Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 13% effective). I have 301 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/10/my-background-story.html

Sunday, May 19, 2013

'Distorteidolias' - Fantastic Perceptive Distortion. A New, Pure Dorsomedial Thalamic Syndrome

A type of thalmic stroke. You try explaining to the doctors that you aren't on drugs when you  talk about voices sounding like dinosaurs. Proves once again that an objective way of diagnosing stroke is required.
The abstract here:
http://www.ncbi.nlm.nih.gov/pubmed/23652461
The blogger discussing it here with a great picture:
http://blogs.discovermagazine.com/neuroskeptic/2013/05/19/fantastic-distortions-of-perception/#.UZjoPcoyv74
A 48-year-old woman woke up one morning without knowing where she was. She recognized her husband and finally realized that she was at home, but reported that she felt that all surroundings appeared ‘strange’ to her. She did not report any changes in the shape of furniture, rooms and people, but complained that voices and noises were ‘dinosaurs shouts’, or were made by ‘prehistorical beasts’…
After arriving at the hospital, she continued to complain that the surrounding sounds were made by dinosaurs, even adding that these were of the meat-eating type. She was not confused, she knew that she was in the hospital, and she reported the exact date.

I wonder what therapy protocol your doctor would prescribe to recover from this?

Saturday, May 18, 2013

Transcranial Direct-Current Stimulation - commercially available




I've only written 10 posts on the subject  No self-prescribing. Your doctor and therapists should have this at their clinic.
http://www.foc.us/
 tDCS Headset








This blogger deconstructs some of the problems with this.
NeuroBollocks Debunking pseudo-neuroscience so you don't have to

Long-term rehabilitation management of stroke: A review of the evidence

When the hell are stroke doctors going to realize that you have to intervene much earlier in the process to get decent recovery prospects. Like stopping the neuronal cascade of death. Less dead neurons would lead to a much better chance of recovery.
It's an incredibly simple cause and effect.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=R09216&phrase=no&rec=120923
NARIC Accession Number: R09216.  What's this?
ISSN: 1074-9357.
Author(s): Teasell, Robert W. (Ed.).
Publisher(s): Thomas Land Publishers, Inc., 255 Jefferson Road, St. Louis, MO 63119.
Publication Year: 2012.
Number of Pages: 109.
Abstract: Articles in this journal issue review the evidence on the effectiveness of treatments provided 6 months or more following the onset of stroke. Topics include: long-term rehabilitation management of stroke patients; cardiovascular conditioning for comfortable gait speed and total distance walked; resistance training for gait speed and total distance walked; systematic review of the effectiveness of pharmacological interventions in the treatment of spasticity of the hemiparetic lower extremity; functional electrical stimulation for improving gait; systematic review and meta-analysis of constraint-induced movement therapy in the hemiparetic upper extremity; evidence for therapeutic interventions for hemiplegic shoulder pain; therapeutic interventions for aphasia initiated more than six months post stroke; and effectiveness of psychological interventions in chronic stage of stroke. In addition, two feature article examine the: (1) relation between the upper extremity synergistic movement components and its implication for motor recovery in poststroke hemiparesis and (2) compelled body weight shift approach in rehabilitation of individuals with chronic stroke. Individual articles may be available for document delivery under accession numbers J65516 through J65526.

5 exercises to improve hand mobility and reduce pain

From an email from Harvard medical school. You know the drill, do nothing without your therapist or doctors ok.
----------------------------------------------------------------------------------
Below you will find five commonly recommended exercises for hand and wrist problems. However, if your hand condition is painful or debilitating, it’s best to get exercise advice from a physical therapist. All exercises should be done slowly and deliberately, to avoid pain and injury. If you feel numbness or pain during or after exercising, stop and contact your doctor.
Range-of-motion exercises
Your muscles and tendons move the joints through arcs of motion, as when you bend and straighten your fingers. If your normal range of motion is impaired — if you can’t bend your thumb without pain, for example you may have trouble doing ordinary things like opening a jar. These exercises move your wrist and fingers through their normal ranges of motion and require all the hand’s tendons to perform their specific functions. Hold each position for 5–10 seconds. Do one set of 10 repetitions, three times a day.
Wrist extension and flexion
• Place your forearm on a table on a rolled-up towel for padding with your hand hanging off the edge of the table, palm down.
• Move the hand upward until you feel a gentle stretch.
• Return to the starting position.
• Repeat the same motions with the elbow bent at your side, palm facing up.
Wrist supination/pronation
• Stand or sit with your arm at your side with the elbow bent to 90 degrees, palm facing down.
• Rotate your forearm, so that your palm faces up and then down.
Wrist ulnar/radial deviation
• Support your forearm on a table on a rolled-up towel for padding or on your knee, thumb upward.
• Move the wrist up and down through its full range of motion.
Thumb flexion/extension

• Begin with your thumb positioned outward.
• Move the thumb across the palm and back to the starting position.
Hand/finger tendon glide
• Start with the fingers extended straight out.
• Make a hook fist; return to a straight hand.
• Make a full fist; return to a straight hand.
• Make a straight fist; return to a straight hand.
For more information on the causes and treatment of hand pain, and strengthening strategies for hands, buy Hands: Strategies for Strong, Pain-Free Hands from Harvard Medical School.

Family’s fury at ambulance response time - Sherburn-in-Elmet, UK

The fury is actually misplaced, it should be directed at the adverts that suggest that strokes can be completely reversed if you get to the hospital in time.  See tPA efficacy is appalling, I don't know about bleeds.
http://www.goolecourier.co.uk/news/local-news/family-s-fury-at-ambulance-response-time-1-5674609
Relatives have spoken of their ‘disgust’ after paramedics took nearly two hours to transport a pensioner who had suffered a stroke to hospital.
Basil Lund, 73, suffered the emergency while cleaning in his home, but two ambulances had to be called before he was taken to hospital.
His wife June was out shopping when he collapsed, and it was only through luck that a passing postman noticed the pensioner on the floor.
The postman rang for an ambulance at approximately 12.30pm but it was 1.10pm before the first crew arrived at Mr Lund’s home in Springfield Road, Sherburn-in-Elmet.
His niece Anne-Marie Barraclough said: “The first crew came from Pontefract but when they arrived didn’t seem to care at all. It was really upsetting and I was so shocked.
“They couldn’t get him away because the tail lift had jammed. It was disgusting just to leave him lying there all that time.”
A second crew was called, but it did not arrive until 2.20pm.
Anne-Marie’s husband Paul, who was alerted to the situation by Mr Lund’s brother Pete, who said the second crew was unable to locate the address.
He said: “The paramedics took an age to find the house.
“They said there was something wrong with the sat nav and that they had come from Dewsbury.
It was worrying because I’ve seen the TV adverts which say the longer someone is on the floor the more damage it does to them.”
Mr Lund is still in hospital and has been able to utter only a few words since his stroke on May 2.
David Williams, deputy director of operations for Yorkshire Ambulance Service NHS Trust apologised to Mr Lund’s family for ‘the distress caused.’
He added: “Representatives from the trust have been speaking to the family directly about their concerns and are looking into these on their behalf.”
“I would like to reassure members of the public that providing high quality and responsive services to patients across Yorkshire is our utmost priority.”

