Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 481 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

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

Saturday, February 6, 2016

Computer models deliver stroke care boost to South West - Devon, UK

This is wonderful, yet tPA has only a 12% full success rate so survivors are still screwed 88% of the time. In a normal world would you ever go to a doctor that can only cure you 12% of the time?
People who have had a stroke in Devon are receiving faster and more effective treatment thanks to research that has used the latest advances in computer simulation.
The ground-breaking project has led to a dramatic increase in the number of patients receiving vital clot-busting treatment, and significantly reduced treatment times.
Researchers from the NIHR CLAHRC South West Peninsula (PenCLAHRC) teamed up with the Royal Devon & Exeter Hospital and the South Western Ambulance Service NHS Foundation Trust to implement the study, which has highlighted the importance of speed when treating people with stroke.
For some patients whose stroke is due to a blood clot (known as ‘ischaemic stroke’), giving emergency treatment to break down the clot can limit brain damage and reduce the likelihood of disability.
To find ways to speed up this process, researchers created a detailed computer simulation of the path stroke patients follow in the hospital, replicating the journey from onset of the condition right through to the point of treatment.
They then used this model to identify and test possible improvements to the system, exploring a range of different scenarios. With several new initiatives established – such as paramedics calling stroke unit specialists ahead of their arrival – the team implemented their findings at the Royal Devon & Exeter Hospital.
The results of the project have been remarkable.
The number of people receiving clot-busting medication after a stroke has tripled, increasing from 4.7% (one in twenty) to 14% (one in seven), and the average time it takes to deliver the treatment has halved.
For over 600 people who are admitted with an acute stroke every year, the RD&E is now matching or beating the performance of the big urban stroke centres elsewhere in the UK and the world.
Dr Martin James, Lead Clinician for Stroke at the Royal Devon & Exeter Hospital, said: “Working out whether a person with stroke is suitable to receive clot-busting treatment can be complicated and time-consuming. We’ve been able to use the latest techniques in computer simulation to speed up this process, so no matter when a person suffers a stroke, day or night, weekday or weekend, we can provide the fastest possible assessment and treatment for them. The computer simulation project has really helped us to make vital changes to the care we give people with stroke in an emergency.”
The project has been so successful that it is now being rolled out to other acute hospitals across the South West in partnership with the South West Cardiovascular Strategic Clinical Network and the South West Academic Health Sciences Network.
Professor Martin Pitt, one of PenCLAHRC’s experts in operational modelling based at the University of Exeter Medical School, said: “This project represents a fantastic example of how modelling and simulation can be used to improve care for patients. We’re always looking for new projects to work on and would encourage colleagues working in the NHS across the South West to get in touch and explore the ways in which we might be able to help.”
Life Sciences Minister George Freeman MP said: “I am delighted to see the pioneering work of the National Institute for Health Research (NIHR) combine with our NHS to deliver faster, more effective treatment for stroke patients.
“This is truly twenty-first century technology, and the outstanding benefits for patients underline precisely why we invest £1 billion into NIHR health research each year.”

Dietary nitrate lowers blood pressure

Well shit, I've been writing about this for years. But still they do not give any food types or amounts that could be used by laypersons to reduce blood pressure. So this is a totally fucking worthless piece of research at least in the abstract. Once again you are on your own. This is why I eat beets.

Dietary Nitrate Lowers Blood Pressure: Epidemiological, Pre-clinical Experimental and Clinical Trial Evidence


Nitric oxide (NO), a potent vasodilator critical in maintaining vascular homeostasis, can reduce blood pressure in vivo. Loss of constitutive NO generation, for example as a result of endothelial dysfunction, occurs in many pathological conditions, including hypertension, and contributes to disease pathology. Attempts to therapeutically deliver NO via organic nitrates (e.g. glyceryl trinitrate, GTN) to reduce blood pressure in hypertensives have been largely unsuccessful. However, in recent years inorganic (or 'dietary') nitrate has been identified as a potential solution for NO delivery through its sequential chemical reduction via the enterosalivary circuit. With dietary nitrate found in abundance in vegetables this review discusses epidemiological, pre-clinical and clinical data supporting the idea that dietary nitrate could represent a cheap and effective dietary intervention capable of reducing blood pressure and thereby improving cardiovascular health.


