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 493 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:

Friday, February 23, 2018

Association of coffee consumption and non-motor symptoms in drug-naïve, early-stage Parkinson's disease

With your chance of getting Parkinsons post stroke and this news my choice of massive coffee consumption seems warranted. But don't listen to me, I'm not medically trained. Of course no amounts are given, so you'll have to guess.

Parkinson’s Disease May Have Link to Stroke

How coffee protects against Parkinson’s Aug. 2014


  • There is an inverse association between coffee consumption and non-motor symptoms (NMSs) of drug-naïve PD patients.
  • Coffee drinkers had a lower severity in several sub-items of the mood/cognition domain compared to non-coffee drinkers.
  • It is important to consider the history of coffee consumption in the assessment of NMSs of PD patients.



Coffee consumption has an inverse association with the risk of Parkinson's disease (PD). The aim of this study was to investigate the association between coffee consumption and non-motor symptoms (NMSs) in patients with PD.


In this cross-sectional study, we included 196 early-stage, treatment-naïve PD patients. Coffee consumption history was obtained via semi-structured interviews. NMSs were assessed using the Non-Motor Symptom assessment scale (NMSS).


Of the 196 patients with PD, 136 (69.3%) were categorized as coffee drinkers and 60 (30.6%) were non-drinkers. Coffee drinkers were younger, predominantly male, were younger in age at symptom onset, had lower Unified Parkinson's Disease Rating Scale motor and Beck Depression Inventory scores, and higher Mini-Mental State Examination scores than non-coffee drinkers. After adjustment, coffee drinking was significantly inversely associated with the prevalence of lack of motivation, anhedonia, and lack of pleasure, which were less frequent in coffee drinkers. Total NMSS scores were lower in coffee drinkers than in non-drinkers (p = 0.047). In particular, coffee drinking was significantly associated with a reduced severity of the mood/cognition domain of NMSS (p = 0.003). After correcting for multiple testing, there were no significant differences in the prevalence of NMSs, but there were significant differences in the severity of NMSs between coffee drinkers and non-drinkers.


There is a negative association between coffee consumption and the severity of the mood/cognition domain of NMSS in patients with PD. Clinicians should consider the history of coffee consumption in the assessment of NMSs in PD.

Novel Stent Retriever Is Quick to Restore Flow

Once again the wrong endpoint is used. The endpoint is 100% recovery, NOT the lazy 50% flow restored. If Dr. Sacco being president of the ASA at one time produced anything useful for survivors it is not commonly known.
  • by Senior Associate Editor, MedPage Today
  • This article is a collaboration between MedPage Today® and:
LOS ANGELES -- A novel stent retriever device achieved high rates of rapid, substantial reperfusion for large vessel ischemic strokes without significant safety concerns, the pivotal ARISE II study showed.
With the EmboTrap device, 80% of recipients reached the primary endpoint of more than 50% flow restored (modified TICI 2b, 2c, or 3 flow) within three passes without aspiration or other rescue therapy, including 65% with near-complete or full flow.
Notably, 51.5% of those treated had this substantial flow restored on the first pass, Osama Zaidat, MD, of St. Vincent Mercy Hospital in Toledo, Ohio, reported here at the International Stroke Conference.
While the final rate of mTICI 2b-3 flow was 93%, on par with other mechanical thrombectomy trials, Zaidat noted that the high early-pass revascularization rate was a "remarkable" advance.
"That's what the trial is, it's pushing the limit," he said at a press conference. "The physicians are taking the right patients and they are taking them fast. And I think that's why I think we achieved one of the highest mRS 0-2 at 67%" compared with other studies.
The proportion of participants with a good functional outcome (modified Rankin Scale score 0-2) was 67.3% at 90 days.
J Mocco, MD, of Mount Sinai Hospital in New York City, who presented another trial at the same session reporting mRS 0-2 achieved in 52% of patients treated with an aspiration-first approach and 49% with a stentriever-first strategy, agreed that this is an important evolving area.
"Sooner and fewer is always better," he told MedPage Today at the press briefing, "although I think that more important right now is to focus on the time component to getting at least TICI 2b or greater. If you can do that with one pass, obviously that will be faster. If it's two passes and it's still very quick, that's just as important. We need to focus on the quality of reperfusion ... we need to move our conversation to 2c and 3, we need to be talking about 90% of the brain getting blood flow or more, not 52%."
"For one pass efficacy, that is something that seems to be clear but does not have clear proof," he added. "However, for achieving 2c or 3 versus TICI 2b, has overwhelming proof" of impact on clinical outcomes.
"The first pass is a nuance, I think," agreed Ralph Sacco, MD, of the University of Miami, and president of the American Academy of Neurology. "It may be a predictor of how fast you can then subsequently open up the vessel, I think that's the data they need to show."(I call that lazy, wrong data to show)
The trial included 227 patients treated with the EmboTrap device for large vessel occlusions within 8 hours of last time known well before onset of symptoms. Median time from onset to puncture was 214 minutes; median time from puncture to revascularization was 35 minutes.
The primary safety endpoint of symptomatic intracranial hemorrhage within 24 hours of treatment or other serious adverse events occurred in 5.3%. No patients died related to the procedure in the first week, although 9.0% died from any cause by day 90.
Device developer Cerenovus has applied for FDA clearance of EmboTrap based on ARISE II.
ARISE II was sponsored by Neuravi (since acquired by Cerenovus, a Johnson & Johnson company).
Zaidat disclosed being a consultant for the company.