Seminar on stroke prevention, rehabilitation - Redding, CA

Be prepared and ask tons of questions, they really know nothing concrete about stroke rehab. You have to prove that to them before they might realize that they need to educate themselves. Everything I've written about they should know intimately.
http://www.redbluffdailynews.com/news/ci_23273734/seminar-stroke-prevention-rehabilitation
May is Stroke Awareness Month, and Shasta Regional Medical Center is hosting a free community health seminar on Stroke Prevention and Rehabilitation with Dr. Atkinson, Neurologist and director of Neurology at Sutter Health, and Dr. Rabiee, Neurologist and director of Shasta Regional's Stroke Program, 6:30-7:30 p.m. Thursday, May 23 in Shasta Regional's Liberty Room 2, 1100 Butte St. in Redding.



Trained medical staff will provide a risk assessment along with providing educational information.

When a person is having a stroke, time wasted means more damage to the brain. Shasta Regional's Stroke Team is available 24/7 and is dedicated to rapid diagnosis and fast-track treatment. Shasta Regional was recognized as the first designated Primary Stroke Center in the North State.

Space is limited, and reservations are recommended. RSVP to 244-5454. Refreshments will be served.  

--------------------------------------------------------------------------------
Questions from these posts will stump them.
You need to go and demand to know why tPA barely works.
Can you get to a 307% reduction in stroke risk and what does that mean?
1. What percentage of patients fully recover?
2. Why is it so low?
3. Are you using hypothermia?
4. What are you doing to stop the neuronal cascade of death in the first week?
5. Why aren't you doing anything?
6. Nothing is available is not a valid answer.
Lots of other questions in here.

http://oc1dean.blogspot.com/2013/03/stroke-risk-reduction-ideas.html
http://oc1dean.blogspot.com/2010/08/what-my-doctor-should-have-told-me.html
 http://www.oc1dean.blogspot.com/2011/02/marijuana-and-stroke-rehab.html
http://oc1dean.blogspot.com/2013/03/what-i-am-going-to-insist-i-get-after.html
http://oc1dean.blogspot.com/2010/09/stroke-research-questions.html
If he sticks to prevention ask him from this list.
http://oc1dean.blogspot.com/2013/03/stroke-risk-reduction-ideas.html
Then ask why he didn't mention marijuana buds.  
 

Mayo stroke awareness discussion - St. James, MN

Be prepared and ask tons of questions, they really know nothing concrete about stroke rehab. You have to prove that to them before they might realize that they need to educate themselves. Everything I've written about they should know intimately.
 http://www.stjamesnews.com/article/20130518/NEWS/130519677?refresh=true
Stroke is a leading cause of death in Minnesota. According to the Centers for Disease Control and Prevention (CDC), one American dies every four minutes from stroke. Understanding the causes and symptoms of stroke is paramount when it comes to prevention and effective treatment.
To help educate community members about stroke, Mayo Clinic Health System in St. James is offering a free stroke awareness presentation on Thursday, May 23 at 5:30 p.m. in the medical center’s conference center.
The event features speakers Jennifer Langbehn, D.O., Mayo Clinic Health System family physician, and Shayna Baker, Mayo Clinic Health System speech/language pathologist.
Dr. Langbehn and Baker will discuss symptoms of stroke, prevention, treatments and share information about a new telestroke service that is coming soon to the medical center. The event will also serve as a kickoff for a potential St. James area stroke support group.
“As we know, stroke is a serious health concern in our community, as well as our country,” says Dr. Langbehn. “The good news is that further education, access to quality medical care and healthy lifestyle choices can help decrease the impact of stroke. We intend to convey that message throughout our presentation.”
There is no cost to attend the event, and snacks, refreshments and giveaways will be available. For more information, please call Mayo Clinic Health System in St. James at 507-375-8602.
-------------------------------------------------------------------------------------
Questions from these posts will stump them.
You need to go and demand to know why tPA barely works.
Can you get to a 307% reduction in stroke risk and what does that mean?
1. What percentage of patients fully recover?
2. Why is it so low?
3. Are you using hypothermia?
4. What are you doing to stop the neuronal cascade of death in the first week.
5. Why aren't you doing anything?
6. Nothing is available is not a valid answer.
Lots of other questions in here.

http://oc1dean.blogspot.com/2013/03/stroke-risk-reduction-ideas.html
http://oc1dean.blogspot.com/2010/08/what-my-doctor-should-have-told-me.html
 http://www.oc1dean.blogspot.com/2011/02/marijuana-and-stroke-rehab.html
http://oc1dean.blogspot.com/2013/03/what-i-am-going-to-insist-i-get-after.html
http://oc1dean.blogspot.com/2010/09/stroke-research-questions.html
If he sticks to prevention ask him from this list.
http://oc1dean.blogspot.com/2013/03/stroke-risk-reduction-ideas.html
Then ask why he didn't mention marijuana buds.  

Friday, May 17, 2013

Need a hand? Wearable robot arms give you two

See what your doctor and therapists are doing to make this a possibility for survivors.
http://www.newscientist.com/article/mg21628885.800-need-a-hand-wearable-robot-arms-give-you-two.html
IF YOU fancy an extra pair of hands, why not take a leaf out of Dr Octopus's book? A pair of intelligent arms should make almost any job a lot easier.
The semi-autonomous arms extend out in front of the body from the hips and are strapped to a backpack-like harness that holds the control circuitry. The prototype is the handiwork of Federico Parietti and Harry Asada of the Massachusetts Institute of Technology, who suggest that one of the first uses could be to help factory workers, or those with tricky DIY tasks to perform.
"It's the first time I've seen robot arms designed to augment human abilities. It's bold and out of keeping with anything I've ever seen to attach two arms to a human," says Dave Barrett, a roboticist and mechanical engineer at Olin College in Needham, Massachusetts.
So how are the arms controlled? Parietti and Asada designed the limbs to learn and hopefully anticipate what their wearer wants. The idea is that the algorithms in charge of the limbs would first be trained to perform specific tasks.

Rest at the link.

“Never give in — never, never, never, never, in nothing great or small, large or petty, never give in.”

Winston Churchill graduation speech. He didn't actually say these words
This is our most frequent quote request. The speech was made 29 October 1941 to the boys at Harrow School. " Never, never, in nothing great or small, large or petty, never give in except to convictions of honour and good sense. Never yield to force; never yield to the apparently overwhelming might of the enemy.'' The full speech is contained in "The Unrelenting Struggle" (London:Cassell and Boston:Little Brown 1942, and is found on pages 274-76 of the English edition). It may also be found in "The Complete Speeches of Winston S. Churchill," edited by Robert Rhodes James (NY:Bowker and London:Chelsea House 1974).
The voiceover here:
http://www.youtube.com/watch?v=r36wikH36JM
The actual words here:
http://www.school-for-champions.com/speeches/churchill_never_give_in.htm

We have to follow this if we expect to get close as possible to our recovery.