Ankle-brachial index and recurrent stroke risk

No clue on what this means but once again we have researchers trying to predict stroke risk rather than solving all the problems in stroke. If we had anything other than our fucking failures of stroke associations we would have a stroke strategy defined that would systematically solve all the problems in stroke. But NO, we will be screwed for decades because NO ONE is in charge.

Ankle-Brachial Index Test

In this systematic review and meta–analysis, the authors sought to explore ankle–brachial index (ABI)’s merit as a marker for stroke recurrence and vascular risk by synthesizing the data currently available in stroke literature. The results confirm the positive association between ABI and stroke recurrence. Further studies are needed to see whether inclusion of ABI will help improve the accuracy of prediction models and management of stroke patients.


  • The authors searched Embase, MEDLINE, and Pubmed databases for prospective cohort studies that included consecutive patients with stroke and transient ischemic attack, measured ABI at baseline, and performed a follow-up assessment at least 12 months after initial stroke or transient ischemic attack.
  • The following end points were chosen for their analysis: recurrent stroke and combined vascular end point (recurrent vascular event or vascular death).
  • Crude risk ratios and adjusted Cox proportional hazard ratios were combined separately using the random-effects model.
  • Study-level characteristics (eg, percent of cohort with a history of hypertension, average cohort age, level of adjustment, and mean follow-up duration) were included as covariates in a metaregression analysis.


  • The authors identified 11 studies (5374 patients) that were not significantly heterogeneous.
  • Pooling adjusted hazard ratios showed that low ABI was associated with both an increased hazard of recurrent stroke (hazard ratio, 1.70; 95% confidence interval, 1.10-2.64) and an increased risk of vascular events or vascular death (hazard ratio, 2.22; 95% confidence interval, 1.67-2.97).
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

Association of breakfast intake with incident stroke and coronary heart disease - Japanese

Not sure that this really proves cause and effect.

Association of breakfast intake with incident stroke and coronary heart disease

he authors sought to prospectively investigate whether the omission of breakfast is related to increased risks of stroke and coronary heart disease in general Japanese populations. The frequency of breakfast intake was inversely associated with the risk of stroke, especially cerebral hemorrhage in Japanese, suggesting that eating breakfast everyday may be beneficial for the prevention of stroke.


  • A total of 82 772 participants (38 676 men and 44 096 women) aged 45 to 74 years without histories of cardiovascular disease or cancer were followed up from 1995 to 2010.
  • Participants were classified as having breakfast 0 to 2, 3 to 4, 5 to 6, or 7 times/wk.
  • The hazard ratios of cardiovascular disease were estimated using Cox proportional hazards models.


  • During the 1 050 030 person–years of follow–up, the authors documented a total of 4642 incident cases, 3772 strokes (1051 cerebral hemorrhages, 417 subarachnoid hemorrhages, and 2286 cerebral infarctions), and 870 coronary heart disease.
  • Multivariable analysis showed that those consuming no breakfast per week compared with those consuming breakfast everyday had hazard ratios (95% confidence interval; P for trend) of 1.14 (1.01–1.27; 0.013) for total cardiovascular disease, 1.18 (1.04–1.34; 0.007) for total stroke, and 1.36 (1.10–1.70; 0.004) for cerebral hemorrhage.
  • Similar results were observed even after exclusion of early cardiovascular events.
  • No significant association between the frequency of breakfast intake and the risk of coronary heart disease was observed.
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

Could blood pressure drugs have a role in Alzheimer's disease treatment?

We'll never know from our stroke associations. Your doctor will just have to guess. How likely is your doctor to try something that hasn't been fully clinically proven? I want the kitchen sink thrown at my problems. Damn the torpedoes, full speed ahead.
The readable analysis:

The research it is based upon:

An integrative genome-wide transcriptome reveals that candesartan is neuroprotective and a candidate therapeutic for Alzheimer's disease.

