The Joint Commission and the American Heart Association/American Stroke Association Launch New Certification Program for Comprehensive Stroke Centers

I wouldn't think much of this new certification because  everything about it is hidden from public view. I bet you as a survivor will get nothing from

please call 630.792.5291 or e-mail dscinfo@jointcommission.org. 

If you do send it to me so I can publish it.

http://www.marketwire.com/press-release/joint-commission-american-heart-association-american-stroke-association-launch-new-certification-1697052.htm

5 Weird Medical Tests You Can Try Right Now and fail at

I failed Romberg's Test at the hospital although I can pass it now.
I can't tell if  I failed Finger Measurement Test because I can't get my left hand into that position. Right hand looks ok.
I failed the Nose Test at the hospital with my left hand and still fail it(I must be constantly intoxicated, damn that red wine and dark beer)
I failed the Heel Test at the hospital with my left leg and still fail it today because my leg spasticity doesn't allow me to bend my knee.
I failed The "Prayer Position" Test and the Pinky Tests because I can't even flatten my left hand at all.
http://health.yahoo.net/articles/healthcare/photos/5-weird-medical-tests-you-can-try-right-now#0

Study looks at rhythms of the brain

May be useful for our visual deficits so ask your researcher what it means for your rehab.
http://therapytoronto.ca/news/?p=5938

Combination of blood thinning drugs shown to be ineffective as stroke preventer

  You have to read the complete article because they refer to lacunar strokes. This is for your doctor to consider so if they don't ask about it tell them.

 http://www.healthcanal.com/brain-nerves/32026-Combination-blood-thinning-drugs-shown-ineffective-stroke-preventer.html

 

An international team led by a neurologist at the University of British Columbia and Vancouver Coastal Health has shown that a combination of aspirin and clopidogrel, both common blood thinners, does not prevent recurrence of a common type of stroke, and may even pose serious risks.
Combining aspirin and clopidogrel (known commercially as Plavix) was thought to hold promise in preventing recurring lacunar strokes – the death of brain cells caused by a narrowing of small blood vessels – by reducing the formation of clots in arteries supplying the brain.
Dr. Oscar Benavente, a UBC professor of neurology and research director of the Stroke and Cerebrovascular Health Program at Vancouver Coastal Health, sought to determine if a combination of clopidogrel and aspirin –another anti-clotting agent that is used to prevent strokes — would lower the recurrence of lacunar strokes more than aspirin alone. The study involved 3,020 patients from 82 sites in North America, Latin America, and Spain who were followed for several years.

White matter dementia

So make sure your doctors test for this  before assuming your cognition problems are a result of the stroke. Then ask for a protocol to correct those problems.
http://tan.sagepub.com/content/5/5/267.abstract?etoc=

Abstract

White matter dementia (WMD) is a syndrome introduced in 1988 to highlight the potential of cerebral white matter disorders to produce cognitive loss of sufficient severity to qualify as dementia. Neurologists have long understood that such a syndrome can occur, but the dominance of gray matter as the locus of higher function has strongly directed neurobehavioral inquiry to the cerebral cortex while white matter has received less attention. Contemporary neuroimaging has been crucial in enabling the recognition of white matter abnormalities in a host of disorders, and the correlation of these changes with cognitive performance. Comprising about half the brain, white matter is prominently or exclusively involved in well over 100 disorders,in each of which white matter dysfunction can potentially cause or contribute to dementia. Neuropsychological findings from ten categories of white matter disorder lead to a convergence of findings that document remarkable neurobehavioral commonality among the dementias produced. More recently, the syndrome of mild cognitive dysfunction (MCD) has been introduced to expand the concept of WMD by proposing a precursor syndrome related to early white matter neuropathology. WMD and MCD inform the understanding of how white matter contributes to normal and abnormal cognition, and the specific neuroanatomic focus of these syndromes may enhance the diagnosis and treatment of many disabling disorders that do not primarily implicate the cerebral cortex. Forming essential connections within widely distributed neural networks, white matter is critical for rapid and efficient information transfer that complements the information processing of gray matter. As neuroimaging continues to advance, further information on white matter structure can be expected, and behavioral neurology will play a central role in elucidating the functional significance of these emerging data. By emphasizing the contribution of myelinated systems to higher function, the study of white matter and cognition represents investigation of the basic neuroscience of human behavior.

Cardiac Benefits of Red Wine Not From the Alcohol

Good luck finding dealcoholized red wine, unless you can substitute grape juice. 
http://www.medpagetoday.com/Cardiology/Hypertension/34610

Action Points

• Explain that a small Spanish open-label, crossover study found that consumption of a moderate amount of dealcoholized red wine over a 4-week period, but not red wine itself or gin, was associated with a modest decrease in both systolic and diastolic blood pressure.
• Note that plasma nitric oxide was also increased when dealcoholized red wine was consumed, leading the authors to speculate that the blood pressure lowering effect might be due to nitric oxide.

 Rest at the link, I suppose that they will next test the dark beers and say that the alcohol in them is not needed either. Taking all the fun out of life.

Degenerative Diseases Of The Brain – New Therapies

Nothing directly for us here but our researchers should be able to posit some hypotheses about this helping our brain problems.
Degenerative Diseases Of The Brain – New Therapies

Late onset diseases like Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS) are degenerative as well as progressive and thereby diminish the quality of life of patients significantly. At present, therapies to treat or reverse degeneration of brain cells are limited and these diseases usually progress into disabilities. However, recent research seems to indicate that it may be possible to limit the damage caused by the onset of AD, PD and ALS by activating innate biological mechanisms.
A consequence of the natural respiration process that is always active in our cells is the production of harmful forms of oxygen, which are known as reactive oxygen species (ROS). Reactive oxygen species like hydroxyl ions and hydrogen peroxide are produced in mitochondria. During periods of wakefulness, our brain consumes 20% of the total oxygen used in the body and it therefore follows that the chances of generating reactive oxygen species in brain cells are very high. These highly destructive molecules are neutralized by two enzyme: heme oxidase-1 (HO-1) and superoxide dismutase (SOD). In the early stages of AD and PD, the activity of these enzymes is either normal or reduced. It is surmised that the capability of the brain to increase the activity of these antioxidants is diminished in the stages preceding the onset of these degenerative diseases. In the case of AD, the protein (beta-amyloid peptide) deposited on nerve cells actually causes an increase in the ROS within nerve cells.
Recent research suggests that inhalation of gases like hydrogen, hydrogen sulfide and carbon monoxide, in low and regulated doses, can actually help to reduce oxidative damage caused by ROS. Although hydrogen sulfide is toxic, small quantities of this gas can actually be therapeutic against ROS. A modified form of aspirin which can release hydrogen sulfide, termed as S-aspirin, is able to protect brain cells from damage caused by the beta-amyloid peptide. Similarly, hydrogen, when inhaled, can reach the brain within an hour and can help to reverse nerve cell damage evident in PD. Hydrogen can be also given to patients in the form of hydrogen water and is faster in action than when inhaled in gas form. In experimental animal models for Parkinson’s disease, treatment with hydrogen water helped to rescue neurons which respond to dopamine from damage caused by ROS.
Hydrogen is capable of reacting with hydroxyl radicals to form water. In addition to this short-term chemical neutralization of reactive oxygen species, exposure to low doses of hydrogen also causes enhanced expression of HO-1 and SOD enzymes. Similar effects are also seen when nerve cells are exposed to carbon monoxide and hydrogen sulfide. These medical gases boost innate protective responses against reactive oxygen species and provide long-term protection that goes beyond immediate and local chemistry in the brain. Exposure of brain cells to hydrogen sulfide also reduces the amount of beta-amyloid peptide in nerve cells thereby limiting the damage caused by this protein.
Since administration of medical gases is a pretty standard procedure in hospitals and clinics, these scientific advances may represent a chance of recovery to patients who have been diagnosed with debilitating diseases like AD, Parkinson’s disease and ALS, at least in the early stages. The efficiency of these treatments in patients suffering from advanced stages of these neurodegenerative diseases is not known yet.

