Why strokes among younger adults have soared

I dislike the picture attached to this article - Stroke Victim written over the picture. That term should never be used. It is part of the nocebo effect and never will help the survivor come to terms with their event and recover.
http://www.emaxhealth.com/11306/why-strokes-among-younger-adults-has-soared

 
Strokes are generally considered to be a condition that occurs among the elderly; however, the rate of strokes has increased significantly in the United States among younger adults. Researchers affiliated with the University of Cincinnati conducted a study to determine the reasons behind this increase. They published their findings online on November 15 in the journal Stroke.
According to the Centers for Disease Control and Prevention (CDC), nearly 800,000 individuals in the United States suffer a stroke every year, and the condition is the most common cause of serious long-term disability. A study conducted in 2007 reported that that almost 5% of people who had suffered a stroke that year were between ages 18 and 44. The investigators noted that substance abuse is a prevalent risk factor for stroke in young adults; therefore, they conducted a study to identify trends in substance abuse detection among stroke patients.
The researchers attempted to identify all patients aged 18 to 54 years experiencing a stroke (ischemic or hemorrhagic) in the Greater Cincinnati and Northern Kentucky Study region during 1993 to 1994, 1999, and 2005. (An ischemic stroke is caused by a blocked vessel while a hemorrhagic stroke is caused by leakage of blood from a blood vessel into the brain.) Demographic and clinical characteristics and substance use data were obtained retrospectively from chart review and adjudicated by physicians. The researchers reviewed medical charts for blood or urine test results of other records of substance abuse for nearly 1,200 stroke patients.
The researchers found that the number of young patients identified with a stroke increased from 1993 to 1994 (297 cases) to 2005 (501 cases). Blacks (61% vs. 51%) and men (61% vs. 47%) reported substance abuse (i.e., current smoking, alcohol abuse, or illegal drug use) more frequently than did whites and women. Overall, the use of substances increased across study periods: 45% in 1993 vs. 62% in 2005). The trend was significant for illegal drug use (3.8% in 1993 vs. 19.8% in 2005) and ever smoking (49% in 1993 vs. 66% in 2005). Documentation of both cocaine and marijuana use increased over time. In 2005, half of young adults with a stroke were current smokers, and 1 in 5 abused illegal drugs.
The authors concluded that substance abuse is common in young adults experiencing a stroke. The observed increase in substance abuse is contributing to the increased incidence of stroke in young adults. They recommended that patients aged younger than 55 years who experience a stroke should be routinely screened and counseled regarding substance abuse.
Take home message:
The results of this study are not surprising, given the deleterious effects of smoking and substance abuse. Smoking is a definite risk factor for cardiovascular disease (heart attacks and strokes). Among illegal substances, cocaine, methamphetamine, and other central nervous stimulants pose the greatest risk of a stroke. These substances significantly increase blood pressure. The increased blood pressure can cause a rupture of a blood vessel in the brain, which produces a hemorrhagic stroke.

But did the data show a higher incidence of hemorrhagic stroke than the general population? Or are you suggesting that stiffer arteries were caused by substance abuse, leading to thrown clots? I can't tell if your conclusion is supported by the evidence.

Why drug discovery is so hard

A couple of interesting writeups on this. I wish I could be confident that drugs to stop the neuronal cascade of death will be found but as Dr. Michael Tymianski, of the Toronto Western Hospital Research Institute in Canada mentions 1000 drugs that showed promise in animal models failed in human trials. I have yet to find out why they failed and what has been learned from those failures.
I could care less about it being hard. A Great stroke association would gladly tackle this issue. But alas we have non-functional ones like the ASA, NSA and WSO. Please respond with your excuses, I will print them.
This is way too important to leave it to drug companies to figure out. We as survivors need to push researchers to explain what they have already done and ruled out and what their plans  look like to successfully come up with a neuroprotective drug.

1.A Broadside Against The Way We Do Things Now 
---------------------------------------------------------------------------------------------

2. Traditional drug-discovery model ripe for reform

--------------------------------------------------------------------------------------------

 

3.What are the main discovery issues facing drug discovery companies right now? 