SUMO wrestling cells reveal new protective mechanism target for stroke

A great name for a brain protein.
http://medicalxpress.com/news/2013-05-sumo-cells-reveal-mechanism.html
The discovery, made by researchers from the University's School of Biochemistry and published in the EMBO journal with additional comment in Nature Reviews, could eventually lead to new therapies for stroke and other brain diseases. The research builds on earlier work by the team which identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain. The team's latest work has now identified the key role that SUMO plays in promoting cell survival. During cell stress a protein response triggers a protective mechanism that allows cell adaptation and survival. This process, known as SUMOylation, involves the attachment of a small protein called Small Ubiquitin-related Modifier (SUMO) to target proteins. This pathway is essential for survival of all plant and animal cells because it regulates how proteins interact with each other and can protect nerve cells against damage. The findings have shown that SUMOylation of a protein called dynamin-related protein 1 (Drp1) is particularly important because it controls the release of chemical signals from mitochondria that instruct the cell to die in a process called apoptosis. SUMOylation of Drp1 reduces mitochondrial release of these 'death' signals and helps nerve cells survive toxic insults associated with stroke. In the future, finding effective methods to enhance SUMOylation of Drp1 may also be beneficial for cell survival in other diseases including heart attacks and Alzheimer's disease. The European Research Council-funded study, entitled 'SENP3-mediated deSUMOylation of dynamin-related protein 1 promotes cell death following ischaemia' published in the EMBO Journal and led by Professor Jeremy Henley from the University's School of Biochemistry. More information: doi:10.1038/emboj.2013.65 Journal reference: EMBO Journal search and more info website Provided by University of Bristol search and more info website

Read more at: http://medicalxpress.com/news/2013-05-sumo-cells-reveal-mechanism.html#jCp
 The discovery, made by researchers from the University's School of Biochemistry and published in the EMBO journal with additional comment in Nature Reviews, could eventually lead to new therapies for stroke and other brain diseases. The research builds on earlier work by the team which identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain. The team's latest work has now identified the key role that SUMO plays in promoting cell survival. During cell stress a protein response triggers a protective mechanism that allows cell adaptation and survival. This process, known as SUMOylation, involves the attachment of a small protein called Small Ubiquitin-related Modifier (SUMO) to target proteins. This pathway is essential for survival of all plant and animal cells because it regulates how proteins interact with each other and can protect nerve cells against damage. The findings have shown that SUMOylation of a protein called dynamin-related protein 1 (Drp1) is particularly important because it controls the release of chemical signals from mitochondria that instruct the cell to die in a process called apoptosis. SUMOylation of Drp1 reduces mitochondrial release of these 'death' signals and helps nerve cells survive toxic insults associated with stroke. In the future, finding effective methods to enhance SUMOylation of Drp1 may also be beneficial for cell survival in other diseases including heart attacks and Alzheimer's disease. The European Research Council-funded study, entitled 'SENP3-mediated deSUMOylation of dynamin-related protein 1 promotes cell death following ischaemia' published in the EMBO Journal and led by Professor Jeremy Henley from the University's School of Biochemistry. More information: doi:10.1038/emboj.2013.65 Journal reference: EMBO Journal search and more info website Provided by University of Bristol search and more info website

Read more at: http://medicalxpress.com/news/2013-05-sumo-cells-reveal-mechanism.html#jCp
The discovery, made by researchers from the University's School of Biochemistry and published in the EMBO journal with additional comment in Nature Reviews, could eventually lead to new therapies for stroke and other brain diseases. The research builds on earlier work by the team which identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain. The team's latest work has now identified the key role that SUMO plays in promoting cell survival. During cell stress a protein response triggers a protective mechanism that allows cell adaptation and survival. This process, known as SUMOylation, involves the attachment of a small protein called Small Ubiquitin-related Modifier (SUMO) to target proteins. This pathway is essential for survival of all plant and animal cells because it regulates how proteins interact with each other and can protect nerve cells against damage. The findings have shown that SUMOylation of a protein called dynamin-related protein 1 (Drp1) is particularly important because it controls the release of chemical signals from mitochondria that instruct the cell to die in a process called apoptosis. SUMOylation of Drp1 reduces mitochondrial release of these 'death' signals and helps nerve cells survive toxic insults associated with stroke. In the future, finding effective methods to enhance SUMOylation of Drp1 may also be beneficial for cell survival in other diseases including heart attacks and Alzheimer's disease. The European Research Council-funded study, entitled 'SENP3-mediated deSUMOylation of dynamin-related protein 1 promotes cell death following ischaemia' published in the EMBO Journal and led by Professor Jeremy Henley from the University's School of Biochemistry. More information: doi:10.1038/emboj.2013.65 Journal reference: EMBO Journal

Read more at: http://medicalxpress.com/news/2013-05-sumo-cells-reveal-mechanism.html#jCp
The discovery, made by researchers from the University's School of Biochemistry and published in the EMBO journal with additional comment in Nature Reviews, could eventually lead to new therapies for stroke and other brain diseases. The research builds on earlier work by the team which identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain. The team's latest work has now identified the key role that SUMO plays in promoting cell survival. During cell stress a protein response triggers a protective mechanism that allows cell adaptation and survival. This process, known as SUMOylation, involves the attachment of a small protein called Small Ubiquitin-related Modifier (SUMO) to target proteins. This pathway is essential for survival of all plant and animal cells because it regulates how proteins interact with each other and can protect nerve cells against damage. The findings have shown that SUMOylation of a protein called dynamin-related protein 1 (Drp1) is particularly important because it controls the release of chemical signals from mitochondria that instruct the cell to die in a process called apoptosis. SUMOylation of Drp1 reduces mitochondrial release of these 'death' signals and helps nerve cells survive toxic insults associated with stroke. In the future, finding effective methods to enhance SUMOylation of Drp1 may also be beneficial for cell survival in other diseases including heart attacks and Alzheimer's disease. The European Research Council-funded study, entitled 'SENP3-mediated deSUMOylation of dynamin-related protein 1 promotes cell death following ischaemia' published in the EMBO Journal and led by Professor Jeremy Henley from the University's School of Biochemistry. More information: doi:10.1038/emboj.2013.65 Journal reference: EMBO Journal

Read more at: http://medicalxpress.com/news/2013-05-sumo-cells-reveal-mechanism.html#jCp
The discovery, made by researchers from the University's School of Biochemistry and published in the EMBO journal with additional comment in Nature Reviews, could eventually lead to new therapies for stroke and other brain diseases. The research builds on earlier work by the team which identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain. The team's latest work has now identified the key role that SUMO plays in promoting cell survival. During cell stress a protein response triggers a protective mechanism that allows cell adaptation and survival. This process, known as SUMOylation, involves the attachment of a small protein called Small Ubiquitin-related Modifier (SUMO) to target proteins. This pathway is essential for survival of all plant and animal cells because it regulates how proteins interact with each other and can protect nerve cells against damage. The findings have shown that SUMOylation of a protein called dynamin-related protein 1 (Drp1) is particularly important because it controls the release of chemical signals from mitochondria that instruct the cell to die in a process called apoptosis. SUMOylation of Drp1 reduces mitochondrial release of these 'death' signals and helps nerve cells survive toxic insults associated with stroke. In the future, finding effective methods to enhance SUMOylation of Drp1 may also be beneficial for cell survival in other diseases including heart attacks and Alzheimer's disease. The European Research Council-funded study, entitled 'SENP3-mediated deSUMOylation of dynamin-related protein 1 promotes cell death following ischaemia' published in the EMBO Journal and led by Professor Jeremy Henley from the University's School of Biochemistry. More information: doi:10.1038/emboj.2013.65 Journal reference: EMBO Journal search and more info website Provided by University of Bristol search and more info website