First Pass Effect A New Measure for Stroke Thrombectomy Devices

Still measuring the wrong thing, complete recanalization is a stupid measurement, it may be easy to measure but the measurement is 100% recovery, NOTHING LESS. Are you that incompetent that you aren't even trying for the correct results?  Association means nothing to survivors, we want results. GET THERE!
Osama O. Zaidat, Alicia C. Castonguay, Italo Linfante, Rishi Gupta, Coleman O. Martin, William E. Holloway, Nils Mueller-Kronast, Joey D. English, Guilherme Dabus, Tim W. Malisch, Franklin A. Marden, Hormozd Bozorgchami, Andrew Xavier, Ansaar T. Rai, Michael T. Froehler, Aamir Badruddin, Thanh N. Nguyen, M. Asif Taqi, Michael G. Abraham, Albert J. Yoo, Vallabh Janardhan, Hashem Shaltoni, Roberta Novakovic, Alex Abou-Chebl, Peng R. Chen, Gavin W. Britz, Chung-Huan J. Sun, Vibhav Bansal, Ritesh Kaushal, Ashish Nanda, Raul G. Nogueira


Background and Purpose—In acute ischemic stroke, fast and complete recanalization of the occluded vessel is associated with improved outcomes. We describe a novel measure for newer generation devices: the first pass effect (FPE). FPE is defined as achieving a complete recanalization with a single thrombectomy device pass.
Methods—The North American Solitaire Acute Stroke Registry database was used to identify a FPE subgroup. Their baseline features and clinical outcomes were compared with non-FPE patients. Clinical outcome measures included 90-days modified Rankin Scale score, National Institutes of Health Stroke Scale score, mortality, and symptomatic intracranial hemorrhage. Multivariate analyses were performed to determine whether FPE independently resulted in improved outcomes and to identify predictors of FPE.
Results—A total of 354 acute ischemic stroke patients underwent thrombectomy in the North American Solitaire Acute Stroke registry. FPE was achieved in 89 out of 354 (25.1%). More middle cerebral artery occlusions (64% versus 52.5%) and fewer internal carotid artery occlusions (10.1% versus 27.7%) were present in the FPE group. Balloon guide catheters were used more frequently with FPE (64.0% versus 34.7%). Median time to revascularization was significantly faster in the FPE group (median 34 versus 60 minutes; P=0.0003). FPE was an independent predictor of good clinical outcome (modified Rankin Scale score ≤2 was seen in 61.3% in FPE versus 35.3% in non-FPE cohort; P=0.013; odds ratio, 1.7; 95% confidence interval, 1.1–2.7). The independent predictors of achieving FPE were use of balloon guide catheters and non-internal carotid artery terminus occlusion.
Conclusions—The achievement of complete revascularization from a single Solitaire thrombectomy device pass (FPE) is associated with significantly higher rates of good clinical outcome. The FPE is more frequently associated with the use of balloon guide catheters and less likely to be achieved with internal carotid artery terminus occlusion.