----------------------------------------------------------------------------------------------------

4.  Drug discovery in jeopardy

-----------------------------------------------------------------------------------------------------

5.  Drug Discovery  The Pending Crisis

------------------------------------------------------------------------------------------------------

6.  Future Directions in Drug Design & Discovery

-----------------------------------------------------------------------------------------

7. Major Issues and Trends in Drug Discovery and Development: India’s Emerging Role

--------------------------------------------------------------------------------------------

8.  The end of drug discovery?

-------------------------------------------------------------------------------------------------------

9.   CNS Drug Discovery & Development 2012: Problems, Promises and Solutions

-----------------------------------------------------------------------------------------------------------

 

 

Opening a 2 quart plastic bottle

One of my challenges, I had to compensate to do it.  I'm buying 2 quart V8 or tomato juice bottles to have something to drink around the house instead of soda. Lycopene you know. They have these indentations in the side to easily hold(hah) and pour it. I'm trying to just open the cap. I tried and tried to get my left hand open enough to grab the bottle that way - failed. I need at least three other hands, one to hold the thumb open, one to open the other four fingers and the last to hold the bottle upright.  The other possibility - hold the bottle with the right hand and grab and twist the cap open with the left hand didn't work either. My left hand can't close tight enough to grab something that small. Finally took a knife and ran it around the cap, separating the cap from the ring. Then it was to the Tommye K. Mayer method of using your hip as a support. I braced the bottle against the countertop and used my hip to hold it in place, using my right hand to unscrew the top. This is a delicate operation since you have to determine the stiffness of the plastic bottle so you don't spray the juice all over as the top is removed.  Or I could just get a large vise-grip and straddle the bottle with my feet. The cap is too big to grab with my teeth. I hate having to compensate.

Your Brain by the Numbers

A great graphic from Scientific American. Take this and ask your doctor what has changed after your stroke. A good question is how many watts does your brain need after stroke and have it correlated to your fatigue. In the US it is 7 million with stroke. I wish they would map in 3d the 400 miles of capillaries. MindHacks tells us this is An amazing picture by Dwayne Godwin and Jorge Cham from PhD Comics.
http://www.scientificamerican.com/article.cfm?id=mind-in-pictures-your-brain-by-the-numbers

Stroke survivors are invisible - Change that - start blogging

I originally wrote this 2 years ago and not one person notified me about starting their blog. With 11 million new survivors a year that's pathetic. Now that I'm getting 1000 hits a day maybe this will take.Start your own stroke blog. Stroke survivors as a whole are invisible, we need to change that.
Bringing stroke out of the shadows I don't want to find out 20 years from now that survivors still do not have a voice in their stroke associations and a way to direct where the future of stroke rehab leads.
Even if all we do is document our own case study that can immeasurably help another survivor.
You can create one here on Google

How to Start a Blog on Google Blogger -

Its free and I am sure there are other sites that allow free blogging.
Create a Blog for Free
Start Blogging & Share with Friends
Add Photos, Easy Blog Posting Tools
KaBlog.com
Start Your Free Blog
Simple, Easy, No Coding Necessary.
100,000+ Use HubPages. Start Today!
HubPages.com
Start a Free, Fun Blog
Pictures, text, privacy controls
Free, easy, fun & safe. Start today
http://www.experienceproject.com/
WordPress.com — Get a Free Blog HereFree blogs managed by the developers of the WordPress software. Includes custom design templates, integrated statistics, automatic spam protection and other ...
wordpress.com/

When you have created one and posted a few entries please send me a link. I want to see thousands/millions out there. If it is not in English please tell me what language it is in. I will add yours to my blog list for others to find. If you want to be found by google read my posting on how to stay informed of stroke rehab


Do it now!!!!!!!

Sony PlayStation EyeToy elicits higher levels of movement than the Nintendo Wii: implications for stroke rehabilitation

Ask your doctor /therapist which one is better for your rehab,
These two
http://www.ncbi.nlm.nih.gov/pubmed/23172403
 or 
1. the xBox Kinect
2. Limbs Alive
3.  KineLabs making egg tart, cleaning the window panes of a tram, and even killing cockroaches
4. Rejoyce Workstation
5. Spatial Augmented Reality system
6. Augmented Reflection Technology
7. interactive game
8. REO Therapy and an Auditory Sensor Feedback
9. Haptic-Rehab
10. a virtual system that incorporates music with visuals
11. Nintendo Wii Fit Plus
12. Neurorehabilitation Training Toolkit (NTT)
13. distributed Virtual Reality
14. 3D immersive videogame
15. Open-source version of Curictus VRS commercial stroke rehabilitation product
Your doctor should know about every one of these.

Abstract

BACKGROUND:Virtual reality (VR) is an emerging trend in stroke rehabilitation. VR gaming consoles in stroke intervention have been shown to increase motivation and enjoyment during exercise. The amount and intensity of movements elicited using these consoles are unknown. Aims. The aims of this study were: 1) to quantify the amount and intensity of movement elicited from both hands of two groups of individuals ([chronic stroke and without a disability [healthy]); 2) to determine the effect of console (Wii/EyeToy) and group (stroke/healthy) on the amount and intensity of upper extremity movement; 3) to determine the effect of console (Wii/EyeToy) and group (stroke/healthy) on the usability and VR experience. DESIGN:A cross-sectional design was taken.