How obesity makes memory go bad

Has your doctor considered this as the cause of your memory problems post-stroke? Or did

Occam's razor

 immediately point your doctor to your stroke as the cause without any critical thinking at all?

University of Alabama at Birmingham researchers are probing how obesity makes memory goes bad, and the underlying molecular mechanism that drives this decline.

They have found that epigenetic changes dysregulate memory-associated genes, and a particular enzyme in brain neurons of the hippocampus appears to be a link between chronic obesity and cognitive decline. Their work is published in the Jan. 27 issue of Journal of Neuroscience.
Obesity plagues developed nations, and among the numerous negative health outcomes associated with obesity is a memory impairment that is seen in middle-aged and older obese people. The cause of this decline? Experiments with obese rodents have given a clue: altered gene expression in the hippocampus area of the brain. Until now, the reasons gene expression was changed, as well as the mechanism by which obesity leads to pathogenic memory impairment, have not been known.
There was one suspect: epigenetic dysregulation in neurons of the hippocampus. Foundational experiments over the past decade have linked the creation of long-term memories to changes in DNA methylation and hydroxymethylation — changes caused by epigenetic mechanisms that sit above the level of the genes.
Such lasting molecular changes to DNA appear to play an important role in promoting or suppressing memory formation through their ability to increase or reduce the expression of genes that help brain neurons create new synaptic connections.
UAB researchers have now shown that epigenetic changes are indeed associated with changes in the expression of memory-associated genes within the hippocampus of obese mice, and these epigenetic changes correlate with diminished object location spatial memory in the obese mice. The UAB researchers have also implicated reduced amounts of one particular memory-associated gene product — SIRT1 — as the principal pathogenic cause of obesity-induced memory impairment. The hippocampus subregion of the brain is important for consolidation of long-term memory.
Obesity and cognitive decline
Evidence that suggests a link between the two includes:
  • People aged 40-45 who were obese had a 74 percent increased risk of dementia 21 years later; and those who were overweight had a 35 percent greater risk. This study cohort had 10,276 men and women. Whitmer, RA, et al., BMJ 2005.
  • A study of 2,223 healthy workers found that a higher body-mass index was associated with lower cognitive scores, after adjustment for age, sex, educational level, blood pressure, diabetes and other co-variables. Also, a higher BMI at baseline was associated with higher cognitive decline at a follow-up five years later. Cournot, M., et al., Neurology 2006.
  • Metabolic syndrome in 73 people with an average age of 60 was associated with significant reductions in recall and overall intellectual functioning, compared with age- and education-matched controls. Hassenstab, J.J., et al., Dementia and Geriatric Cognitive Disorders 2010.
  • A study of 8,534 twin individuals who were 65 or older showed that being overweight or obese at mid-life, with an average age of 43, was related to later dementia at the older age. Xu, W.L., et al., Neurology 2011.
Corresponding author J. David Sweatt, Ph.D., first author Frankie D. Heyward, Ph.D., and colleagues in the UAB Department of Neurobiology, Evelyn F. McKnight Brain Institute, write that these data “provide the first evidence that high-fat-diet-induced obesity leads to the time-dependent development of aberrant epigenetic modifications within the hippocampus, as well as corresponding reduction in the expression of various memory-related genes.”
Sweatt noted, “We feel this is a very exciting finding that identifies a new linkage between diet, epigenetics and cognitive function, especially in light of the burgeoning obesity epidemic in the U.S. and elsewhere.”
This work, they write, “offers a novel working model that may serve as a conceptual basis for the development of therapeutic interventions for obesity-induced memory impairment.”
In details about the cause of altered gene expression, the UAB researchers found that:
  • Mice with diet-induced obesity at 20 weeks had impaired performance in object location memory tests, and their hippocampus had impaired synaptic plasticity, as measured by long-term potentiation.
  • Four memory-associated genes — Ppargc1a, Ppp1cb, Reln and Sirt1 — showed significantly decreased gene expression at 23 weeks of diet-induced obesity, as has been seen before, and the latter three had significantly increased DNA methylation in their gene promoter regions. Increased methylation is known to decrease gene expression. Furthermore, the Sirt1 promoter region also had significantly decreased DNA hydroxymethylation. Gene expression increases or decreases as DNA hydroxymethylation increases or decreases.
  • Obesity-induced memory impairment develops over time. At just 13 weeks of diet-induced obesity, seven weeks earlier than the experiments above, mice did not have significant object location memory impairment, and at 16 weeks of diet-induced obesity, also seven weeks earlier than above, none of the genes showed significant increases in DNA methylation. Only one gene at 16 weeks — Ppargc1a — showed significant decreases in gene expression and DNA hydroxymethylation.
To probe the mechanism by which obesity leads to pathogenic memory impairment, the UAB researchers focused on the gene Sirt1, which makes an enzyme that is active in the neuron during energy expenditure and fat mobilization. This enzyme appears to be depleted and dysfunctional in obesity, and the deletion of the Sirt1 gene in the brain shortly after birth is known to impair memory and the ability to form new neural synapses. These roles for the SIRT1 gene product — in both high-fat-diet-induced molecular pathology and in memory impairment — suggest that it might be a link between chronic obesity and cognitive decline.
Heyward, Sweatt and colleagues found that the hippocampus of obese mice had significantly diminished protein expression of SIRT1, and a substrate of the enzyme, acetlylated-p53, was significantly increased, suggesting reduced enzymatic activity. Also, a targeted deletion of Sirt1 in the forebrain region that includes the hippocampus at age 8-12 weeks showed decreased Sirt1 mRNA and protein in the hippocampus, and these mice showed impaired object-location memory when tested two weeks later.
Furthermore, chemical activation of SIRT1 in diet-induced obese mice by feeding them resveratrol showed decreased levels of acetylated-p53, suggesting increased SIRT1 enzymatic activity, and the resveratrol-fed obese mice had a normal object-location memory, as compared with the control obese mice. The resveratrol-fed obese mice did not show an enhanced memory compared with normal mice. This suggests that resveratrol preserved their hippocampus-dependent spatial memory and SIRT1 function in the hippocampus.
Besides Heyward and Sweatt, co-authors of the paper, “Obesity weighs down memory through a mechanism involving the neuroepigenetic dysregulation of Sirt1,” are Daniel Gilliam, Mark Coleman, Cristin Gavin, Ph.D., Jing Wang, Ph.D., Garrett Kaas, Ph.D., Richard Trieu, John Lewis and Jerome Moulden, all of the UAB Department of Neurobiology.
Heyward is now a postdoctoral fellow at Harvard Medical School, the Broad Institute and Beth Israel Deaconess Medical Center. While at UAB, Heyward was supported by a UNCF/Merck Graduate Science Research Dissertation Fellowship that helps train and develop African-American biomedical scientists.
About 10 years ago, Sweatt’s lab made the seminal discovery that everyday experiences tap into epigenetic mechanisms in subregions of the brain, and the resulting epigenetic changes in DNA are critically important for long-term memory formation and the stable storage of long-term memory. The 2007 Neuron paper “Covalent modification of DNA regulates memory formation,” by Courtney Miller, Ph.D., and Sweatt, was the first to show that active regulation of the chemical structure of DNA is involved in learning and experience-driven changes in the brain.
This work was supported by National Institutes of Health grants T32HL105349, MH57014, P60DK079626 and P30DK56336. The T32 pre-doctoral fellow grant to Heyward from the UAB Nutrition and Obesity Research Center supported his training in the biological basis of obesity.