Thursday, February 22, 2018

Compound repairs features of Alzheimer’s disease in mice

With our quite likely chances of getting dementia/Alzheimers maybe you want your doctor to pretreat you with this. Not medical advice since I am not medically trained.
Compound repairs features of Alzheimer’s disease in mice

At a Glance

  • Researchers found that a compound called an NAD+ precursor helped mice with features of Alzheimer’s disease perform better on learning and memory tests.
  • The findings pave the way for studies of the compound’s potential as an intervention for people with Alzheimer’s disease.
Mouse brain with hallmarks of Alzheimer’s disease A mouse brain showing hallmarks of Alzheimer’s disease similar to that of the mice used in this study. Abnormal protein clumps are blue, blood vessels are red, and nerve cells are green.Alvin Gogineni, Genentech
Alzheimer’s disease is a brain disorder that slowly destroys thinking, memory, and language skills. It’s the most common cause of dementia among older people. Experts estimate that more than 5 million Americans are living with the disease. Symptoms usually begin after age 60. There is no cure.
The brain’s usual DNA repair activity is impaired in Alzheimer’s disease, leading to inflammation and dysfunction. A compound that the brain needs to regulate DNA repair and other key signaling pathways is known as nicotinamide adenine dinucleotide (NAD+). Because NAD+ declines with age, scientists have wondered whether boosting the level of NAD+ could help aging brain cells (neurons) to function better. One way to increase the cellular level is by giving an NAD+ precursor compound, such as nicotinamide riboside (NR). NR is a form of vitamin B3.
An international research team led by Dr. Vilhelm A. Bohr at NIH’s National Institute on Aging (NIA) set out to test whether NR supplements could normalize NAD+ levels in the brains of mice and counteract deficits in thinking and memory. The study was published online on February 5, 2018, in the Proceedings of the National Academy of Sciences.
The research team used findings from their previous studies with human cadaver brain tissue to develop a new strain of mice. These mice had the main features of human Alzheimer’s disease, such as the abnormal buildup of the proteins tau and amyloid-beta. The research team added the NR supplement to the mice’s drinking water for three months.
The team found that the NR-treated mice had less DNA damage, lower levels of neuron damage and death, increased production of new neurons, and lower brain inflammation than control mice. Mice who received NR had reduced tau in their brains, too, but amyloid-beta levels were unchanged. The NR-treated mice performed better than control mice on many learning and memory tests, such as a water maze. In addition, NR-treated mice had better muscle strength and endurance than controls.
The research team also tested human cells from people with and without Alzheimer’s disease. As in the mouse studies, NR decreased DNA damage in the cells from people with Alzheimer’s.
“The pursuit of interventions to prevent or delay Alzheimer’s and related dementias is an important national priority,” says NIA Director Dr. Richard J. Hodes. “We are encouraging the testing of a variety of new approaches, and this study’s positive results suggest one avenue to pursue further.”
“We are encouraged by these findings that see an effect in this Alzheimer’s disease model,” Bohr says. “We are looking forward to further testing of how NR or similar compounds might be pursued for their possible therapeutic benefit for people with dementia.”
The team is continuing to study the biological mechanisms of Alzheimer’s disease in preparation for possible studies of the approach in people.

Letter by Dijkland et al Regarding Article, “Development and Validation of a Predictive Model for Functional Outcome After Stroke Rehabilitation: The Maugeri Model”

I totally disagree that prediction is useful in stroke rehab. If you had decent stroke protocols leading to 100% recovery then prediction models wouldn't be needed. Have you no brains in your heads at all? Isn't your goal to get all stroke survivors 100% recovered? Or are you so fucking lazy that the status quo is ok?
Letter by Dijkland et al Regarding Article,“Development and Validation of a Predictive Model for Functional Outcome After Stroke Rehabilitation: The Maugeri Model”