AHA Scientific Sessions Offers Outstanding Late-Breaking Science

From a AHA email I received.  You will notice there is not one session on stroke rehabilitation or prevention of neuronal cascade of death. Scientific Sessions will again offer the latest science via its popular Late-Breaking Clinical Trials. Attendees will have the opportunity to hear 28 LBCTs. These presentations are selected based on their unique approach to the topic, their design methods and the overall quality of the statistical plan. In addition, 19 trials will be presented in the format of Clinical Science: Special Report sessions and will focus on registries, updates to existing trials and important clinical science.

The following presentations are scheduled, as of Aug. 13, 2012. LBCTs Practice Implications for CAD and VTE Aspirin for the Prevention of Recurrent Venous Thromboembolism After a First Unprovoked Event: Results of the ASPIRE Randomized Controlled Trial A Randomized Trial of Bedside Platelet Function Monitoring to Adjust Antiplatelet Therapy Versus Standard of Care in Patients Undergoing Drug Eluting Stent Implantation: The ARCTIC Study First Large-Scale Platelet Function Evaluation in an Acute Coronary Syndromes Trial--The TRILOGY ACS Platelet Function Sub-study Results of the Trial to Assess Chelation Therapy Main Results of the Future REvascularization Evaluation in patients with Diabetes mellitus: Optimal management of Multivessel disease (FREEDOM) Trial Health Economics and Quality of Life in Contemporary Trials Prospective Evaluation of Outcomes With Stress Perfusion Imaging Versus Stress Wall Motion Imaging During Dobutamine or Exercise Echocardiography Economic Outcomes of Percutaneous Coronary Intervention Performed at Sites With and Without On-Site Cardiac Surgery Quality of Life Outcomes in the Trial to Assess Chelation Therapy (TACT) Cost-Effectiveness of PCI With Drug Eluting Stents Versus Bypass Surgery for Patients with Diabetes and Multi-vessel Coronary Artery Disease: Results from the FREEDOM Trial Treatments for Prevention of Cardiovascular Events: A Population Perspective Omega-3 Fatty Acids for the Prevention of Recurrent Symptomatic Atrial Fibrillation: Results of a Double-Blind Randomized Clinical Trial (FORWARD) (NCT00597220) Fish Oil for the Prevention of Post-Operative Atrial Fibrillation--The Omega-3 Fatty Acids for Prevention of Post-Operative Atrial Fibrillation (OPERA) Trial A Randomized Trial of a Multivitamin in the Prevention of Cardiovascular Disease in Men: The Physicians' Health Study II Use of a Multidrug Pill In Reducing cardiovascular Events (UMPIRE) Novel Treatments for Managing Lipid Disorders Reduction of LDL-C with PCSK9 Inhibition in Heterozygous Familial Hypercholesterolemia Disorder (RUTHERFORD): Interim Results From a Phase 2, Randomized, Double-Blind, Placebo-Controlled Trial Goal Achievement after Utilizing an Anti-PCSK9 Antibody in Statin Intolerant Subjects (GAUSS): Interim Results From a Randomized, Double-Blind, Placebo-Controlled Study Effects of 12 Weeks of Treatment with RN316 (PF-04950615), a Humanized IgG2Δa Monoclonal Antibody Binding Proprotein Convertase Subtilisin Kexin Type 9, in Hypercholesterolemic Subjects on High and Maximal Dose Statins CaPre®, A Novel Class of Omega-3-Phospholipids, Therapy in Patients With Mild-to-High Hypertriglyceridemia (From The Multicenter Placebo-Controlled, Randomized, Double-Blind 12-week Trial for Efficacy of Capre on Hypertriglyceridemia [TRIFECTA]) Effects of the Cholesteryl Ester Transfer Protein Inhibitor Dalcetrapib in Patients With Recent Acute Coronary Syndrome Cell-Based Therapies for Myocardial Regeneration Results of the Swiss Multicenter Intracoronary Stem Cells Study in Acute Myocardial Infarction (Swiss Ami) Trial The ALCADIA (Autologous Human Cardiac-Derived Stem Cell to Treat Ischemic Cardiomyopathy) Trial The Effect of Timing of Stem Cell Delivery Following Acute Myocardial Infarction: The NHLBI and CCTRN TIME Trial Randomized Comparison of Allogeneic Versus Autologous Mesenchymal Stem Cells in Patients With Ischemic Cardiomyopathy Effect of Cardiac Stem Cells in Patients with Ischemic Cardiomyopathy: Interim Results of the SCIPIO Trial up to Two Years After Therapy Management of LV Dysfunction: Devices and Drugs MADIT Randomized Trial to Reduce Inappropriate Therapy (MADIT-RIT) Biventricular Versus Right Ventricular Pacing in Patients With Left Ventricular Dysfunction and Atrioventricular Block (BLOCK HF Study) Pilot Trial of Two Levels of Hypothermia in Comatose Survivors From Out-of-Hospital Cardiac Arrest The RELAXin in Acute Heart Failure (RELAX-AHF-1) Trial Cardiorenal Rescue Study in Acute Decompensated Heart Failure: Results of CARRESS-HF, for the Heart Failure Clinical Research Network

Clinical Science: Special Report sessions Prevention and Treatment of Ischemic Heart Disease: Novel Approaches Low Dose Colchicine for Secondary Prevention of Cardiovascular Disease [LoDoCo]: A Randomized Controlled Trial Results of the Responses of Myocardial Ischemia to Escitalopram Treatment Trial Safety and Efficacy of Losmapimod in Non-ST-Segment Elevation Acute Myocardial Infarction: Results of the SOLSTICE Phase 2 Randomized Trial EnligHTN™I, First-in-Man Multi-Center Study of a Novel Multi-Electrode Renal Denervation Catheter in Patients with Drug-Resistant Hypertension New Insights into Management of Common Cardiovascular Disorders A Randomized Trial to Assess Catheter Ablation Versus Rate Control in the Management of Persistent Atrial Fibrillation in Chronic Heart Failure Pulmonary Antrum Radial-Linear Ablation of Paroxysmal Atrial Fibrillation: First-in-Human Multicenter Clinical Outcome Prospective Randomized Study to Assess the Efficacy of Site and Rate of Atrial Pacing on Long-Term Progression of Atrial Fibrillation in Sick Sinus Syndrome--Septal Pacing for Atrial Fibrillation Suppression Evaluation [SAFE] Study Left Ventricular Systolic Dysfunction Associated With Pulmonary Hypertension Riociguat Trial (LEPHT) Sildenafil and Diastolic Dysfunction After Acute Myocardial Infarction in Patients With Preserved Ejection Fraction--A Prospective, Double-Blind Placebo-Controlled Randomized Trial (SIDAMI) Emerging Therapeutics for Diabetes and Dyslipidemia Impact of LX4211, a Dual Inhibitor of Sodium Glucose Transporter 1 and 2 on Cardiovascular Risk Factors in Type 2 Diabetes LAPLACE-TIMI 57 Primary Results Efficacy and Safety of a Fully Human Monoclonal Antibody Against PCSK9 as Monotherapy for Hypercholesterolemia: Results From the MENDEL Study, a Global Phase 2 Trial of AMG 145 AMG 145, a Fully Human Monoclonal Antibody Against Proprotein Convertase Subtilisin Kexin type 9 (PCSK9), Facilitates Achievement of NCEP LDL-Cholesterol Goals in High-Risk Patients Valvular Heart Disease, PAD, Atrial Fibrillation: International Perspectives Mitral Valve Annuloplasty Plus CABG Versus CABG Only in Moderate Functional Ischemic Mitral Regurgitation: Final Results of the Randomized Ischemic Mitral Evaluation (RIME) Trial EndOVascular Treatment for Infra-Inguinal Vessel, in Patients With Critical Limb Sichemia (olive) Registry in Japan Management and One Year Outcome of Atrial Fibrillation in Middle Eastern Cohort Enrolled in the Observational Gulf Survey of Atrial Fibrillation Events (Gulf SAFE) Clinical Implications of Device-Detected Atrial Tachyarrhythmias: Results From the Registry of Atrial Tachycardia and Atrial Fibrillation Episodes in the Cardiac Rhythm Management Device Population (RATE) Antithrombotic Treatments and Associated Outcomes in Patients With Atrial Fibrillation: The Global Anticoagulant Registry in the FIELD (GARFIELD) Randomized Comparison of the Effects of Two Doses of Dabigatran Etexilate on Clinical Outcomes Over 4.3 Years: Results of the Rely-able Double-Blind Randomized Trial Watch all six Late-Breaking Clinical Trial sessions live at your convenience and from anywhere in the world. The AHA will live stream 2012's LBCT Sessions I through VI. View these ground-breaking presentations from the convenience of your personal computer--as if you were with us in Los Angeles. Sessions will be available for purchase beginning Oct. 24. Only $79 per session for AHA professional members. $99 per session for all others. If you would like to be notified when LBCT Live is available for purchase, contact us today and ask to be added to the LBCT Live site alert.