SETTING:

Outpatient rehabilitation setting and healthy participant's homes.

POPULATION:

Participants included ten adults with stroke and ten adults without a disability. Methods. Participants experienced two games from each console. Amount and intensity of movement was measured using accelerometers on both wrists, while the virtual experience and usability was determined with questionnaires.

RESULTS:

No significant differences were found between the consoles usability and experience. EyeToy elicited significantly greater activity count than Wii among the healthy participants (P=0.028) and significantly greater movement intensity in both the stroke (P=0.005) and healthy (P=0.005) groups.

CONCLUSION:

Both consoles rated high for usability, enjoyment and satisfaction highlighting their suitability for a range of individuals in stroke rehabilitation. EyeToy provides increased movement and movement intensity.

CLINICAL REHABILITATION IMPACT:

Both consoles are suitable for use in stroke rehabilitation however this information can be helpful to clinicians while selecting a gaming console according to the type and intensity of movements that he/she aims to encourage during therapy.

Etazolate, an α-secretase activator, reduces neuroinflammation and offers persistent neuroprotection following traumatic brain injury in mice

Get those human clinical trials going. Trillions of neurons need saving everyday we waste.  Call the ASA, NSA and WSO and ask what they are doing to save neurons.

http://www.sciencedirect.com/science/article/pii/S0028390812005461

Abstract

Traumatic brain injury (TBI) evokes an intense neuroinflammatory reaction that is essentially mediated by activated microglia and that has been reported to act as a secondary injury mechanism that further promotes neuronal death. It involves the excessive production of inflammatory cytokines and the diminution of neuroprotective and neurotrophic factors, such as the soluble form alpha of the amyloid precursor protein (sAPPα), generated by the activity of α-secretases. Hence, the aim of this study was to examine the effects of etazolate, an α-secretase activator, on acute and belated post-TBI consequences. The mouse model of TBI by mechanical percussion was used and injured mice received either the vehicle or etazolate at the dose of 1, 3 or 10 mg/kg at 2 h post-TBI. Neurological score, cerebral œdema, IL-1β and sAPPα levels, microglial activation and lesion size were evaluated from 6 to 24 h post-TBI. Spontaneous locomotor activity was evaluated from 48 h to 12 weeks post-TBI, memory function at 5 weeks and olfactory bulb lesions at 13 weeks post-TBI. A single administration of etazolate exerted a dose-dependent anti-inflammatory and anti-œdematous effect accompanied by lasting memory improvement, reduction of locomotor hyperactivity and olfactory bulb tissue protection, with a therapeutic window of at least 2 h. These effects were associated with the restoration of the levels of the sAPPα protein post-TBI. Taken together, these results highlight for the first time the therapeutic interest of an α-secretase activator in TBI.

---

Highlights

► The post-TBI levels of sAPPα were restored by etazolate treatment. ► Etazolate decreases IL-1β levels, cerebral oedema and microglial activation. ► Locomotor hyperactivity and memory deficit were attenuated by etazolate treatment. ► Etazolate protects olfactory bulb tissue in a persistent manner. ► The therapeutic window of etazolate is at least 2 h.

Mem­ory Loss Could Be The Fault Of Your Meds, Not Your Age

Your doctor should eliminate all the other reasons for memory loss before blaming the stroke..
http://www.ibtimes.com/memory-loss-could-be-fault-your-meds-not-your-age-861858

Memory loss isn't always an inevitable sign of getting old – in some cases, common medications that seniors take to treat insomnia, anxiety, or even allergies could be to blame.

"Seniors can play an important role in reducing the risks associated with these medications,” Montreal Geriatric University Institute researcher Cara Tannenbaum said in a statement Tuesday.

Tannenbaum and her colleagues recently investigated what kinds of medication are most likely to affect both memory and concentration. In a meta-analysis of 162 experiments on various drugs, Tannenbaum concluded that the recurrent use of several kinds of medications can have impacts on cognitive function.

Sixty-eight of the studies they examined focused on benzodiazepines, which are often used to treat insomnia and anxiety. Consistently, these medications led to impared memory and concentration, with stronger impacts at higher doses. Tannenbaum says her findings confirm recent recommendations from the American Geriatric Society that seniors avoid tricyclic antidepressants, certain antihistamines and all sleeping pills.

“Patients need this information so that they are more comfortable talking to their doctors and pharmacists about safer pharmacological or non-pharmacological treatment options," Tannenbaum said.

Benzodiazepines aren't the only kinds of medication that could impact memory. In February, the U.S. Food and Drug Administration added new warnings about memory loss and an increased risk for Type 2 diabetes to the labels of cholesterol-fighting statin medications.