Foot woes in Ecuador

Walking in my Chaco sandals on the first day, sand cut my right big toe under the strap. A heavy duty bandage salvaged it so I could walk in Chacos again with just minor pain. The second day(Friday) at the beach we walked three miles north on the sand to a gravel cliff, so I took off my socks and shoes since we were in the wave line most of the time, 18,280 steps. 
My feet sunburned quite badly, and yes I didn't put on sunscreen like I should have. The next day(Saturday), 9,000 steps, I managed to get my socks and shoes on even though my feet were swollen so we could walk one mile south on the beach to the town of San Jacinto. On Sunday played in the waves a bit in my Chacos, luckily the straps crossing the foot didn't pop any blisters. Was able to walk barefoot the 2 blocks to the hotel restaurant, for dinner that night, couldn't have managed to get shoes on to walk farther.
Took 20 minutes to get my Chacos on over socks on Monday so we could take a take a taxi to Manta and eventually fly to Quito, 7,200 steps. That night in the hotel discovered that the blister had drained but not torn. Bret insisted I sit outside the shower and run cold water over the foot along with a couple Advil and it started feeling better. Forced my feet into Chacos once again on Tuesday for the plane rides from Quito to Panama City to Fort Lauderdale to Detroit, 6905 steps. Luckily did not have to remove my sandals thru the checkpoints, I just kept them on and walked thru.
Had another vacation day on Wednesday so I never left the apartment, resting up my feet. On Thursday had to go back to work so had to put socks and shoes on once again, putting on socks one-handed over a blister does not work, It immediately tore wide open. Even though I only did 2610 steps today(Thursday) my foot now looks like hell since all the blisters have torn away.  The major pain associated with this is when the left foot goes in complete spasm mode. I was hopeful I could get back to 70,000 steps a week again but that will have to wait a couple of weeks.
Regardless of all the foot woes the Ecuador trip was a lot of fun and will need to be visited again(volcanoes, rain forest, equator line, Galapagos)
Bandaid on right toe, left foot the night after it occurred
After Saturdays walk, fluid filled, no leaking
Swollen feet in Chacos
Cold shower on the foot

The coconut Batidos in San Jacinto, 80 cents
Blister tore off

Migraine linked to risk of many cardiovascular diseases, especially in year 1 after diagnosis

I guess they didn't get the memo that stroke is now in neurological diseases not cardiovascular diseases. Oh well, what difference does it make to them being 12 years out of date? WHO - 2006
Incompetence is endemic in stroke, what else is new?
Liz Meszaros, MDLinx
In the first year after diagnosis, migraine headaches may be an important risk factor for several cardiovascular diseases, particularly stroke, and these associations may be stronger in patients with migraine with auras and women, according to a study recently published in The BMJ.

Migraine and risk of CVD events

The risk of cardiovascular disease was highest in the first year, with an 8-fold increase risk of both IS and HS, and an approximately 2-fold increased risk of MI, VT, and AF or atrial flutter.
The associations between migraine and ischemic stroke (IS) and myocardial infarction (MI) are well documented. Less is known about the possible associations between migraine and other cardiovascular diseases.
“Around one billion people worldwide are affected by migraine. Migraine has considerable impact on quality of life and imposes a substantial burden on society. Migraine is primarily a headache disorder, but previous studies have suggested a link between migraine and stroke and MI, particularly among women, while the link between migraine and other heart problems is less well known,” lead author Kasper Adelborg, MD, PhD, postdoctoral fellow, Department of Clinical Epidemiology, Aarhus University Hospital, Denmark, told MDLinx.
“In this large, register-based Danish study published in The BMJ, we confirmed that migraine is associated with increased risks of stroke and MI, but we also found that migraine was associated with increased risks of other cardiovascular diseases (specifically, venous thromboembolism [VT] and atrial fibrillation [AF]). Migraine was not associated with increased risks of heart failure (HF) or peripheral artery disease (PAD),” he added.
In this nationwide, population-based cohort study, Dr. Adelborg and colleagues included 51,032 patients with a first-time primary or secondary diagnosis of migraine from the Danish National Patient Registry (median age at diagnosis: 35 years; 71% women) between 1995 and 2013. The researchers compared the patients with 510,320 subjects from the general population who were matched in age, sex, and calendar year.
Researchers assessed cardiovascular risk factors in all patients, including diabetes, obesity, hyperlipidemia, hypercholesterolemia, hypertension, valvular heart disease, chronic obstructive pulmonary disease, renal failure, liver disease, cancer, alcoholism-related disorders, and thyroid disease.
They found that cardiovascular risk factors and comorbidity at index date were slightly higher in patients with migraine, and that patients with migraine had higher absolute risks for most of these outcomes.
After 19 years of follow-up, the cumulative incidences (per 1,000 people) in the migraine cohort compared with the general population were:
  • MI: 25 vs 17
  • IS: 45 vs 25
  • Hemorrhagic stroke (HS): 11 vs 6
  • PAD: 13 vs 11
  • VT: 27 vs 18
  • AF or atrial flutter: 47 vs 34
  • HF: 19 vs 18
Dr. Adelborg and colleagues also found a positive association between migraine and MI (adjusted HR: 1.49; 95% CI: 1.36-1.64), IS (adjusted HR: 2.26; 95% CI: 2.11-2.41), HS (adjusted HR: 1.94; 95% CI: 1.68-2.23), VT (adjusted HR: 1.59; 95% CI: 1.45-1.74), and AF or atrial flutter (adjusted HR: 1.25; 95% CI: 1.16-1.36).
They found no meaningful associations, however, between migraine and PAD (adjusted HR: 1.12; 95% CI: 0.96-1.30) or HF (adjusted HR: 1.04; 95% CI: 0.93-1.16).
In patients with aura, these associations were stronger in the short-term after diagnosis (years 0-1) than in the long-term (up to 19 years) compared with those without aura, and in women compared with men.
The risk of cardiovascular disease was highest in the first year, with an 8-fold increase risk of both IS and HS, and an approximately 2-fold increased risk of MI, VT, and AF or atrial flutter.
“In general, the associations were strongest in the first year after diagnosis but persisted in the long term (up to 19 years after diagnosis). Most associations applied to both migraine patients with aura (warning signs before a migraine, such as seeing flashing lights) and in those without aura, and in both women and in men,” said Dr. Adelborg.
Why are migraine and cardiovascular disease seemingly so closely linked?
According to Dr. Adelborg, “The underlying mechanisms are likely multifactorial and different for the individual cardiovascular outcomes. For example, one potential mechanism may involve vasospasm in the cerebral arteries leading to migraine, which at the same time may increase the risk of stroke. Another mechanism may involve migraine-associated immobilization, which in turn increases the risk of VT.”     
This recent study stands out for several reasons, noted Dr. Adelborg.
“In contrast to most previous studies, our study had a very large sample size and an age- and sex- matched comparison cohort from the general population, which allowed us to put migraine in a population context and to perform several subgroup analyses,” he said.
For clinicians, the message is clear, he added.
“Now, accumulating evidence supports that migraine should be considered as a risk factor for most cardiovascular diseases in both men and women. Although the absolute risks of cardiovascular diseases were low at the individual level, it translates into a substantial increase in risk at the population level, because migraine is a very common disease.
“Establishing the link between migraine and cardiovascular risk was an important first step. Now, we need data to inform the development of clinical recommendations and strategies that reduce the risk of cardiovascular disease for patients with migraine. For example, current migraine guidelines do not recommend use of anticoagulant treatment with aspirin and clopidogrel in the prophylaxis of migraine, but future studies should address whether patients at particularly high risk of cardiovascular diseases would benefit from anticoagulant treatment. Additionally, it will be important to determine whether prevention strategies in patients with migraine can reduce the burden of cardiovascular disease in patients with this common disorder,” Dr. Adelborg concluded.
This study was funded by Aarhus University and the Program for Clinical Research Infrastructure (PROCRIN), established by the Lundbeck Foundation and the Novo Nordisk Foundation.