Towards more effective robotic gait training for stroke rehabilitation: a review

This is probably more for your therapists and their management, so hand it to them and ask when it will be implemented. If we as survivors don't push new ideas it will take 30 years to get to clinical practice. So yes, I am blaming survivors for not pushing back on their medical staff for a lack of evidence-based practice for stroke rehab.
http://www.jneuroengrehab.com/content/9/1/65/abstract

Abstract (provisional)

Background

Stroke is the most common cause of disability in the developed world and can severely degrade walking function. Robot-driven gait therapy can provide assistance to patients during training and offers a number of advantages over other forms of therapy. These potential benefits do not, however, seem to have been fully realised as of yet in clinical practice.

Objectives

This review determines ways in which robot-driven gait technology could be improved in order to achieve better outcomes in gait rehabilitation.

Methods

The literature on gait impairments caused by stroke is reviewed, followed by research detailing the different pathways to recovery. The outcomes of clinical trials investigating robot-driven gait therapy are then examined. Finally, an analysis of the literature focused on the technical features of the robot-based devices is presented. This review thus combines both clinical and technical aspects in order to determine the routes by which robot-driven gait therapy could be further developed.

Conclusions

Active subject participation in robot-driven gait therapy is vital to many of the potential recovery pathways and is therefore an important feature of gait training. Higher levels of subject participation and challenge could be promoted through designs with a high emphasis on robotic transparency and sufficient degrees of freedom to allow other aspects of gait such as balance to be incorporated.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

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

I do remember my OT telling me I needed confidence in my bad legs ability  to hold myself up. And I bet I would have had a lot more confidence if fall-based therapy had been available.
http://nnr.sagepub.com/content/26/8/999.abstract?etoc

Abstract

Background. Confidence about balance may be an important factor affecting self-efficacy for daily activities after stroke. Objective. The authors investigated whether confidence changes and the parameters that may predict changes in self-perceived balance within the first year of community reintegration. Methods. In this prospective study, 98 hemiparetic participants who could walk at least 10 m independently were assessed 1, 3, 6, and 12 months postdischarge from rehabilitation by the Berg Balance Scale, Timed Up and Go, 6-minute walking distance, and depression and anxiety scales. The 98 age-/sex-matched controls were assessed at enrollment and the same intervals. Multilevel modeling was used to determine if assessed covariates predicted changes in balance confidence by the Activities-Specific Balance Confidence Scale. Results. Stroke subjects had lower initial balance confidence than controls and showed a statistically significant increase in confidence over 1 year at each assessment. Poor balance and high state anxiety were associated with lower balance confidence. Significant interactions were observed between greater depression, along with more impaired walking capacity and balance tests, in predicting lower change trajectories in confidence. Falls predicted a reduced rate of improvement. Conclusions. Balance confidence after stroke remained lower than controls over the first year. Physical therapies and supportive interventions designed to treat confidence should be initiated at discharge from inpatient rehabilitation.

Theta Burst Stimulation in the Rehabilitation of the Upper Limb A Semirandomized, Placebo-Controlled Trial in Chronic Stroke Patients

A cooler name like theta probably makes  getting grants for repeating similar research easier.
http://nnr.sagepub.com/content/26/8/976.abstract?etoc

Abstract

Background. Noninvasive cortical stimulation could represent an add-on treatment to enhance motor recovery after stroke. However, its clinical value, including anticipated size and duration of the treatment effects, remains largely unknown. Objective. The authors designed a small semi-randomized clinical trial to explore whether long-lasting clinically important gains can be achieved by adding theta burst stimulation (TBS), a form of repetitive transcranial magnetic stimulation (TMS), to a rehabilitation program for the hand. Methods. A total of 41 chronic stroke patients received excitatory TBS to the ipsilesional hemisphere or inhibitory TBS to the contralesional hemisphere in 2 centers; each active group was compared with a group receiving sham TBS. TBS was followed by physical therapy for 10 working days. Patients and therapists were blinded to the type of TBS. Primary outcome measures (9-hole Peg Test [9HPT], Jebsen Taylor Test [JTT], and grip and pinch-grip dynamometry) were assessed 4, 30, and 90 days post treatment. The clinically important difference was defined as 10% of the maximum score. Results. There were no differences between the active treatment and sham groups in any of the outcome measures. All patients achieved small sustainable improvements—9HPT, 5% of maximum (confidence interval [CI] = 3%-7%); JTT, 5.7% (CI = 3%-8%); and grip strength, 6% (CI = 2%-10%)—all below the defined clinically important level. Conclusions. Cortical stimulation did not augment the gains from a late rehabilitation program. The effect size anticipated by the authors was overestimated. These results can improve the design of future work on therapeutic uses of TMS.

Effects of Fast Functional Exercise on Muscle Activity After Stroke

If I could do anything fast I would.
http://nnr.sagepub.com/content/26/8/968.abstract?etoc

Abstract

Background. In stroke rehabilitation, considerable emphasis is placed on improving muscle strength with less focus on the speed of movement. Muscle power (product of force and velocity) is essential for balance and mobility but velocity of movement is impaired after stroke. Objective. The purpose of this efficacy study is to determine if a single session of fast functional movements can increase muscle activation and the speed of movement in participants with a subacute stroke. Methods. In total, 32 individuals poststroke and 32 age- and sex-matched controls performed a single session of 50 fast squats and steps. Electromyographic (EMG) activity was measured bilaterally in the rectus femoris (RF), biceps femoris (BF), tibialis anterior (TA), and soleus muscles. The average EMG area and the movement speed were calculated over 10 trials. The effect of exercise was determined as the change from the second set (Start) to the last set (End) of 10 trials. Results. The stroke group had significant increases in EMG area of the TA, BF, and RF during the squatting exercise. There was an increase in EMG area of the RF and BF when the paretic leg was stepping. Improvements in EMG area of the soleus and RF when the paretic leg was in stance accompanied increases in EMG area when the nonparetic leg was stepping. There was a trend for improved movement speed for both exercises. Conclusion. A single session of exercises emphasizing speed of movement can be used to improve muscle activation in persons with mild to moderately severe strokes.

Amount of Exercise in the First Week After Stroke Predicts Walking Speed and Unassisted Walking

I bet with some additional  research  they could correlate penumbra damage with predictions on walking speed and that would be objective and repeatable.

Amount of Exercise in the First Week After Stroke Predicts Walking Speed and Unassisted Walking

Abstract

Background. 

 

Predicting walking outcomes poststroke is a challenge for clinicians.  

Objective. 

 

To identify the extent to which exercise dose (repetitions of leg movements) in the first week of a comprehensive stroke unit stay predicts discharge mobility.  

Methods. 

 

A cohort study was conducted on 200 consecutive people admitted to a comprehensive stroke unit who required physical therapy.  

Results. 

 

Discharge and predictor data were available for 191 survivors (99%). On admission, 86 participants were able to walk, and the average walking velocity was 0.42 m/s. On discharge, the average walking velocity was 0.77 m/s, and 152 participants were able to walk. A discharge walking velocity of greater than 0.8 m/s was predicted by the exercise dose achieved in the first week after admission. Adding other predictors did not significantly increase the predictive ability of the model. Completion of more than the median number of exercise repetitions (703) in the first week of admission was associated with a quicker recovery of unassisted walking. This effect persisted after adjustment for walking velocity on admission, cognition, and comorbidity.  

Conclusion. 

 

Exercise dose in the first week after admission for stroke is an important indicator of walking speed at discharge and the time to achieve unassisted walking.

Getting Neurorehabilitation Right What Can Be Learned From Animal Models?

And Dale Corbett is one of the authors.

Getting Neurorehabilitation Right What Can Be Learned From Animal Models?