Friday, February 5, 2016

Intravenous Thrombolysis in Patients Dependent on the Daily Help of Others Before Stroke

And why pray tell would being dependent on others for your care have anything to do with eligibility for tPA?  This previous criteria should have been massively pushed back on by our incompetent stroke associations. You better hope your hospital has adjusted the tPA protocol before your next stroke if you are already dependent on others.
  1. for the Thrombolysis in Stroke Patients (TriSP) Collaborators
+ Author Affiliations
  1. From the Stroke Center and Department of Neurology, University Hospital Basel, Basel, Switzerland (H.G., S.C., D.J.S., C.T., N.P., L.H.B., P.A.L., S.T.E.); Department of Neurology, Helsinki University Central Hospital, Helsinki, Finland (D.S., J.P., S.C., G.S., T.T.); Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands (S.M.Z., T.P.Z., Y.B.R., P.J.N.); Department of Neurology and Center for Stroke Research, Charité-Universitätsmedizin Berlin, Berlin, Germany (J.F.S., H.E., P.K., C.H.N.); Department of Neurology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland (O.B., P.M.); Department of Neurology, University Hospital Heidelberg, Heidelberg, Germany (C.H., P.R.); University Lille, Inserm, CHU Lille, U1171-Degenerative and Vascular Cognitive Disorders, Lille, France (S.M., D.L., C.C.); Stroke Unit, Department of Neuroscience, Nuovo Ospedale Civile S. Agostino-Estense, AUSL Modena, Modena, Italy (A.Z., L.V.); Department of Neurology, Kantonsspital St. Gallen, St Gallen, Switzerland (G.K.); Department of Clinical and Experimental Sciences, Neurology Clinic, University of Brescia, Brescia, Italy (A.P.); Department of Neurology, Clinical Centre of Serbia, Beograd, Serbia (V.P.); Department of Neurology, University Hospital, and Dijon Stroke Registry, University of Burgundy, Dijon, France (Y.B.); Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden (T.T.); and Department for Medicine of Aging and Rehabilitation, University Center, Felix Platter Hospital, Basel, Switzerland (S.T.E.).
  1. Correspondence to Henrik Gensicke, MD, Department of Neurology, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland. E-mail


Background and Purpose—We compared outcome and complications in patients with stroke treated with intravenous thrombolysis (IVT) who could not live alone without help of another person before stroke (dependent patients) versus independent ones.
Methods—In a multicenter IVT-register–based cohort study, we compared previously dependent (prestroke modified Rankin Scale score, 3–5) versus independent (prestroke modified Rankin Scale score, 0–2) patients. Outcome measures were poor 3-month outcome (not reaching at least prestroke modified Rankin Scale [dependent patients]; modified Rankin Scale score of 3–6 [independent patients]), death, and symptomatic intracranial hemorrhage. Unadjusted and adjusted odds ratios (ORs) with 95% confidence intervals (OR [95% confidence interval]) were calculated.
Results—Among 7430 IVT-treated patients, 489 (6.6%) were dependent and 6941 (93.4%) were independent. Previous stroke, dementia, heart, and bone diseases were the most common causes of preexisting dependency. Dependent patients were more likely to die (ORunadjusted, 4.55 [3.74–5.53]; ORadjusted, 2.19 [1.70–2.84]). Symptomatic intracranial hemorrhage occurred equally frequent (4.8% versus 4.5%). Poor outcome was more frequent in dependent (60.5%) than in independent (39.6%) patients, but the adjusted ORs were similar (ORadjusted, 0.95 [0.75–1.21]). Among survivors, the proportion of patients with poor outcome did not differ (35.7% versus 31.3%). After adjustment for age and stroke severity, the odds of poor outcome were lower in dependent patients (ORadjusted, 0.64 [0.49–0.84]).
Conclusions—IVT-treated stroke patients who were dependent on the daily help of others before stroke carry a higher mortality risk than previously independent patients. The risk of symptomatic intracranial hemorrhage and the likelihood of poor outcome were not independently influenced by previous dependency. Among survivors, poor outcome was avoided at least as effectively in previously dependent patients. Thus, withholding IVT in previously dependent patients might not be justified.