Should Stroke Physicians Assess Cognition and Mood?

And what is the point of assessing cognition and mood? There are no protocols to address either.
Terence J. Quinn, Emma Elliott, Peter Langhorne

Profound effects of combining choline and piracetam on memory enhancement and cholinergic function in aged rats

Only 37 fucking years and I bet nothing was ever done with this for stroke survivors. God, the lack of leadership from anyone in stroke is criminal.
Neurobiol Aging. 1981 Summer;2(2):105-11.


In an attempt to gain some insight into possible approaches to reducing age-related memory disturbances, aged Fischer 344 rats were administered either vehicle, choline, piracetam or a combination of choline or piracetam. Animals in each group were tested behaviorally for retention of a one trial passive avoidance task, and biochemically to determine changes in choline and acetylcholine levels in hippocampus, cortex and striatum. Previous research has shown that rats of this strain suffer severe age-related deficits on this passive avoidance task and that memory disturbances are at least partially responsible. Those subjects given only choline (100 mg/kg) did not differ on the behavioral task from control animals administered vehicle. Rats given piracetam (100 mg/kg) performed slightly better than control rats (p less than 0.05), but rats given the piracetam/choline combination (100 mg/kg of each) exhibited retention scores several times better than those given piracetam alone. In a second study, it was shown that twice the dose of piracetam (200 mg/kg) or choline (200 mg/kg) alone, still did not enhance retention nearly as well as when piracetam and choline (100 mg/kg of each) were administered together. Further, repeated administration (1 week) of the piracetam/choline combination was superior to acute injections. Regional determinations of choline and acetylcholine revealed interesting differences between treatments and brain area. Although choline administration raised choline content about 50% in striatum and cortex, changes in acetylcholine levels were much more subtle (only 6-10%). No significant changes following choline administration were observed in the hippocampus. However, piracetam alone markedly increased choline content in hippocampus (88%) and tended to decrease acetylcholine levels (19%). No measurable changes in striatum or cortex were observed following piracetam administration. The combination of choline and piracetam did not potentiate the effects seen with either drug alone, and in certain cases the effects were much less pronounced under the drug combination. These data are discussed as they relate to possible effects of choline and piracetam on cholinergic transmission and other neuronal function, and how these effects may reduce specific memory disturbances in aged subjects. The results of these studies demonstrate that the effects of combining choline and piracetam are quite different than those obtained with either drug alone and support the notion that in order to achieve substantial efficacy in aged subjects it may be necessary to reduce multiple, interactive neurochemical dysfunctions in the brain, or affect activity in more than one parameter of a deficient metabolic pathway.
[Indexed for MEDLINE]

