Daniel S. Scholz1, Liming Wu1, Jonas Pirzer1, Johann Schneider1, Jens Rollnik2, Michael Großbach1,
Eckart Altenmüller1*
1 Institute of Music Physiology and Musicians' Medicine, University of Music, Drama and Media,
Hannover, Germany
2 BDH-Klinik, Hessisch Oldendorf, Germany
*Corresponding author:
Eckart Altenmüller,
University of Music, Drama and Media
Institute of Music Physiology and Musicians' Medicine
Emmichplatz 1
30175 Hannover
Germany
eckart.altenmueller@hmtm-hannover.de

Abstract
Despite cerebral stroke being one of the main causes of acquired impairments of motor skills
worldwide, well-established therapies to improve motor functions are sparse. Recently, attempts
have been made to improve gross motor rehabilitation by mapping patient movements to sound,
termed sonification. Sonification provides additional sensory input, supplementing impaired
proprioception. However, to date no established sonification-supported rehabilitation protocol
strategy exists.
In order to examine and validate the effectiveness of sonification in stroke rehabilitation, we
developed a computer program, termed “SonicPointer”: Participants' computer mouse movements
were sonified in real-time with complex tones. Tone characteristics were derived from an invisible
parameter mapping, overlaid on the computer screen. The parameters were: tone pitch and tone
brightness. One parameter varied along the x, the other along the y-axis. The order of parameter
assignment to axes was balanced in two blocks between subjects so that each participant performed
under both conditions. Subjects were naive to the overlaid parameter mapping and its change
between blocks. In each trial a target tone was presented and subjects were instructed to indicate its
origin with respect to the overlaid parameter mapping on the screen as quickly and accurately as
possible with a mouse click. Twenty-six elderly healthy participants were tested. Required time and
two-dimensional accuracy were recorded. Trial duration times and learning curves were derived.
We hypothesized that subjects performed in one of the two parameter-to-axis–mapping better,
indicating the most natural sonification.
Generally, subjects' localizing performance was better on the pitch axis as compared to the
brightness axis. Furthermore, the learning curves were steepest when pitch was mapped onto the
vertical and brightness onto the horizontal axis. This seems to be the optimal constellation for this
two-dimensional sonification.