Abstract

Animal models suggest that a month of heightened plasticity occurs in the brain after stroke, accompanied by most of the recovery from impairment. This period of peri-infarct and remote plasticity is associated with changes in excitatory/inhibitory balance and the spatial extent and activation of cortical maps and structural remodeling. The best time for experience and training to improve outcome is unclear. In animal models, very early (<5 and="and" conversely="conversely" damage.="damage." days="days" from="from" histological="histological" increased="increased" intense="intense" late="late" lead="lead" may="may" onset="onset" rehabilitation="rehabilitation" to="to" training="training">30 days) is much less effective both in terms of outcome and morphological changes associated with plasticity. In clinical practice, rehabilitation after disabling stroke involves a relatively brief period of inpatient therapy that does not come close to matching intensity levels investigated in animal models and includes the training of compensatory strategies that have minimal impact on impairment. Current rehabilitation treatments have a disappointingly modest effect on impairment early or late after stroke. Translation from animal models will require the following: (1) substantial increases in the intensity and dosage of treatments offered in the first month after stroke with an emphasis on impairment; (2) combinational approaches such as noninvasive brain stimulation with robotics, based on current understanding of motor learning and brain plasticity; and (3) research that emphasizes mechanistic phase II studies over premature phase III clinical trials.

Symptomatic therapy in multiple sclerosis: the role of cannabinoids in treating spasticity

I don't care if we accept workable clinical trials from Germany, if it works in MS lets test it in stroke survivors and get this done. Then we can get our states to allow medical marijuana. One step at a time but only if we as survivors demand it. Ask your doctor to sponsor such research and legislation. If I didn't have to fight spasticity all the time, recovering movement would be a breeze, contrary to Dr. William Landaus' opinion and research articles.

http://tan.sagepub.com/content/5/5/255.abstract?etoc=

Abstract

A large proportion of patients with multiple sclerosis (MS) have spasticity, which has a marked impact on their quality of life. Anecdotal evidence suggests a beneficial effect of cannabis on spasticity as well as pain. Recently, randomized, double-blind, placebo-controlled studies have confirmed the clinical efficacy of cannabinoids for the treatment of spasticity in patients with MS. Based on these data, nabiximols (Sativex), a 1:1 mix of Δ-9-tetrahydrocannabinol and cannabidiol extracted from cloned Cannabis sativa chemovars, received approval for treating MS-related spasticity in various countries around the globe. In this article we review the current understanding of cannabinoid biology and the value of cannabinoids as a symptomatic treatment option addressing spasticity in patients with MS.

How Does the Brain Recover After Stroke?

You have to read this bloggers description of what happens and then educate your doctor on it.
http://brainblogger.com/2012/09/05/how-does-the-brain-recover-after-stroke/
The last paragraph;
This study demonstrates that the brain is extremely capable at repairing itself, and suggests exciting new possibilities for improving recovery after traumatic brain injury and stroke in humans. Developing treatments that enhance this rewiring, sprouting and branching process may improve the likelihood of recovery for people who have lost cognitive or motor function due to injury.

Vitamin D supplement fails to lower cholesterol in short term

So ask your doctor what you should do.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=123605&CultureCode=en
Taking vitamin D supplements to compensate for vitamin D deficiency didn’t improve cholesterol — at least in the short term, according to new research in Arteriosclerosis, Thrombosis and Vascular Biology, an American Heart Association journal.
Researchers studied 151 people with vitamin D deficiency who received either a mega-dose (50,000 internationals units) of vitamin D3 or placebo weekly for eight weeks. Participants’ cholesterol levels were measured before and after treatment.
Correcting vitamin D deficiencies with high doses of oral vitamin D supplements did not change cholesterol levels, researchers found. This was despite effectively increasing vitamin D to recommended levels. Vitamin D levels nearly tripled in the group that received actual supplements, but were unchanged in the placebo group.
“Our study challenges the notion that vitamin D repletion improves cholesterol levels” said Manish Ponda, M.D., M.S., study lead author and assistant professor of clinical investigation in Dr. Jan Breslow’s laboratory of biochemical genetics and metabolism at The Rockefeller University in New York, N.Y. “These clinical trial results confirm those from a recent data mining study.”
The researchers also tested the effect of vitamin D supplementation on more sophisticated biomarker measures of cholesterol, such as particle size and number. “These measures of cholesterol, which are not used in routine clinical practice, also did not change in response to vitamin D therapy,” Ponda said.
As expected, replenishing subjects with high-dose supplements of oral vitamin D decreased parathyroid hormone levels and increased calcium levels — physical functional changes that were linked to participants’ increase in low-density lipoprotein (LDL, bad cholesterol).
“For example, participants receiving vitamin D who had an increase in calcium levels experienced a 7 percent increase in LDL cholesterol, while those whose calcium levels fell or did not change had a 5 percent decrease in LDL cholesterol,” Ponda said.
The study questions the use of vitamin D supplements to improve cholesterol, Ponda said. While the dose of vitamin D in this study was high, it was appropriate for correcting a vitamin D deficiency over an eight week period.
However, longer-term studies on the impact of the changes in LDL cholesterol as a result of high dose vitamin D supplementation are needed to make stronger recommendations. And questions remain about whether increasing vitamin D levels with exposure to sunlight, the predominant natural source, would have a different effect than with high-dose oral supplements.
To address these issues, Ponda and Breslow will begin another clinical trial this fall, comparing the effect of oral vitamin D to ultraviolet light exposure with a longer follow-up period.

I am however taking this because it might help fatigue. 
Or maybe to prevent muscle atrophy.
Or fall prevention.

Statins are killers and cause major artery damage, say researchers

Inflammatory article from WDDTY - What Doctors don't tell you.
http://www.wddty.com/statins-are-killers-and-cause-major-artery-damage-say-researchers.html
The abstract this is based on is here; unless the complete study says something different, I don't see it.

Progression of Vascular Calcification Is Increased With Statin Use in the Veterans Affairs Diabetes Trial (VADT).

Ask your doctor to clarify.

Exercises to Target Specific Hamstring Muscles

There is no way I can even summarize  this so ask your therapist  to put it into  understandable words if your hamstring needs help.
http://sportsmedresearch.blogspot.com/2012/08/hamstring-exercise-rankings.html

Blood Sugar Levels Linked to Brain Loss

We've already had enough brain loss so make sure your doctor doesn't allow any more of your brain to be lost.
http://www.medpagetoday.com/Neurology/GeneralNeurology/34588
Higher blood glucose levels were associated with brain atrophy among healthy individuals in their early 60s, even when levels remained within the official normal range, an Australian study demonstrated.
After adjustment for age, sex, body mass index (BMI), hypertension, alcohol use, smoking, and APOE genotype, the associations between glucose and left and right hippocampal volumes were −131 and −148 (P=0.001 for both), with a positive association reflecting less atrophy, according to Nicolas Cherbuin, PhD, of Australian National University in Canberra, and colleagues.

The rest at the link.

Moving Physical Therapy Forward

You can listen to Joseph Brence, DPT talk about the need for PTs to have evidence to  support their therapy. This was talked about here in 1994 by Carr and Shepherd. Why should he have to repeat this 18 years later?
http://pttalker.com/2012/09/moving-physical-therapy-forward/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+PtTalker+%28PT+Talker%29
But then we might not get any therapy at all, for those like me who have large areas of dead brain, What will therapists provide as evidence? I remember my OT telling me that studies showed that survivors that didn't have this type of finger movement wouldn't recover finger movement. I still do not have finger movement  but she kept trying and I will eventually prove it can be done.