Popular drugs like Lipitor, Crestor and Vytorin fell under the scope of February's decision by the FDA, which was based on results from new clinical trials and reports of side effects from patients, doctors and pharmaceutical companies.

Memory loss associated with statins tends to go away once a patient stops using the drug, the FDA said.

The link between anti-cholesterol medication and memory impairment becomes somewhat less surprising when you consider how fatty brain tissue is. While high levels of cholesterol are bad for your heart, they help form vital neural connections in the brain.

“We can’t understand how a drug that affects such an important pathway would not have adverse reactions,” Ralph Edwards, former director of the World Health Organization’s drug-monitoring center in Sweden told Scientific American in 2010.

Many drugs that cause mild cognitive impairment are anti-cholinergic, meaning that they inhibit the activity of the neurotransmitter acetylcholine.

Some drugs are specifically taken for their anti-cholinergic effects and can help relieve bladder irritability or intestinal cramping. But patients, doctors and pharmacists may not be aware of the anti-cholinergic activity of other kinds of drugs, like antidepressants and antihistamines.

Tannenbaum acknowledges that each person should be dealt with individually.

"Despite the known risks, it may be better for some patients to continue their medication instead of having to live with intolerable symptoms,” she says. “Each individual has a right to make an informed choice based on preference and a thorough understanding of the effects the medications may have on their memory and function."

Thick collagen-based 3D matrices including growth factors to induce neurite outgrowth.

Something for you to tell your researchers about, a way to easily watch their neurogenesis and angiogenesis experiments, probably better than scaffolding.
The abstract here:
http://www.ncbi.nlm.nih.gov/pubmed/22617741
A blogger explaining it here:

Growing 3D Cells

Double Duty: Immune System Regulator Found to Protect Brain from Effects of Stroke

My other post on microRNA suggested it was useful for neurogenesis. So demand answers from your doctor or stroke association. Or are you going to let them fail at their job and negatively affect your recovery. Get going, it takes years to get new things thru the medical morass. 

Double Duty: Immune System Regulator Found to Protect Brain from Effects of Stroke

A small molecule known to regulate white blood cells has a surprising second role in protecting brain cells from the deleterious effects of stroke, Johns Hopkins researchers report. The molecule, microRNA-223, affects how cells respond to the temporary loss of blood supply brought on by stroke -- and thus the cells' likelihood of suffering permanent damage.

---

"We set out to find a small molecule with very specific effects in the brain, one that could be the target of a future stroke treatment," says Valina Dawson, Ph.D., a professor in the Johns Hopkins University School of Medicine's Institute for Cell Engineering. "What we found is this molecule involved in immune response, which also acts in complex ways on the brain. This opens up a suite of interesting questions about what microRNA-223 is doing and how, but it also presents a challenge to any therapeutic application." A report on the discovery is published in the Nov. 13 issue of the Proceedings of the National Academy of Sciences.
RNA is best known as a go-between that shuttles genetic information from DNA and then helps produce proteins based on that information. But, Dawson explains, a decade ago researchers unearthed a completely different class of RNA: small, nimble fragments that regulate protein production. In the case of microRNA, one member of this class, that control comes from the ability to bind to RNA messenger molecules carrying genetic information, and thus prevent them from delivering their messages. "Compared with most ways of shutting genes off, this one is very quick," Dawson notes.
Reasoning that this quick action, along with other properties, could make microRNAs a good target for therapy development, Dawson and her team searched for microRNAs that regulate brain cells' response to oxygen deprivation.
To do that, they looked for proteins that increased in number in cells subjected to stress, and then examined how production of these proteins was regulated. For many of them, microRNA-223 played a role, Dawson says.
In most cases, the proteins regulated by microRNA-223 turned out to be involved in detecting and responding to glutamate, a common chemical signal brain cells use to communicate with each other. A stroke or other injury can lead to a dangerous excess of glutamate in the brain, as can a range of diseases, including autism and Alzheimer's. Because microRNA-223 is involved in regulating so many different proteins, and because it affects glutamate receptors, which themselves are involved in many different processes, the molecule's reach turned out to be much broader than expected, says Maged M. Harraz, Ph.D., a research associate at Hopkins who led the study. "Before this experiment, we didn't appreciate that a single microRNA could regulate so many proteins," he explains.
This finding suggests that microRNA-223 is unlikely to become a therapeutic target in the near future unless researchers figure out how to avoid unwanted side effects, Dawson says.
Other authors on the paper are Stephen M. Eacker, Ph.D., Xueqing Wang, Ph.D., and Ted M. Dawson, M.D., Ph.D., from the Johns Hopkins University School of Medicine.
This work was supported by a grant from the National Institutes of Health (grant DA000266) and by a Maryland Stem Cell Research Fund fellowship.