New Exoskeleton Suit from UC Berkeley Helps Paraplegics Walk

This should be able to be repurposed for hemiplegics if our fucking failures of stroke associations wanted to actually do something for survivors.
By Greg Watry, Digital Reporter
It’s been an over a 10-year journey. In 2000, Univ. of California, Berkeley Prof. Homayoon Kazerooni began working with a team to develop a series of exoskeletons. The research was funded by the Defense Advanced Research Projects Agency (DARPA).
Recently, SuitX, founded by Kazerooni and spun off from the university’s Robotics and Human Engineering Laboratory, unveiled the Phoenix, a 27-lb exoskeleton that can help paraplegic users achieve a walking speed of 1.1 mph.
“We can’t really fix their disease,” said Kazerooni. “We can’t fix their injury. But what it would do is postpone the secondary injuries due to sitting. It gives a better quality of life.”
Adaptable to a users’ size, the Phoenix, on a single charge, can walk for four hours continuously, or eight hours intermittently. The battery is stored in a backpack carried by the user.
The exoskeleton is controlled by users via crutches, which are outfitted with buttons, allowing the user to control standing up, sitting down, and walking.
The Phoenix costs around $40,000. While that’s a hefty price tag, it’s more affordable and lightweight than competitors like the ReWalk suit, which costs around $70,000 and weighs 50 lbs, according to MIT Technology Review.  
Kazerooni told the media outlet that one of the goals is to design a Phoenix model for children, which may be able to assist in walking training for those with neurological disorders.
“My injury came about from a BMX bicycle accident,” said Steven Sanchez, one of the Phoenix’s test pilots, in a video. Sanchez’s fall resulted in him breaking his back. He was paralyzed instantly.
“I feel much more with myself and human-like being in this device, being able to stand up eye-to-eye with somebody,” Sanchez said in the video, while footage of him kicking a soccer plays. “It’s strange that this robot makes me feel more a part of this planet than a wheelchair does.”
As the technology continues to advance and the price decreases, these devices may one day be monetarily feasible options for paraplegics.


With 13 pages and 58 references in here this is too much for a stroke-addled non-medical person like myself to have any understanding of how to apply this to survivors. So either you are going to have to become a genius or you wait 200 years before this is translated into stroke protocols. Your choice. Your doctor has already had two years to figure this out and I bet has done absolutely nothing.
If your doctors aren't salivating over having all these possibilities laid out for them to help survivors you have idiots for doctors. This should in any reasonable world trigger dozens of clinical trials. But it won't because SOMEONE ELSE WILL SOLVE THOSE FUCKING PROBLEMS.
But not in your lifetime.

In clinical practice, these drugs are classified
into two major groups: nootropics of direct ac-
tion (cognitive enhancers) and neuroprotective
agents [31, 32]:
I. Cognitive enhancers or «true» nootropics:
1. Pyrrolidone nootropics(racetams) with pre-
dominant metabolite action: Piracetam, Fenotro-
pil combined racetams (Thiocetam, Olatropil, and
2. Cholinergic agents: enhancers of synthesis and
release of acetylcholine (Phosphatidylserine, leci-
thin, Citicoline); cholinergic receptor agonists (Oxo-
tremorine, Bethanechol); and acetylcholi nes terase
inhibitors (Physostigmine, Galantha mine, etc.)
3. Neuropeptides and neurotrophic cerebroprotec-
tors: Semax, Cerebrolysin, Cortexin, Cerebrocu rin.
4. Modulators of glutamatergic system:
a) low-affinity NMDA receptor polyamine site antago-
nists and partial agonists of AMPA receptors: Me-
mantine, Ademol);
b) AMPA receptor agonists: Nooglutyl;
c) AMPA receptor partial agonists, as well as en-
hancers of noradrenaline and dopamine release:
(Ritalin, Donepezil);
d) NMDA receptor co-agonists: glycine;
e) NMDA mimetics: glutamic acid, D-cycloserine.
5. Dopamine receptor agonists: Pronoran;
6. GABA receptor agonists: Baclofen.
II. Neuroprotective agents:
1. Activators of brain metabolism: Mildronat,
Phosphatidylserine, xanthine derivatives of Pen-
toxifylline, etc.
2. Cerebral vasodilators: Vincamine, Vinpocet-
ine, Nicergoline, etc.
3. Calcium channel blockers: Nimodipine, Cin-
narizine, Flunarizine, etc.
4. Antioxidants: Mexidol, a-tocopheryl acetate,
Thiotriazoline, Emoxipin, Cytoflavin, Glutoxim.
5. Substances affecting the GABA system
: Ami-nalon (Gammalon), Pathogen, Picamilon, Fenib-
ut (Noofen), sodium hydroxybutyrate.
6. Different groups of substances: orotic acid,
Naftidrofuryl, ginseng, lemongrass, Ginkgo bi lo-
ba, and Siberian ginseng.
For the direct nootropics the effect on memory
is the main action, although they have other phar-
macological properties (anticonvulsant, antihy-
poxic, circulatory, antioxidant, etc.) as well. The
direct nootropics include substances with very
different structure, from the relatively simple ra-
cetams to the complex peptide formations. The
neuroprotective agents comprise brain metabo-
lism activators, cerebral vasodilators, calcium an-
tagonists, antioxidants, and substances affecting
GABA system.