Researchers Compare Walking Ability of Post-Stroke Patients and Non-Disabled Adults

Something  we should have had for years, evidence-based practice.
http://www.ptproductsonline.com/news/2012-09-06_01.asp
Individuals with stroke have reduced walking activity, although it is unknown whether this deficit is due to a reduction in all aspects of walking activity or only in specific areas. Researchers from Delaware and Maine performed a study to examine the walking activity in post-stroke individuals compared with older adults without disability. The results were published in the September 2012 issue of Physical Therapy. 
Margaret A. Roos, PT, DPT, PhD, NCS, from the department of physical therapy at the University of Delaware, Newark, Del, led the cross-sectional study of 54 post-stroke participants and 18 older adults reported as having no disability. All participants wore a step activity monitor for 3 days, which calculated steps per day (SPD), bouts per day (BPD), steps per bout (SPB), total time walking per day (TTW), percentage of time walking per day (PTW), and frequency of short, medium, and long walking bouts.
The researchers classified 29 participants as household and limited community ambulators (HHA-LCA group) and 22 participants as unlimited community ambulators (UCA group). According to the results, the SPD, TTW, PTW, and BPD measurements were the greatest in the older, non-disabled adults and the lowest in the HHA-LCA group. In addition, walking in the short, medium, and long categories was found to be lowest in the HHA-LCA group, greater in the UCA group, and greatest in the non-disabled group.
The specific descriptors of walking activity presented can provide insight into walking deficits post-stroke that cannot be determined by looking at steps per day alone. The researchers stress the need to analyze the structure of walking activity, concluding that the deficits found during this study could be addressed through appropriate exercise prescription.

What is your stroke protocol?

Definition:  The plan for a course of medical treatment or for a scientific experiment.

Isn't this by definition what Physiatrists or PM&R doctors supposed to do? Or is yours like mine was; hand you off to the therapists with ET, evaluate and treat, nothing scientific there and no way to monitor progress against your goals. You did discuss your goals with your doctor, didn't you? 100% recovery. I had no goal discussion with my doctor.
Wouldn't you think that stroke rehab would have the same type of detail as below?

Check out what colon cancer has from  Medscape
http://emedicine.medscape.com/article/2005487-overview

Adjuvant chemotherapy for patients with resectable colon cancer

Stage 0 and I:

• Patients do not require adjuvant therapy

Adjuvant chemotherapy for resectable colon cancer

Stage IIA, B and C (node-negative)^{[1, 2, 3]} :
The value of adjuvant therapy in stage II disease is at best controversial; however, the following regimens may be used:

• Capecitabine 1250 mg/m² PO BID on days 1-14; repeat cycle every 21d for 8 cycles or
• Leucovorin 500 mg/m² given as a 2-h infusion and repeated weekly for 6wk plus  5-fluorouracil (5-FU) 500 mg/m² given as a bolus 1h after the start of leucovorin and repeated 6 times weekly; every 8wk for 4 cycles or
• Leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU bolus 400 mg/m², then  1200 mg/m²/day for 2d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk

Stage II adjuvant chemotherapy in high-risk or intermediate-risk patients:
Adjuvant therapy for high-risk patients with stage II is an option, and common regimens include use of 5-FU and leucovorin with or without oxaliplatin or capecitabine.^[1]

• mFOLFOX6: Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2d continuous infusion; repeat every 2wk or
• FLOX: 5-FU 500 mg/m² IV weekly plus  leucovorin 500 mg/m² IV weekly for 6wk (days 1, 8, 15, 22, 29, and 36) of each 8-wk cycle plus  oxaliplatin 85 mg/m² IV administered on days 1, 15, and 29 of each 8-wk cycle for 3 cycles or
• Capecitabine 1250 mg/m² PO BID on days 1-14; repeat cycle every 21d for 8 cycles

Adjuvant therapy for resectable cancer

Stage III (node-positive)^{[2, 3]} :
The following regimens are acceptable adjuvant therapies for stage III disease for resectable colon cancer:

• mFOLFOX6: Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk or
• FLOX: 5-FU 500 mg/m² IV weekly plus  leucovorin 500 mg/m² IV weekly for 6wk (days 1, 8, 15, 22, 29, and 36) of each 8-wk cycle plus  oxaliplatin 85 mg/m² IV administered on days 1, 15, and 29 of each 8-wk cycle for 3 cycles or
• Capecitabine 1250 mg/m² PO BID on days 1-14; repeat cycle every 21d for 8 cycles or
• CapeOx: Oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² PO BID on days 1-14 every 3wk for 8 cycles or
• Leucovorin 500 mg/m² given as a 2-h infusion and repeated weekly for 6wk plus  5-FU 500 mg/m² given as a bolus 1h after the start of leucovorin and repeated 6 times weekly; every 8wk for 4 cycles or
• Leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU bolus 400 mg/m², then  1200 mg/m²/day for 2d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk

Neoadjuvant therapy for resectable metastatic disease

Neoadjuvant therapy for resectable metastatic disease is usually administered for approximately 2-3mo, limiting the development of hepatotoxicity.^[3] Regimens for adjuvant and neoadjuvant therapy are similar.

• mFOLFOX6: Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk or
• FOLFIRI: Irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk
• CapeOx with or without bevacizumab: Oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² PO BID for 14d; repeat every 3wk plus bevacizumab 7.5 mg/kg IV every 3wk

Chemotherapy for advanced or metastatic disease

Stage IV:
Chemotherapy for advanced or metastatic disease includes the use of multiple drugs as single agents or as combination regimens.^{[4, 5, 6, 7, 8, 9]}
First-line chemotherapy for bevacizumab candidates:

• mFOLFOX6 plus bevacizumab: Bevacizumab 5 mg/kg over 30-90min on day 1 plus  oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk for 4-6 cycles with reevaluation for maintenance therapy (1 g of calcium gluconate and 1 g of magnesium sulfate may be give over 15min preinfusion and postinfusion to reduce the risk of neurotoxicity) or
• FLOX plus bevacizumab: Bevacizumab 5 mg/kg over 30-90min on days 1, 15, and 29 plus  oxaliplatin 85 mg/m² on days 1, 15, and 29 plus  leucovorin 500 mg/m² on days 1, 8, 15, 22, 29, and 36 plus  5-FU 500 mg/m² on days 1, 8, 15, 22, 29, and 39 for 2 cycles followed by reevaluation or
• FOLFIRI plus bevacizumab: Bevacizumab 5 mg/kg over 30-90min on day 1 plus  irinotecan 180 mg/m² IV over 30-90 min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4-6 cycles with reevaluation for maintenance therapy or
• CAPEOX plus bevacizumab: Bevacizumab 7.5 mg/kg over 30-90min on day 1 plus  oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² PO BID for 14d; repeat every 21d for 4 cycles followed by reevaluation for maintenance therapy or
• Capecitabine plus bevacizumab (in patients not able to undergo treatment with oxaliplatin or irinotecan): Bevacizumab 7.5 mg/kg on day 1 plus  capecitabine 1250 mg/m² PO BID for 14d; repeat cycle every 21d for 8 cycles, then  reevaluate for maintenance or
• DeGramont regimen plus bevacizumab (in patients not able to undergo treatment with oxaliplatin or irinotecan): Bevacizumab 5 mg/kg over 30-90min on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU bolus 400 mg/m², then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4-6 cycles with reevaluation for maintenance therapy or
• Bevacizumab plus 5-FU and leucovorin (Roswell Park) (in patients unable to undergo treatment with oxaliplatin or irinotecan): Bevacizumab 5 mg/kg over 30-90min on day 1 plus  leucovorin 500 mg/m² over 2h plus  5-FU 500 mg/m² bolus every 2wk for 4-6 cycles with reevaluation for maintenance therapy

First-line chemotherapy for patients who are not candidates for bevacizumab^{[7, 8, 9, 10]} :

• mFOLFOX6: Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk for 4 cycles or
• FLOX: Oxaliplatin 85 mg/m² on days 1, 15, and 29 plus  leucovorin 500 mg/m² on days 1, 8, 15, 22, 29, and 36, followed by 5-FU 500 mg/m² on days 1, 8, 15, 22, 29, and 39 for 2 cycles followed by reevaluation or
• FOLFIRI: Irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4 cycles or
• Capecitabine: Capecitabine 1250 mg/m² PO BID on days 1-14; repeat cycle every 21d until progression or
• Roswell Park regimen: Leucovorin 500 mg/m² IV weekly for 6wk over 2h followed by 5-FU 500 mg/m² IV bolus weekly for 6wk; repeat cycle every 8wk or
• CapeOx: Oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² BID for 14d every 21d for 4 cycles followed by reevaluation for maintenance therapy or
• mFOLFOX6 plus cetuximab (only for KRAS wild-type tumors): Cetuximab 400 mg/m² loading dose on day 1, then  cetuximab 250 mg/m² weekly plus  oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk for 4 cycles, then reevaluate or
• FOLFIRI plus cetuximab (only for KRAS wild-type tumors): Cetuximab 400 mg/m² loading dose over 2h on day 1, then  cetuximab 250 mg/m² over 1h weekly plus  irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4 cycles, then reevaluate or
• Referral for clinical trial