Read more at: http://medicalxpress.com/news/2013-05-sumo-cells-reveal-mechanism.html#jCp
The discovery, made by researchers from the University's School of Biochemistry and published in the EMBO journal with additional comment in Nature Reviews, could eventually lead to new therapies for stroke and other brain diseases. The research builds on earlier work by the team which identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain. The team's latest work has now identified the key role that SUMO plays in promoting cell survival. During cell stress a protein response triggers a protective mechanism that allows cell adaptation and survival. This process, known as SUMOylation, involves the attachment of a small protein called Small Ubiquitin-related Modifier (SUMO) to target proteins. This pathway is essential for survival of all plant and animal cells because it regulates how proteins interact with each other and can protect nerve cells against damage. The findings have shown that SUMOylation of a protein called dynamin-related protein 1 (Drp1) is particularly important because it controls the release of chemical signals from mitochondria that instruct the cell to die in a process called apoptosis. SUMOylation of Drp1 reduces mitochondrial release of these 'death' signals and helps nerve cells survive toxic insults associated with stroke. In the future, finding effective methods to enhance SUMOylation of Drp1 may also be beneficial for cell survival in other diseases including heart attacks and Alzheimer's disease. The European Research Council-funded study, entitled 'SENP3-mediated deSUMOylation of dynamin-related protein 1 promotes cell death following ischaemia' published in the EMBO Journal and led by Professor Jeremy Henley from the University's School of Biochemistry. More information: doi:10.1038/emboj.2013.65 Journal reference: EMBO Journal search and more info website Provided by University of Bristol search and more info website

Read more at: http://medicalxpress.com/news/2013-05-sumo-cells-reveal-mechanism.html#jCp
The discovery, made by researchers from the University's School of Biochemistry and published in the EMBO journal with additional comment in Nature Reviews, could eventually lead to new therapies for stroke and other brain diseases. The research builds on earlier work by the team which identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain. The team's latest work has now identified the key role that SUMO plays in promoting cell survival. During cell stress a protein response triggers a protective mechanism that allows cell adaptation and survival. This process, known as SUMOylation, involves the attachment of a small protein called Small Ubiquitin-related Modifier (SUMO) to target proteins. This pathway is essential for survival of all plant and animal cells because it regulates how proteins interact with each other and can protect nerve cells against damage. The findings have shown that SUMOylation of a protein called dynamin-related protein 1 (Drp1) is particularly important because it controls the release of chemical signals from mitochondria that instruct the cell to die in a process called apoptosis. SUMOylation of Drp1 reduces mitochondrial release of these 'death' signals and helps nerve cells survive toxic insults associated with stroke. In the future, finding effective methods to enhance SUMOylation of Drp1 may also be beneficial for cell survival in other diseases including heart attacks and Alzheimer's disease. The European Research Council-funded study, entitled 'SENP3-mediated deSUMOylation of dynamin-related protein 1 promotes cell death following ischaemia' published in the EMBO Journal and led by Professor Jeremy Henley from the University's School of Biochemistry. More information: doi:10.1038/emboj.2013.65 Journal reference: EMBO Journal search and more info website Provided by University of Bristol search and more info website

Read more at: http://medicalxpress.com/news/2013-05-sumo-cells-reveal-mechanism.html#jCp

Effectiveness of psychological interventions in chronic stage of stroke: A systematic review

There is really no intervention that  would help me right now unless it is a physical improvement.
But you might be different.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J65524&phrase=no&rec=120920
NARIC Accession Number: J65524.  What's this?
ISSN: 1074-9357.
Author(s): Mehta, Swati; Pereira, Shelialah; Janzen, Shannon; McIntyre, Amanda; McClure, Andrew; Teasell, Robert W..
Publication Year: 2012.
Number of Pages: 9.
Abstract: Study examined the effectiveness of interventions for psychological issues faced by individuals post stroke when initiated in the chronic stage of stroke. MEDLINE, CINAHL, EMBASE, and Scopus databases were searched for relevant randomized controlled trials (RCTs). Similar interventions were grouped and results summarized. Data on the study design, participant characteristics, interventions, outcomes, and adverse events were extracted from each of the selected studies. Nine RCTs met the inclusion criteria. All 9 studies examined effectiveness on mood and 3 on adjustment. Repetitive transcranial magnetic stimulation had the strongest evidence of effectiveness in improving mood followed by pharmacotherapy. Exercise appeared to be effective in improving adjustment and coping among individuals in the chronic stage of stroke. Overall, interventions provided in the chronic stage of stroke appear to be effective in improving mood and adjustment up to 3 months after intervention. The use of multidisciplinary interventions and acceptance models may be important in the overall adjustment process.
Descriptor Terms: CHRONIC ILLNESS, INTERVENTION, LITERATURE REVIEWS, OUTCOMES, PSYCHOLOGICAL ASPECTS, STROKE.

Can this document be ordered through NARIC's document delivery service?: Y.

Gender, health ambiguity, and depression among survivors of first stroke: A pilot study

It proves my point that with no damage diagnosis and no idea of how well you will recover you are likely to be depressed.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J65474&phrase=no&rec=120783
NARIC Accession Number: J65474.  What's this?
ISSN: 0003-9993.
Author(s): McCarthy, Michael J.; Lyons, Karen S.; Powers, Laurie E.; Bauer, Elizabeth A..
Publication Year: 2013.
Number of Pages: 3.
Abstract: Study investigated the relationship between health ambiguity and depressive symptoms among stroke survivors and whether survivor gender moderates this association. Thirty-six survivors of first stroke were recruited through provider referral, support groups, and print and Web-based sources. Participants completed questionnaires via face-to-face interviews. Health ambiguity was measured with the ambiguity subscale of the Mishel Uncertainty in Illness Scale. Depressive symptoms were measured by the Patient Health Questionnaire-9. Paired samples t tests were used to examine differences between male and female survivors on key variables. Ordinary least squares regression was used to examine main and interaction effects of ambiguity and gender on depressive symptoms. A simple slopes test was used to examine the interaction effect. Health ambiguity, gender, and the interaction of the 2 variables were significantly associated with depressive symptoms. Simple slopes tests indicated that the association between health ambiguity and depressive symptoms was stronger for male versus female survivors. This study indicated that gender and health ambiguity impact survivor depressive symptoms, independently and in conjunction with one another. Further research with larger samples and more comprehensive statistical models is needed to confirm these findings.
Descriptor Terms: DEPRESSION, FEMALES, FUNCTIONAL STATUS, MALES, OUTCOMES, SELF CONCEPT, STROKE.

Can this document be ordered through NARIC's document delivery service?: Y.

Constraint-induced movement therapy combined with conventional neurorehabilitation techniques in chronic stroke patients with plegic hands: A case series

So maybe there is hope for my hand after all. Although they only mention the arm improving.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J65463&phrase=no&rec=120772
NARIC Accession Number: J65463.  What's this?
ISSN: 0003-9993.
Author(s): Taub, Edward; Uswatte, Gitendra; Bowman, Mary H.; Mark, Victor W.; Delgado, Adriana; Bryson, Camille; Morris, David; Bishop-McKay, Staci.
Project Number: H133G050222.
Publication Year: 2013.
Number of Pages: 9.
Abstract: Study investigated whether the combination of constraint-induced movement therapy (CIMT) and conventional rehabilitation techniques can produce meaningful motor improvement in chronic stroke patients with initially fisted hands. Six patients who were more than 1 year poststroke with plegic hands participated in the study. Treatment consisted of an initial period of 3 weeks (phase A) when adaptive equipment in the home, orthotics, and splints were employed to improve ability to engage in activities of daily living. This was continued in phase B, when CIMT and selected neurodevelopmental treatment techniques were added. Outcome measures included the Motor Activity Log (MAL), accelerometry, and the Fugl-Meyer Motor Assessment (FMA). Patients exhibited a large improvement in spontaneous real-world use of the more-affected arm (mean lower-functioning MAL change = 1.3 points) and a similar pattern of increase in an objective measure of real-world more-affected arm movement (mean change in ratio of more- to less-affected arm accelerometer recordings = 0.12 points). A large improvement in motor status was also recorded (mean FMA change = 5.3 points). The findings suggest that stroke patients with plegic hands can benefit from CIMT combined with some conventional rehabilitation techniques, even long after brain injury.
Descriptor Terms: BODY MOVEMENT, LIMBS, MOTOR SKILLS, PARALYSIS, PHYSICAL THERAPY, STROKE.