Sensory-Targeted Ankle Rehabilitation Strategies for Chronic Ankle Instability

Would this be helpful in preventing ankle rollovers that lots of survivors have? I should stop asking questions because our fucking failures of stroke associations will never condescend to doing the difficult work needed to solve all the problems in stroke and help survivors. You're screwed.

Written by: Nicole Cattano

McKeon PO & Wikstrom EA. Med Sci Sports Exerc. Published Online First: December 10, 2015; DOI: 10.1249/MSS.0000000000000859

Take Home Message: Sensory-targeted rehabilitation strategies (STARS) result in improvements in patient-reported and clinical outcomes.  Certain deficits may be specifically targeted by different techniques.

Chronic ankle instability (CAI) with recurrent episodes of giving way and functional limitations can cause long-term complications.  Sensorimotor deficits may play a significant role in those with CAI.  Therefore, the authors of this randomized control study compared the effects of 3 sensory-targeted ankle rehabilitation strategies (STARS; i.e., ankle joint mobilization, plantar massage, or triceps surae stretching) on improvements in clinician- and patient-reported outcomes among individuals with CAI.  The authors randomized 80 participants to 4 groups (3 STARS interventions and a control group). 75 participants completed the entire duration of the study at the 1-month follow-up.  STARS programs consisted of six total treatment sessions over the course of 2 weeks.  Joint mobilization participants received 2 two-minute sets of grade III (one-second large amplitude) oscillations.  Participants within the plantar massage group received 2 two-minute sets of effleurage and petrissage on the plantar aspect of the foot.  Trcieps surae stretching participants performed 2 sets of three 30-second stretches with their knee flexed.  Control participants received no treatments. Participants were assessed at baseline, within 72 hours of their last treatment, and at a 1-month follow-up.  Patient reported outcomes included self-reported disability (Foot and Ankle Ability Measure; FAAM) and self-reported physical activities levels (NASA Physical activity status scale).  Clinician measures of interest were dorsiflexion range of motion (weight-bearing lunge test) and single-limb balance.  Overall, the plantar massage and calf stretching groups had the best improvements in patient and clinician reported outcomes.  After 2 weeks, all 3 STARS programs had improvements compared with the control group. The plantar massage and calf stretching groups had the largest improvements in patient-reported disability and number of episodes of giving way.  The calf stretching and joint mobilization groups had improvements in range of motion, while all 3 groups had improvements in single leg balance. The plantar massage group had the most pronounced improvement in balance after two weeks. 

Each STARS group had unique improvements.  For example, joint mobilization offered the most meaningful benefit for improving dorsiflexion, plantar massage led to the most meaningful change in balance, and stretching offered benefits in various outcomes. Amazingly, these benefits were achieved with just six 5-minute treatment sessions during a 2-week period.  Clinicians could carefully add a specific treatment to their rehabilitation protocol based on deficits found during assessment.  It would have been interesting to see if any of the clinical findings (i.e., single limb balance & range of motion) had lasting effects at the 1-month follow-up.  It would also be interesting to see if a combination of these techniques resulted in better short and long-term outcomes.  For example, the joint mobilizations showed the best outcomes immediately post-treatments, while plantar massage showed better outcomes at the 1-month follow-up.  The findings of this study help to confirm that clinicians should consider STARS to target improvements in certain areas for patients with CAI. 

Questions for Discussion:  Are there any other therapy decisions that you have used with individuals with CAI?  What has your experience been with trying to improve patient and clinical outcomes in patients with CAI?