Second-line chemotherapy for metastatic disease^{[11, 12, 13]} :

• FOLFIRI (if FOLFOX, CapeOx, CapeOx plus bevacizumab or FOLFOX plus bevacizumab used as first-line chemotherapy): Irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4 cycles, then reevaluate or
• FOLFIRI plus cetuximab (only for KRAS wild-type tumors and if FOLFOX, CapeOx, CapeOx plus bevacizumab or FOLFOX plus bevacizumab used as first–line chemotherapy): Cetuximab 400 mg/m² loading dose over 2h on day 1, then  cetuximab 250 mg/m² over 1h weekly plus  irinotecan 180 mg/m² IV over 30-90min on day 1 plus  leucovorin 400 mg/m² IV infusion to match duration of irinotecan infusion on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d (total 2400 mg/m² over 46-48h) continuous infusion; repeat every 2wk for 4 cycles and then reevaluate or
• mFOLFOX6 (if FOLFIRI or FOLFIFI plus bevacizumab used as first-line chemotherapy): Oxaliplatin 85 mg/m² IV over 2h on day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2-d continuous infusion; repeat every 2wk for 4 cycles or
• CapeOx: Oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² BID for 14d every 21d for 4 cycles followed by reevaluation for maintenance therapy or
• mFOLFOX6 plus cetuximab (only for KRAS wild-type tumors and if FOLFIRI or FOLFIRI plus bevacizumab used as first-line chemotherapy): Cetuximab 400 mg/m² loading dose on day 1 over 2h, then  cetuximab 250 mg/m² over 1h weekly plus  oxaliplatin 85 mg/m² IV over 2h day 1 plus  leucovorin 400 mg/m² IV over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1, then  1200 mg/m²/day for 2d continuous infusion; repeat every 2wk for 4 cycles and then reevaluate or
• Irinotecan 125 mg/m² over 90min weekly with reevaluation after 8wk or
• Cetuximab 400 mg/m² over 2h on day 1, then  250 mg/m² over 1h weekly with reevaluation after 8wk or
• Panitumumab 6 mg/kg over 60-90min every 2wk with reevaluation after 8wk or
• Modified FOLFOX6 plus bevacizumab (if FOLFIRI used upfront and bevacizumab never used as first-line chemotherapy; note higher dose of bevacizumab as second-line chemotherapy): Bevacizumab 10 mg/kg over 30-90min on day 1 plus  oxaliplatin 85 mg/m² over 2h on day 1 plus  leucovorin 400 mg/m² over 2h plus  5-FU 400 mg/m² IV bolus on day 1, followed by 5-FU 2400 mg/m² IV continuous infusion over 46h every 2wk for 4-6 cycles with reevaluation for maintenance therapy (1 g of calcium gluconate and 1 g of magnesium sulfate may be give over 15min preinfusion and postinfusion to reduce the risk of neurotoxicity) or
• CAPEOX plus bevacizumab (if FOLFIRI used upfront and bevacizumab never used as first-line chemotherapy; note higher dose of bevacizumab as second-line chemotherapy): Bevacizumab 15 mg/kg over 30-90min on day 1 plus  oxaliplatin 130 mg/m² over 2h on day 1 plus  capecitabine 1000 mg/m² BID for 14d every 21d for 4 cycles followed by reevaluation for maintenance therapy or
• FOLFIRI plus bevacizumab (if FOLFOX or CAPEOX used upfront and bevacizumab never used as first-line chemotherapy): Bevacizumab 10 mg/kg over 30-90min on day 1 plus  irinotecan 180 mg/m² over 90min on day 1 plus  leucovorin 400 mg/m² over 2h on day 1 plus  5-FU 400 mg/m² IV bolus on day 1 followed by 5-FU 2400 mg/m² IV continuous infusion over 46h every 2wk for 4-6 cycles with reevaluation for maintenance therapy or
• Aflibercept 4 mg/kg IV infused over 1 hr q2weeks plus FOLFIRI in mCRC resistant to or has progressed after an oxaliplatin regimen; administer before any component of FOLFIRI regimen on the day of treatment
• Referral for clinical trial

Note: In the above regimens, cetuximab can be replaced with panitumumab at 6mg/kg every 2wk if anaphylaxis is experienced with cetuximab.
Third-line chemotherapy for metastatic disease:

• Panitumumab 6 mg/kg over 60-90min every 2wk for KRAS wild-type tumors only with reevaluation after 8wk or
• Any regimen incorporating an EGFR antibody for patients with KRAS wild-type disease using a cytotoxic backbone not previously tried or
• Referral for clinical trial

Summary of guiding principles in the treatment of metastatic colorectal cancer

• Importance of differentiating between M1a (1 organ site of metastatic disease) and M1b (more than 1 organ site) in view of curative potential of 1 organ site
• Selection of oxaliplatin or irinotecan as part of cytotoxic backbone upfront in metastatic disease is based primarily on toxicity profile
• Bevacizumab improves survival as first-line and second-line therapy and works with irinotecan- and oxaliplatin-based therapy
• Addition of bevacizumab to irinotecan, fluorouracil, and leucovorin (IFL) significantly improved the response rate, overall survival, and progression-free survival
• The addition of bevacizumab to fluorouracil-based combination chemotherapy results in statistically significant and clinically meaningful improvement in survival among patients with metastatic colorectal cancer
• Interruption in therapy is not ideal for patients; some form of therapy should always be continued after a stable disease state is obtained
• Single-agent maintenance bevacizumab may be a feasible option for patients receiving bevacizumab + CapeOx as induction therapy
• There are no data on maintenance anti-EGFR therapy
• Anti-EGFR antibody therapy should be given only to patients with KRAS wild-type tumors
• Anti-EGFR antibody therapy and bevacizumab should never be combined
• Progression-free survival (PFS) and overall survival (OS) in randomized clinical trials using both FOLFOX and FOLFIRI cytotoxic backbones has been improved only in those patients with KRAS wild-type tumors
• The data on BRAF status are still preliminary in terms of predictive value, but there is a suggestion that even in the setting of KRAS wild-type tumors, BRAF mutation abrogates the effect of anti-EGFR antibody therapy; it is, however, prognostic of a worse outcome
• Optimal use of all therapeutic agents improves survival in patients with metastatic disease
• It is reasonable to leave the primary therapy in place and start treatment for metastatic disease
• A multidisciplinary approach is necessary to deal with the complicated issue of potentially resectable or marginally resectable metastatic disease
• Pharmacogenomics profiling beyond KRAS mutation status is not yet standard of care

Etiologic work-up crucial after stroke

Etiology is the study of causation, or origination. The word is derived from the Greek αἰτιολογία, aitiologia, "giving a reason for". And after the workup they should put that into a stroke causation database so  everyone can read about it.
 http://www.news-medical.net/news/20120905/Etiologic-work-up-crucial-after-stroke.aspx

Connexin 36 Promotes Cortical Spreading Depolarization and Ischemic Brain Damage

What is the logical conclusion after this research and what theory can be tested  to help survivors?

Connexin 36 Promotes Cortical Spreading Depolarization and Ischemic Brain Damage

Abstract

Cortical spreading depolarization (CSD) promotes the progression of neuronal injury after cerebral ischemia. However, the mechanisms of propagation of postischemic CSD events are still unclear. In this study we characterized the role of the main neuronal gap junction protein connexin 36 (Cx36) in generating postischemic CSDs.

In Cx36-deficient mice and controls we occluded the distal middle cerebral artery. To detect CSD events we recorded the direct current and laser Doppler flow. In addition, locomotor function and the infarct size were determined.

Cx36-deficient mice had significantly fewer and shorter CSD events than wild-type controls. Additionally, Cx36 deletion is neuroprotective, leading to a better functional outcome and decreased infarct size after ischemia.

These results suggest a detrimental role for Cx36 after ischemia, possibly by promoting CSD.