Can this document be ordered through NARIC's document delivery service?: Y.

Effects on decreasing upper-limb poststroke muscle tone using transcranial direct current stimulation: A randomized sham-controlled study

I hate my bicep and lat spasticity.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J65451&phrase=no&rec=120760
NARIC Accession Number: J65451.  What's this?
ISSN: 0003-9993.
Author(s): Wu, Dongyu; Qian, Long; Zorowitz, Richard D.; Zhang, Lei; Qu, Yaping; Yuan, Ying.
Publication Year: 2013.
Number of Pages: 8.
Abstract: Study assessed the efficacy of transcranial direct current stimulation (tDCS) on decreasing upper-limb (UL) muscle tone after stroke. Ninety inpatients with poststroke UL spasticity were randomized into the tDCS group or the control group. The tDCS group received tDCS to the primary sensorimotor cortex of the affected side with cathodal stimulation, 20 minutes per day, 5 days per week, for 4 weeks and conventional physical therapy. The control group received sham stimulation (same area as the tDCS group) and conventional physical therapy. Outcome measures included the Modified Ashworth scale (MAS), Fugl-Meyer Assessment of motor recovery, and Barthel Index. All outcomes were measured at admission, at the end of the 4-week treatment, and at a 4-week follow-up. A clinically important difference (CID) was defined as a reduction of 1 or more in the MAS score. Compared with the sham tDCS group, UL muscle tone was significantly decreased and UL motor function and activities of daily living (ADL) assessment significantly improved in the active tDCS group after treatment and at follow-up. For the active tDCS group, MAS scores of elbow and wrist significantly decreased after tDCS and kept decreasing at follow-up. For the sham tDCS group, MAS scores almost kept unchanged after tDCS and increased significantly at follow-up. UL muscle tone after stroke can be decreased using cathodal tDCS. Combined with conventional physical therapy, tDCS appears to improve motor function and ADL. Cathodal tDCS over ipsilesional primary sensorimotor cortex may inhibit primary sensorimotor cortex hyperactivation, resulting in significant reductions in muscle tone.
Descriptor Terms: BRAIN, ELECTRICAL STIMULATION, LIMBS, MUSCLES, PHYSICAL THERAPY, SPASTICITY, STROKE.

Can this document be ordered through NARIC's document delivery service?: Y.

Naming practice for people with aphasia in a mobile web application: Early user experience

Have at it.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=O18808&phrase=no&rec=120927
NARIC Accession Number: O18808.  What's this?
Author(s): Hagood, Khalyle; Moore, Terrance; Pierre, Tiffany; Messamer, Paula; Ramsberger, Gail; Lewis, Clayton.
Project Number: H133E090003.
Publication Year: 2010.
Number of Pages: 2.
Abstract: Article describes Bangaten, a new version of Banga, a smart phone application that uses computer-presented images to support naming (word finding) practice, a form of therapy for people with aphasia. Banga combines delivery on easily portable smart phone devices with remote management, allowing a therapist to monitor a patient’s practice, and change the materials on a patient’s device, without requiring office visits. Early user experience shows that Bangaten offers useful cross-platform operation, on both Android and iPhone devices, including remote management of a client's device. Bangaten demonstrates the growing usefulness of emerging HTML5 technology for implementing assistive technology applications, while also illustrating some remaining limitations.

Corticospinal responses of quadriceps are abnormally coupled with hip adductors in chronic stroke survivors

So ask your therapist what therapy protocol will correct that problem. You do expect them to know how to fix it, don't you? Sounds right up your alley Amy. And I know I'm being a bastard. I expect a lot from myself and even more from my medical team.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J65578&phrase=no&rec=120874

NARIC Accession Number: J65578.  What's this?
ISSN: 0014-4886.
Author(s): Krishnan, Chandramouli; Dhaher, Yasin.
Project Number: H133E070013.
Publication Year: 2012.
Number of Pages: 8.
Abstract: Study investigated whether the neural substrates mediating abnormal activation patterns after stroke are of cortical origin. Eight chronic stroke survivors, seven able-bodied young control subjects and four older adults participated in this research study. Data from older adults were used to evaluate whether aging contributes to abnormal coupling of the corticospinal responses. A novel transcranialmagnetic stimulation (TMS) protocol was developed to evaluate the extent of abnormal across-joint coupling of corticospinal responses in chronic stroke survivors. It was hypothesized that the stroke subjects would demonstrate abnormal higher corticospinal responses of the quadriceps muscle group during an isometric hip adduction task. TMS-elicited motor evoked potentials (MEPs) were recorded from the paretic leg of the stroke survivors and from the dominant leg of the control subjects using surface electromyography. Results indicated that, in stroke survivors, the magnitudes of MEPs of the vastus lateralis and vastus medialis during isometric hip adduction were significantly higher than those recorded during knee extension at similar background activity. Furthermore, MEP coupling ratios of the quadriceps muscles were significantly different than those observed in healthy controls. No significant differences in MEP coupling ratios were observed between the younger and older adults. These findings provide evidence for the first time that stroke subjects exhibit abnormal excitability of the quadricepsmuscle corticospinal neurons when performing isometric hip adduction. Importantly, the abnormal corticospinal responses observed in stroke subjects were not mediated by aging.

Development of a haptic keypad for training finger individuation after stroke

Every clinic and hospital dealing with stroke should have this available in the next month.  What is your clinics excuse?  Finger/hand use is the biggest problem for lots of patients. I have no individual use of any finger.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=O18774&phrase=no&rec=120843
NARIC Accession Number: O18774.  What's this? Download article in Full Text .
Author(s): Lord, Thomas J.; Keefe, Diana M.; Li, Yu; Stoykov, Nikolay; Kamper, Derek.
Project Number: H133E070013.
Publication Year: 2011.
Number of Pages: 2.
Abstract: This paper presents a low-cost virtual-reality environment for training finger individuation in stroke survivors with chronic hand impairment. Users play an ergonomic 5-key virtual piano while receiving either assistance or resistance from a pneumatically actuated glove. The level of assistance and the difficulty of the task can be modulated by a therapist.

Overground walking speed changes when subjected to body weight support conditions for nonimpaired and post stroke individuals

When I used the Lite-Gait, the lack of weight caused my gait to get noticeably worse because my spasticity then had full rein to express itself. And it expressed itself very badly. The  Lokomat worked because the legs were strapped down and the spasticity couldn't take over.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J65577&phrase=no&rec=120873
NARIC Accession Number: J65577.  What's this?
ISSN: 1743-0003.
Author(s): Burgess, Jamie K.; Weibel, Gwendolyn C.; Brown, David A..
Project Number: H133E070013.
Publication Year: 2010.
Number of Pages: 10.
Abstract: Study examined changes in self-selected walking speed in non-impaired subjects and individuals who had suffered a stroke when subjected to body weight support (BWS). Eleven non-impaired subjects and 12 post-stroke subjects walked at a self-selected speed over a 15-meter walkway. BWS was provided to participants at 0, 10, 20, 30, and 40 percent of the subject's weight while they walked overground using a robotic gait and balance training system. Gait speed, cadence, and average step length were calculated for each subject using recorded data on their time to walk 10 meters and the number of steps taken. Results indicated that when subjected to greater levels of BWS, self-selected walking speed decreased for the non-impaired subjects. However, post-stroke subjects showed an average increase of 17 percent in self-selected walking speed when subjected to some level of BWS compared to the 0-percent BWS condition. Most subjects showed this increase at the 10-percent BWS level. Gait speed increases corresponded to an increase in step length, but not cadence.