Tests for silent neck artery narrowing to curb stroke risk: Waste of resources

Well are there other options? like;
Do you want the lawnmower?
http://www.articlecity.com/videos/health/Lawnmower-For-Clogged-Arteries-175286465.php
Or Drano? I would be worried about this, sloughing off chunks
http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=26404
 and the waste of resources here:
http://www.sciencecodex.com/tests_for_silent_neck_artery_narrowing_to_curb_stroke_risk_waste_of_resources-97904
This was the starting point of my stroke and could have been solved if when my Dad was diagnosed with 85% blockage his doctor had recommended that any children get tested, At the time of my stroke it was estimated at 85 % blockage(This was 3 years later) when an ultrasound was done and I found out that the right carotid was totally blocked. The blockage was never found during my hospital stay. I consider that a complete failure on my doctors part. I luckily did not have any further strokes during that 3 year window of high danger.

Who Best to Create a Sense of Urgency for Acute Stroke Treatment? Commentary on “Neurohospitalists Improve Door-to-Needle Times for Patients With Ischemic Stroke Receiving Intravenous tPA”

I'm sorry but the urgency  they are trying to create to speed up tPA time is the wrong focus. A separate and just as important focus should be to find multiple ways to stop the neuronal cascade of death. And that will have to come from survivors. 17 years to find  out that tPA is hard to implement is a colossal failure. Fire them and put survivors in charge if you want something done. 

http://nho.sagepub.com/content/2/4/117.full?etoc

In the 17 years since the efficacy of intravenous tissue plasminogen activator (tPA) for acute ischemic stroke was first established,¹ we have struggled to develop the infrastructures and systems of care that are necessary to deliver this therapy as quickly and efficiently as possible.

Speed matters. Although delays in presenting to the emergency department account for most of the unrealized potential of thrombolysis,² the time from when a patient arrives in the emergency department to when the tPA infusion begins—the door-to-needle time—presents a more readily accessible target for hospital-level interventions. Pooled data from 6 randomized trials³ and analyses of large observational data sets⁴ consistently show that faster door-to-needle times are associated with better patient outcomes. In fact, each 15-minute decrease in door-to-needle time is associated with a 5% lower odds of in-hospital mortality.⁴ Therefore, the American Heart Association: Target Stroke initiative has set a specific goal of raising the percentage of patients treated within 60 minutes from the current level of 29% to over 50%.⁴

Precisely how to actually achieve this goal involves evaluating a variety of factors, but certainly one important consideration is ensuring that appropriate staffing is available for these neurological emergencies. In this issue of The Neurohospitalist, Bhatt and Shatila examine the impact of neurohospitalists on door-to-needle times for acute ischemic stroke.⁵ The study includes data from 107 consecutive patients treated with intravenous (IV) tPA at 2 community hospitals between July 2009 and September 2011. The study was a natural experiment of sorts: halfway though the study period, coverage for acute stroke calls from the emergency department changed from a rotating schedule of 4 community neurologists with shared inpatient and outpatient responsibilities to a neurohospitalist model staffed by 2 inpatient-based neurologists. Occasional weekend coverage continued to be provided by locums tenens and community neurologists.

The primary finding was that among patients treated with IV thrombolysis for stroke, 51% (24 of 47) of those evaluated by neurohospitalists were treated in 60 minutes or less, compared with 15% (9 of 60) of those evaluated by nonneurohospitalists—a difference that may be due, at least in part, to the greater likelihood that a neurohospitalists is in hospital for an emergency in-person consultation.

Bhatt and Shatila are generally careful not to assert a causal relationship between a neurohospitalist’s involvement and faster door-to-needle times, with the notable exception of the article’s title. Such caution is warranted. First, there are likely to be unmeasured confounders and secular trends at play. For example, a t test comparing the mean performance of the 2 groups may obscure a secular trend of improved door-to-needle times over time. Other analytic methods such as interrupted time series analysis are often used to mitigate this possibility in other quality improvement studies. Next, relevant details on how the availability of neurohospitalists would actually impact the response time are unavailable. These details would be especially important to understand and evaluate because the acute stroke response involves interactions between multiple disciplines—not just the neurohospitalist—and since shared knowledge and best practices at the team- or hospital-level would be expected to diffuse to the care of all patients over time. Finally, upward of 90% of the observed difference was driven by the performance of the neurohospitalist with specific certification in vascular neurology—someone with both the experience and interest to shepherd the performance improvement seen here.

So can we attribute these improvements to neurohospitalist staffing, to vascular neurology training, or perhaps to the involvement of a motivated, invested, and accountable champion for change regardless of specialty? I would say that what probably matters most is the watchful eye and the sustained involvement of someone with an interest in improving these processes and outcomes—a motivated neurohospitalist may be ideally situated to take on this role.

New technique helps determine degree of muscle wasting in critically ill patients

While we as stroke patients may not be critically ill we do have muscle wastage that should be objectively measured and come up with ways to correct it. So ask your doctor what they are doing about this problem. I know I had this because my AFO got looser rather rapidly and my doctor never checked on it.
 http://www.alphagalileo.org/ViewItem.aspx?ItemId=123625&CultureCode=en
 Researchers have identified a new technique that can help determine the severity of muscle loss in critically ill patients. The breakthrough could lead to new research to help prevent muscle-wasting and new therapeutic interventions to help treat critically ill patients.
The results of the study will be presented today (2 September 2012) at the European Respiratory Society’s Annual Congress in Vienna.
Patients who are critically ill with multi-organ failure often have significant muscle wasting after recovering from their illness. This can delay their discharge from an intensive care unit and is a major cause of disability affecting quality of life once patients have left the hospital.
Until now, there has been no clinically useful way of measuring muscle wastage, or identifying patients who are at a high-risk of this. The researchers hypothesised that they could measure the rectus femoris, one of the four quadriceps muscles in the leg, to determine the level of muscle wasting.
63 patients were recruited to the study within 24 hours of admission to hospital. Muscle wasting was assessed using an ultrasound to measure muscle circumference of the rectus femoris. Researchers also monitored the number of failed organ systems during the patient’s time in intensive care, to assess which patients were at a high risk of muscle wasting.
The researchers determined that circumference measurements of the rectus femoris area by ultra sound can objectively track muscle loss early in critical illness. They also determined that the greatest reduction in muscle circumference was seen in patients with multi-organ failure. In patients with multi-organ failure, the circumference of the rectus femoris was reduced by approximately 21.53%. This compared with an approximate reduction of 7.2% in people with single organ failure.
Lead author, Dr Zudin Puthucheary from University College London, UK, said: “Our research has determined that measuring the rectus femoris using ultrasound is a useful tool to analyse the degree of muscle wasting in critically ill patients. This is clinically relevant as it can help healthcare professionals detect those at high-risk of muscle loss and provide interventions to help improve their quality of life. It is also an important discovery for research as it can help scientists track muscle response to different interventions, so we can find new solutions to addressing this problem in our critically ill patients.”

Fly through the brain of a mouse

Ok, not too useful for us but the eventual possibilities for understanding our brains are great.
http://www.newscientist.com/blogs/nstv/2012/09/matrix-like-fly-through-shows-brain-in-amazing-detail.html?

Aqua-wheelchair performs flips underwater

Ask your therapist for this. I could easily see the fantastic therapeutic stroke rehab possibilities. I would have been able to reduce the spasticity preventing me from raising my left arm. That alone  would make it cost feasible.
http://www.newscientist.com/blogs/nstv/2012/08/aqua-wheelchair-performs-flips-underwater.html?

Statins linked with development of cataracts

Another discussion point with your doctor, if you are keeping track I'll be indexing all of statin side effects under that name  for your ease of doctor questioning.
http://www.theheart.org/article/1434435.do?utm_medium=email&utm_source=20120903_TopTen&utm_campaign=newsletter
Statin users are more than 50% likelier to develop age-related cataracts, according to the results of a new study [1]. And type 2 diabetics who use statins are at even greater risk of cataracts, report investigators.

"The bioplausibility of these results lies in the fact that the crystalline lens membrane requires high cholesterol for proper epithelial cell development and lens transparency," write Dr Carolyn Machan (University of Waterloo, ON) and colleagues in the August 2012 issue of Optometry and Vision Science. "Increased cataract formation has been seen in both animals and humans with hereditary cholesterol deficiency, and the risk exists that statins can inhibit cholesterol biosynthesis in the human lens."

Asked to comment on the paper for heartwire, Dr Richard Karas (Tufts University School of Medicine, Boston, MA), called the findings "an interesting observation [that] isn't alarmist." There is, he says, a "suggestion" here that statins may increase the risk of cataracts, but this visual problem eventually afflicts everyone of a certain age anyhow, he says, adding that further study of this association will be required.

Waterloo Eye Study includes almost 6500 patients

The analysis included 6397 patients with and without diabetes. As the researchers note, diabetes is a risk factor for the development of cataracts, leading the group to analyze the prevalence of cataracts among patients with diabetes taking statins (n=452) and the prevalence among those taking statins but without diabetes (n=5884). The mean age of patients with diabetes was 14 years older than those without diabetes and included a slightly higher proportion of female subjects. The prevalence of statin use in patients 38 years of age and older was 56% for those with type 2 diabetes and 16% for those without diabetes.

In the study, known as the Waterloo Eye Study, diabetes was associated with an 86% higher risk of developing cataracts (odds ratio [OR] 1.86; 95% CI 1.34-2.59) across the lifespan after researchers controlled for multiple variables, including age, female sex, smoking, and blood pressure. A diagnosis of diabetes was also associated with an increased risk of different subtypes of cataracts: an 84% greater risk of nuclear sclerosis, a 38% higher risk of cortical cataract, and a 52% rise in posterior subcapsular cataract

Statin use was also associated with a significantly increased risk of developing age-related cataracts (OR 1.57; 95% CI 1.15-2.13) and some subtypes, including a 48% higher risk of nuclear sclerosis and a 48% rise in posterior subcapsular cataract but no increased risk of cortical cataract.

In an analysis of cataract prevalence among patients with and without diabetes taking statins, Machan and colleagues found that the prevalence of cataract increased at a faster rate in patients with diabetes who used statins. "Similar prevalence levels were seen in patients with diabetes who did not use statins and in patients without diabetes who did use statins," according to the researchers. "The prevalence of cataract increased at the slowest rate in patients without diabetes who did not use statins."

Are you on your own for stroke recovery?

Did your doctor and therapists not have a plan B? Then your plan B will have to be Steven Wolfs contention, 'Stroke patients need to rely more on their own problem solving to regain mobility', I can't give you any medical advice but if you read all the entries in my blog, wink,wink, you might be able to figure what to do to continue your recovery. Your recovery can continue as long as you keep working at it. I'm going to be doing this till the day I die.

Muscle action and explanation for stroke rehab

I'm sure your therapists throw a lot of muscle names at you. This site can explain what they are referring to and for those of the do-it-yourself plan  you can use it for your mental imagery and action observation.
http://www.getbodysmart.com/
My first lookup was the latissimus dorsi to find out which muscle is causing me so much grief in trying to raise my arm due to spasticity. And as Steven Wolf says, 'Stroke patients need to rely more on their own problem solving to regain mobility',  this would be a good start for your problem solving.

Red Meat Consumption and Risk of Stroke: A Meta-Analysis of Prospective Studies.

And even our American Heart Association promotes the conflating of corellation and causation. They should be working on figuring out how to stop the neuronal cascade of death. How about it, Ms. Nancy Brown?
http://www.ncbi.nlm.nih.gov/pubmed/22851546

Stroke. 2012 Jul 31. [Epub ahead of print]

Abstract

BACKGROUND AND PURPOSE:

Prospective studies of red meat consumption and risk of stroke have provided inconsistent results. We performed a meta-analysis to summarize the evidence regarding the effects of red meat (fresh, processed, and total) consumption on stroke risk. (Where's the hard work stopping neuronal death?)

METHODS:

Studies were identified by searching the PubMed database through May 26, 2012, and by reviewing the reference lists of retrieved articles. Prospective studies that reported relative risks (RR) with 95% confidence intervals (CI) for the association between red meat consumption and risk of stroke were eligible.

RESULTS:

Five articles including results from 6 prospective studies with 10ü630 cases of stroke and 329ü495 participants were included in the meta-analysis. For each serving per day increase in fresh red meat, processed meat, and total red meat consumption, the RR (95% CI) of total stroke were 1.11 (1.03-1.20), 1.13 (1.03-1.24), and 1.11 (1.06-1.16), respectively, without heterogeneity among studies (P>0.16). Among 4 articles with results for stroke subtypes, the risk of ischemic stroke was positively associated with consumption of fresh red meat (RR, 1.13; 95% CI, 1.00-1.27), processed meat (RR, 1.15; 95% CI, 1.06-1.24), and total red meat (RR, 1.12; 95% CI, 1.05-1.19); no statistically significant associations were observed for hemorrhagic stroke.

CONCLUSIONS:

Results from this meta-analysis indicate that consumption of fresh red meat and processed red meat as well as total red meat is associated with increased risk of total stroke and ischemic stroke, but not hemorrhagic stroke.

Eating small bar of chocolate cuts risks of stroke in men

I hate these articles, correlation does not prove causation. And it dumps all responsibility for preventing stroke damage on the patient. Rather than doing the hard research necessary to prevent the neuronal cascade of death. I expect better from our researchers and no one is calling out them on their taking the easy way out.
http://www.healthcareglobal.com/administration/eating-small-bar-of-chocolate-cuts-risks-of-stroke-in-men

According to a new study, eating a small bar of chocolate every week can considerably lessens the risk of stroke in men. The study conducted on more than 37,000 Swedish men showed that those eating chocolates were least likely to have a stroke.  

Other studies have suggested that eating chocolate can definitely improve the health of the heart.  The participants of the study were asked about their habits of eating and for a decade their health was monitored.  

Based on the amount of chocolate, they were split into four groups, with the bottom group eating, on average, no chocolate each week. Meanwhile, the top group had 63 grams, slightly more than an average bar. Study also found that those eating the most chocolate were 17% less likely to have a stroke.  

Prof Susanna Larsson, said, “The beneficial effect of chocolate consumption on stroke may be related to flavonoids in the chocolate.” “Flavonoids appear to be protective against cardiovascular disease through antioxidants, anti-clotting and anti-inflammatory properties,” said Prof Susanna.  

The study also stated that milk chocolate was ideal option in Sweden and the dark chocolate has been linked to benefits for the heart in the past.

Dr. Clare Walton, from the Stroke Association, UK said, “Past research has shown that eating dark chocolate might go some way to reduce your stroke risk if it’s eaten as part of a healthy, balanced diet.”  Or maybe richer/healthier persons can afford to buy dark chocolate.

Dr Walton also said, “This study suggests that eating a moderate amount of other types of chocolate could also be beneficial in men.”  It is sensible enough to understand that eat chocolates in moderation as it contains high sugar and fat content.

Chocolate is a raw or processed food produced from the seed of tropical Theobroma cacao tree. It mostly comes in dark, milk, and white varieties with cocoa solids and contributes to brown coloration.

My theory on motor recovery - stroke rehab

I put this out there with no professional background, borrowed from Cassalita and my original OT on eccentric vs. concentric contractions.Most therapists focus on functional recovery because that's what they are paid for. From some questions directed to me, a lot of survivors have a specific movement they want to recover - not necessarily functional. And no one is giving them any help in planning out how to recover that.  And as Steven Wolf says, 'Stroke patients need to rely more on their own problem solving to regain mobility', Prerequisites are a decent muscle anatomy or body-building book or anatomy software that shows the complete range of movement of the muscles you are interested in. My example is the bicep.
1. First you need to see where you have some control. straighten your arm out, see if you can exert force at any point in the contraction phase, this might entail having someone lift your arm up bit by bit to see if you have some muscle control at any point, try this standing and lying down. That determines if you have some concentric contractions. Then get the lower arm to 90 degrees to your body and try to lower it. You may need someone to pull on your hand to tell if you can resist. That determines if you have eccentric contractions.
2. If you have control at any point, start there and move it back and forth, thousands to millions of times.
3. If that doesn't produce anything it's time to go to the dead brain recovery options - these are not really proven yet and some can be quite dangerous(videos and mirrors)
    a. Mental imagery
    b. Passive movement
    c. Mirror therapy
    d. Thermal therapy
    e. Action observation
4. If 3 works go back and repeat 1 and 2.

Remember, this is not for personal use, ask your doctors and therapists for validation first.

If your doctor or therapist has given you something better, please post it, it must be worth a lot since it is not public information.