Systematic review of the effectiveness of pharmacological interventions in the treatment of spasticity of the hemiparetic lower extremity more than six months post stroke

Demand your doctor get this and let you read it. I bet nothing has worked for your spasticity yet so you better find out if anything works. The abstract looks pretty hopeless.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J65519&phrase=no&rec=120915
NARIC Accession Number: J65519.  What's this?
ISSN: 1074-9357.
Author(s): McIntyre, Amanda; Lee, Taeweon; Janzen, Shannon; Mays, Rachel; Mehta, Swati; Teasell, Robert.
Publication Year: 2012.
Number of Pages: 12.
Abstract: Study examined the effectiveness of pharmacological interventions in reducing spasticity of the lower limb in chronic stroke survivors. PubMed, CINAHL, and EMBASE were searched for randomized controlled trials (RCTs) in which patients who were at least 6 months post stroke received a pharmacological intervention aimed at treating lower-limb spasticity. Methodological quality of each study was assessed using the Physiotherapy Evidence Database (PEDro) tool. Nine RCTs (PEDro scores, 4 to 9) met the inclusion criteria and included a pooled sample size of 605 individuals with a mean age of 54.8 years. Four RCTs provided evidence that botulinum toxin type A was effective in reducing spasticity compared to participants receiving placebo or a phenol neurolytic. One study provided evidence that both alcohol and phenol neurolytics were effective in reducing spasticity. Finally, 4 studies provided evidence that oral and intrathecal medications were effective in reducing lower-limb spasticity compared to placebo. Findings indicated that pharmacological treatment initiated 6 months post stroke reduced lower-limb spasticity. Relevant areas of exploration for future research could include the period of effectiveness, long-term complications, and a cost-benefit analysis of such treatments.

An evidence-based review of cognitive rehabilitation in medical conditions affecting cognitive function

I would think that cognition would be the first thing worked on after stroke but thats just me.
Your doctor may think that should be the last because you wouldn't want anybody questioning the medical protocols that don't exist for stroke.
http://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J65493&phrase=no&rec=120804
NARIC Accession Number: J65493.  What's this?
ISSN: 0003-9993.
Author(s): Langenbahn, Donna M.; Ashman, Teresa; Cantor, Joshua; Trott, Charlotte.
Publication Year: 2013.
Number of Pages: 16.
Abstract: This review examined evidence for the efficacy of cognitive rehabilitation in individuals diagnosed with medical conditions known to affect cognitive function, and formulated evidence-based recommendations for clinical practice based on that evidence. Ovid Medline and PubMed databases were searched using the terms cognition, cognitive, crossed with the terms rehabilitation, remediation, retraining, training, crossed with 11 medical diagnostic categories. Articles through December 2008 were accessed, resulting in 2,284 abstracts. A total of 211 articles were selected from the initial abstract review. These articles were then assessed by committee members using 9 exclusion and 3 inclusion criteria. A total of 34 remaining articles were submitted to full review. Articles were reviewed under diagnostic categories using specific criteria recorded on structured data sheets. Classification was performed according to guidelines of the American Academy of Neurology, with agreement between 2 committee members necessary for final decisions. Of the 34 studies fully evaluated, 1 was rated as class I, 6 as class II, 2 as class III, and 25 as class IV. Evidence within each diagnostic area was synthesized for the formulation of Practice Standards, Practice Guidelines, and Practice Options, as possible. Two clinical practice recommendations were advanced, 1 each in the diagnostic areas of brain neoplasms and epilepsy/seizure disorders. Discussion included comments on the research status of the effectiveness of cognitive rehabilitation for cognitive deficits related to these medical conditions, as well as suggestions for future directions in research.

Comparing chiropractic neck adjustment to hanging

This is over the top but I need even more readers.
From Science-Based Medicine by Mark Crislip comes this quote.
I once calculated that the force of a neck crack is about 40% that of hanging by the neck and it has the same pathologic changes if it goes wrong. Every time I see a death in the movie where the neck is twisted to break it, I think chiropractic, although some tolerate it better than others.
Full post here:
Whack em hard/Whack em once and Stroke

This  is the paper that supposedly supports chiropractic.
Risk of Vertebrobasilar Stroke and Chiropractic Care
Results of a Population-Based Case-Control and Case-Crossover Study
Spine. 2008 Feb 15;33(4 Suppl):S176-83.
by Cassidy JD, Boyle E, Côté P, He Y, Hogg-Johnson S, Silver FL, Bondy SJ.
(5)
Dissected(pun intended) quite ably here;
Chiropractic and Stroke: Evaluation of One Paper

I will never have this done. Would you trust your chiropractor to not go over 40%?  Does your chiropractor even know about this limit?

Forget coffee, now you can get caffeine in your TOOTHBRUSH

You can read about all the great results of using caffeine here;
http://oc1dean.blogspot.com/2012/10/caffeine-good-vs-bad.html

Of course, you will need to make sure you don't use this for your nightly brushing. And since the caffeine gum is discontinued this would be a great solution. Do you really think your hospital will read research on caffeine and provide these toothbrushes to stroke patients?
http://www.dailymail.co.uk/sciencetech/article-2325500/Forget-coffee-caffeine-TOOTHBRUSH.html?ico=sciencetech^headlines
  • Firm has applied for patents for a range of brushes with flavours and even an appetite suppressant on them
  • Could also be used to deliver correct doses of drugs to patients

The patent application from the Colgate-Palmolive Company revealed technology that would allow chemicals to be embedded into the heads of standard toothbrushes and slowly released during use.
The firm showed off plans for everything from mint and apple flavoured patches to a caffeine patch to wake up the weary in the morning.

Diagrams and more at the link.

QI Program Leads to Better Stroke Outcomes

This is the Get With the Guidelines program.
http://www.medpagetoday.com/MeetingCoverage/AdditionalMeetings/39186?
Hospitals participating in a national quality improvement program provided better outcomes for patients with acute ischemic stroke, researchers found.
Centers that participated in the Get With The Guidelines-Stroke program had significantly higher rates of patients getting discharged to home and lower rates of mortality at 30 days and 1 year, when compared with similar hospitals that did not join the program, according to Sarah Song, MD, MPH, of Rush University Medical Center in Chicago.
Those advantages were seen both shortly after joining the program and up to 540 days after participation began, Song reported at the American Heart Association's Quality of Care and Outcomes Research meeting in Baltimore.
The study suggests that even for hospitals that are primary stroke centers and are meeting all the quality metrics established by the Centers for Medicare & Medicaid Services (CMS), "this program might have an additional benefit," Song said in an interview. "This could be a really big impetus to join the program, and I think it should be."
Committing to the guidelines is a reflection of a commitment to being prepared to handle acute stroke cases, according to Patrick Lyden, MD, of Cedars-Sinai Medical Center in Los Angeles, which participates in the program.
"I think the data [are] extremely informative to the public," said Lyden, who was not involved in the study. "You want to go to a stroke center that has some form of preparedness and the easiest way to be prepared is to comply with Get With The Guidelines."
Although previous studies have shown that participation in Get With The Guidelines-Stroke is associated with improvement in various processes of care, an attempt had not been made to compare patient outcomes in an analysis matching participating hospitals with similar non-participating centers, Song said.

More at link.
This from a commenter is interesting.
These are marginal effects and require hospitals to invoke herculean efforts to attain them. It requires stroke coordinators, daily monitoring of quality measures, numerous meetings and intra- departmental collaborations to actually see the results. While it is likely cost-effective, you would think the major payor in stroke treatment (a la CMS) would develop, encourage and implement some standardized treatment algorithms to improve the country's performance on this treatable and preventable disease.


This just points out how badly needed stopping the neuronal cascade of death is.

Depression May Be Stroke Trigger in Women

So I guess the takeaway is don't get depressed or you'll trigger your own stroke. What a depressing scenario. Be careful out there.
http://www.medpagetoday.com/Cardiology/Strokes/39192?
Depression appears to be a risk factor for stroke among middle-age women, even after accounting for other variables, an Australian study showed.
Among women in their late 40s and early 50s who were followed for up to 12 years, meeting criteria for depression was associated with more than double the likelihood of having a stroke (OR 2.41, 95% CI 1.78-3.27), according to Caroline Jackson, PhD, and Gita Mishra, PhD, of the University of Queensland in Australia.
The relationship was partly explained by age, socioeconomic status, lifestyle, and physiological factors, but remained statistically significant after adjustment for those variables (OR 1.94, 95% CI 1.37- 2.74), they reported online in Stroke: Journal of the American Heart Association.

More at link.

Thursday, May 16, 2013

Brain training after stroke pain

No research listed so its hard to tell. Have your doctor track this down. I do wonder if the are detecting brain waves from the motor cortex, if so it wouldn't work on me.
http://news.investors.com/051613-656426-brain-training-after-stroke-pain.htm
A new device detects brain waves and could lead to renewed control of paralyzed limbs or possibly control of a prosthetic device. Hong Kong Polytechnic Univ. researchers created what's thought to be the 1st brain training device, which could give new hope to stroke survivors. The patented Brain Training System inside a helmet uses an algorithm that guides stroke survivors to ID voluntary acts and to relearn how to reconnect paralyzed limbs. Plans are being made to develop a portable system for home use.

Research Derivation and validation of QStroke score for predicting risk of ischaemic stroke in primary care and comparison with other risk scores: a prospective open cohort study

Check out yours here;
http://www.qstroke.org/index.php
Putting in the factors at time of your stroke. Mine was .8% in the next 10 years.I bet it calculates just as bad for most of you, especially you youngsters.
 That way all us survivors could check it out and see if it could have predicted our strokes.
Ask your doctor for your next stroke prediction with your risk reductions as listed here.

http://www.bmj.com/content/346/bmj.f2573

Abstract

Objective To develop and validate a risk algorithm (QStroke) to estimate risk of stroke or transient ischaemic attack in patients without prior stroke or transient ischaemic attack at baseline; to compare (a) QStroke with CHADS2 and CHA2DS2VASc scores in patients with atrial fibrillation and (b) the performance of QStroke with the Framingham stroke score in the full population free of stroke or transient ischaemic attack.
Design Prospective open cohort study using routinely collected data from general practice during the study period 1 January 1998 to 1 August 2012.
Setting 451 general practices in England and Wales contributing to the national QResearch database to develop the algorithm and 225 different QResearch practices to validate the algorithm.
Participants 3.5 million patients aged 25-84 years with 24.8 million person years in the derivation cohort who experienced 77 578 stroke events. For the validation cohort, we identified 1.9 million patients aged 25-84 years with 12.7 million person years who experienced 38 404 stroke events. We excluded patients with a prior diagnosis of stroke or transient ischaemic attack and those prescribed oral anticoagulants at study entry.
Main outcome measures Incident diagnosis of stroke or transient ischaemic attack recorded in general practice records or linked death certificates during follow-up.
Risk factors Self assigned ethnicity, age, sex, smoking status, systolic blood pressure, ratio of total serum cholesterol to high density lipoprotein cholesterol concentrations, body mass index, family history of coronary heart disease in first degree relative under 60 years, Townsend deprivation score, treated hypertension, type 1 diabetes, type 2 diabetes, renal disease, rheumatoid arthritis, coronary heart disease, congestive cardiac failure, valvular heart disease, and atrial fibrillation
Results The QStroke algorithm explained 57% of the variation in women and 55% in men without a prior stroke. The D statistic for QStroke was 2.4 in women and 2.3 in men. QStroke had improved performance on all measures of discrimination and calibration compared with the Framingham score in patients without a prior stroke. Among patients with atrial fibrillation, levels of discrimination were lower, but QStroke had some improved performance on all measures of discrimination compared with CHADS2 and CHA2DS2VASc.
Conclusion QStroke provides a valid measure of absolute stroke risk in the general population of patients free of stroke or transient ischaemic attack as shown by its performance in a separate validation cohort. QStroke also shows some improvement on current risk scoring methods, CHADS2 and CHA2DS2VASc, for the subset of patients with atrial fibrillation for whom anticoagulation may be required. Further research is needed to evaluate the cost effectiveness of using these algorithms in primary care.

Explaining stroke 101 - from the NSA

Look at it first before I color your impression.
http://www.stroke.org/site/DocServer/Explaining_Stroke_101.pptx?docID=8321
Page 2 -You notice nothing on actually finding solutions to diagnosis, treatment, recovery. No mention of research. In other words, they are just a  press release organization. I will never donate to any org that doesn't do real work. They can easily look to the Alzheimers Foundation or the Michael J. Fox Foundation for examples. I wonder how their board of directors can live with themselves.
Page 4, 7 million survivors in the US and nothing being done for them. They are missing a huge pool of donations if they had any help in recovery for these chronic survivors.
Pages5-8, No links to references. If they expect to be taken seriously you have to document your sources.
Page 10, definition, I wish they would mention the real reason to be concerned, blood carries oxygen and neurons don't survive long without it.
Page 11, shows a carotid artery obstruction. This is not a stroke. With a fully functioning Circle of Willis that blockage as shown is harmless. It would only become harmful if the clot continued travelling and lodged in an artery in the brain.
Pages 18-20, stroke prevention. These are all so bland and non-specific as to be useless.
Page 23, no mention of how badly tPA works or the use of gluing. Nothing on any treatments that can stop the neuronal cascade of death. It seems they don't even know anything about the progression of stroke.
Page 24, recovery statistics. These are appalling and need to show changes since the NSA started.
Page 28, purpose of NSA. In my opinion they have failed because their purpose is wrong.

Body Fat Is Associated With Reduced Aortic Stiffness Until Middle Age

I'm sure there is a correlation between stiff arteries and stroke, but I don't know about it. You can test if you have stiff arteries here and here.
You can fix them via this. Don't listen to me I have no medical training. Your doctor can tell you if fixing your stiff arteries would lead to dangerously low blood pressure and the risk of stroke from that.
Stiff arteries relax like younger blood vessels after taking alagebrium

I'm probably carrying an extra 20 pounds and I am middle-aged. So I should do something about that. Exercise, exercise, exercise.
http://hyper.ahajournals.org/content/early/2013/04/22/HYPERTENSIONAHA.113.01177.reprint

Abstract

Obesity is a major risk factor for cardiometabolic disease, but the effect of body composition on vascular aging and arterial stiffness remains uncertain. We investigated relationships among body composition, blood pressure, age, and aortic pulse wave velocity in healthy individuals. Pulse wave velocity in the thoracic aorta, an indicator of central arterial stiffness, was measured in 221 volunteers (range, 18–72 years; mean, 40.3±13 years) who had no history of cardiovascular disease using cardiovascular MRI. In univariate analyses, age (r=0.78; P < 0.001) and blood pressure (r=0.41; P< 0.001) showed a strong positive association with pulse wave velocity. In multivariate analysis, after adjustment for age, sex, and mean arterial blood pressure, elevated body fat% was associated with reduced aortic stiffness until the age of 50 years, thereafter adiposity had an increasingly positive association with aortic stiffness (β=0.16; P < 0.001). Body fat% was positively associated with cardiac output when age, sex, height, and absolute lean mass were adjusted for (β=0.23; P=0.002). These findings suggest that the cardiovascular system of young adults may be capable of adapting to the state of obesity and that an adverse association between body fat and aortic stiffness is only apparent in later life.

More explanation about this here: From Imperial College, London.
Body fat hardens arteries after middle age

Infectious burden and cognitive function

So when your doctor tells you your cognition has been affected by the stroke. Ask whether they have ruled out these eleven first or did they just blindly follow Occams' razor.
Or is the actual stroke itself?  Ask for proof as to the conclusion.
1. Decline in executive control during acute bouts of exercise
2. Time to Recognize Mild Cognitive Disorder?
3.  Low-T in men
4.  Alcohol intake in the elderly affects risk of cognitive decline and dementia
5.   long-term exposure to particulate matter speeded up cognitive decline in older women.
6.  Older Brains Actually Become ‘Full’
7. Mem­ory Loss Could Be The Fault Of Your Meds, Not Your Age
8. How marijuana makes you forget
9.  Silent strokes -New Clues as to Why Some Older People May Be Losing Their Memory
10.  Doorways - What did I come in here for? Study explains why we forget simple tasks
11.  Afib Linked to Cognitive Decline
And the new infection reason here;
http://www.neurology.org/content/80/13/1209.abstract

Abstract

Objective: We hypothesized that infectious burden (IB), a composite serologic measure of exposure to common pathogens (i.e., Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpes simplex virus 1 and 2) associated with vascular risk in the prospective Northern Manhattan Study (NOMAS), would also be associated with cognition.
Methods: Cognition was assessed using the Mini-Mental State Examination (MMSE) at enrollment and the modified Telephone Interview for Cognitive Status (TICS-m) at annual follow-up visits. Adjusted linear and logistic regressions were used to measure the association between IB index and MMSE. Generalized estimating equation models were used to evaluate associations with TICS-m and its change over time.
Results: Serologies and cognitive assessments were available in 1,625 participants of the NOMAS cohort. In unadjusted analyses, higher IB index was associated with worse cognition (change per standard deviation [SD] of IB for MMSE was −0.77, p < 0.0001, and for first measurements of TICS-m was −1.89, p < 0.0001). These effects were attenuated after adjusting for risk factors (for MMSE adjusted change per SD of IB = −0.17, p = 0.06, for TICS-m adjusted change per SD IB = −0.68, p < 0.0001). IB was associated with MMSE ≤24 (compared to MMSE >24, adjusted odds ratio 1.26 per SD of IB, 95% confidence interval 1.06–1.51). IB was not associated with cognitive decline over time. The results were similar when IB was limited to viral serologies only.
Conclusion: A measure of IB associated with stroke risk and atherosclerosis was independently associated with cognitive performance in this multiethnic cohort. Past infections may contribute to cognitive impairment.

Factors associated with misdiagnosis of acute stroke in young adults

The assumptions made here are totally incorrect, you don't need more stroke centers or better training on diagnosis. You need an OBJECTIVE way to determine a stroke is occurring. Like these seventeen. Are people that stupid that they can't even solve a simple problem as described?
http://www.ncbi.nlm.nih.gov/pubmed/20719534
copyrighted so hopefully I  won't get in trouble for pointing out this stupidity.

Abstract

Misdiagnosis or delayed diagnosis of acute ischemic stroke can result in neurologic worsening or a missed opportunity for thrombolysis. Because stroke in young adults is less common than stroke in the elderly, we sought to determine clinical characteristics associated with misdiagnosis of stroke in young adults. Patients from the prospectively maintained Young Stroke Registry in our comprehensive stroke center were reviewed. Demographic information, past medical history, presentation within the 3-hour time window, and outcomes were assessed. We compared patients misdiagnosed and those correctly diagnosed to identify factors associated with misdiagnosis of acute stroke. A total of 57 patients aged 16-50 were enrolled in the registry during 2001-2006. Eight patients (14%; 4 men and 4 women; mean age, 38 years) were misdiagnosed. Seven of these 8 patients were discharged from the emergency department initially. Patients age < 35 years (P = .05) and patients with posterior circulation stroke (P = .006) were more likely to be misdiagnosed. All 8 misdiagnosed patients were initially evaluated at hospitals that were not certified primary stroke centers. Patients presenting with vertebrobasilar territory ischemia have a greater rate of misdiagnosis. Our study demonstrates the increasing need for "young stroke awareness" among emergency department personnel. Initial misdiagnosis can potentially lead to a lost opportunity for thrombolysis in otherwise good candidates.

Wednesday, May 15, 2013

Study Finds Plasmin—Delivered Through A Bubble—More Effective Than tPA In Busting Clots

And to make this even better you could use xenon gas in the bubbles.
http://www.healthcanal.com/blood-heart-circulation/38656-study-finds-plasmin%E2%80%94delivered-through-a-bubble%E2%80%94more-effective-than-tpa-in-busting-clots.html
A new study from the University of Cincinnati (UC) College of Medicine has found that, when delivered via ultrasound, the natural enzyme plasmin is more effective at dissolving stroke-causing clots than the standard of care, recombinant tissue plasminogen activator (rt-PA).
The novel delivery method involved trapping plasmin into bubble-like liposomes, delivering them to the clot intravenously and bursting it via ultrasound. That method is necessary, says UC associate professor of emergency medicine George "Chip” Shaw III, MD, PhD, because plasmin cannot be delivered through traditional methods. Intravenous delivery of rt-PA is designed to solve that problem by catalyzing the conversion of existing plasminogen inside the body to plasmin, which in turn degrades blood clots.

"Plasmin is the enzyme that actually chews up the fibrin in clots,” says Shaw. "The problem is you can only give plasmin inter-arterially, which has safety risks and takes longer to deliver. IV therapy is always easier and quicker, but if you give plasmin intravenously, the body inhibits it immediately. If you can encapsulate it, it doesn’t get inhibited and you can target it to the clot.” 

In their in-vitro study, Shaw and researchers Madhuvathi Kandadai, PhD, and Jason Meunier, PhD, enclosed plasmin and a gas bubble inside a liposome. They then delivered the liposome to a clot in an in-vitro lab clot model and dissolved it using ultrasound waves, thus delivering the plasmin enzyme to the clot. After 30 minutes, clots treated with plasmin showed significantly greater breakdown than clots treated with rt-PA. 

They worked with colleague Christy Holland, PhD, professor in UC’s cardiovascular diseases division, to develop the technique. As director of the  Image-guided Ultrasound Therapeutics Laboratories at UC, Holland has studied the use of liposomes and ultrasound to deliver drugs in a less invasive, more targeted fashion.

The standard of care for acute ischemic stroke is intravenous delivery of U.S. Food and Drug Administration-approved rt-PA within three hours of stroke onset. Ischemic stroke is the most common type of stroke, accounting for about 87 percent of all stroke cases. 

But Shaw says there is a "critical need” for a safer and more effective thrombolytic, as rt-PA carries a risk of bleeding. Intracranial hemorrhage currently occurs in 6 percent of patients receiving rt-PA therapy.

More at link.