Theanine prevents memory impairment induced by repeated cerebral ischemia in rats

You'll have to ask your doctor if this was followed up with human testing in the past 10 years. Or if NOTHING WAS DONE LIKE USUAL. 


New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection

Pages and pages for your doctor to read to see what neuroprotection can come out of this.  But that won't occur since your doctor needs to continually prove incompetence on not staying up-to-date on research. Only 89 references to back this up.

Azizul Haque 1,*, Rachel Polcyn 1, Denise Matzelle 2,3 and Naren L. Banik 1,2,3
Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29401, USA
Department of Neurosurgery, Medical University of South Carolina, Charleston, SC 29401, USA
Ralph H. Johnson Veterans Administration Medical Center, Charleston, SC 29401, USA
Correspondence:; Tel.: +1-843-792-9466; Fax: +1-843-792-2464
Received: 18 January 2018 / Accepted: 13 February 2018 / Published: 18 February 2018


Neurodegeneration is a complex process that leads to irreversible neuronal damage and death in spinal cord injury (SCI) and various neurodegenerative diseases, which are serious, debilitating conditions. Despite exhaustive research, the cause of neuronal damage in these degenerative disorders is not completely understood. Elevation of cell surface α-enolase activates various inflammatory pathways, including the production of pro-inflammatory cytokines, chemokines, and some growth factors that are detrimental to neuronal cells. While α-enolase is present in all neurological tissues, it can also be converted to neuron specific enolase (NSE). NSE is a glycolytic enzyme found in neuronal and neuroendocrine tissues that may play a dual role in promoting both neuroinflammation and neuroprotection in SCI and other neurodegenerative events. Elevated NSE can promote ECM degradation, inflammatory glial cell proliferation, and actin remodeling, thereby affecting migration of activated macrophages and microglia to the injury site and promoting neuronal cell death. Thus, NSE could be a reliable, quantitative, and specific marker of neuronal injury. Depending on the injury, disease, and microenvironment, NSE may also show neurotrophic function as it controls neuronal survival, differentiation, and neurite regeneration via activation of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways. This review discusses possible implications of NSE expression and activity in neuroinflammation, neurodegeneration, and neuroprotection in SCI and various neurodegenerative diseases for prognostic and therapeutic potential.

Central Infusion of IGF-1 Increases Hippocampal Neurogenesis and Improves Neurobehavioral Function following Traumatic Brain Injury

Would this help post stroke?  What leader in stroke will make sure followup occurs? 

Central Infusion of IGF-1 Increases Hippocampal Neurogenesis and Improves Neurobehavioral Function following Traumatic Brain Injury

To cite this article:
Dr. Shaun W. Carlson and Dr. Kathryn E Saatman. Journal of Neurotrauma. February 2018, ahead of print.
Online Ahead of Editing: February 17, 2018


Traumatic brain injury (TBI) produces neuronal dysfunction and cellular loss that can culminate in lasting impairments in cognitive and motor abilities. Therapeutic agents that promote repair and replenish neurons after TBI hold promise in improving recovery of function. Insulin-like growth factor-1 (IGF-1) is a neurotrophic factor capable of mediating neuroprotective and neuroplasticity mechanisms. Targeted overexpression of IGF-1 enhances the generation of hippocampal newborn neurons in brain-injured mice; however, the translational neurogenic potential of exogenously administered IGF-1 after TBI remains unknown. In a mouse model of controlled cortical impact (CCI), continuous intracerebroventricular infusion of recombinant human IGF-1 (hIGF) for 7 days, beginning 15min post-injury, resulted in a dose-dependent increase in the number of immature neurons in the hippocampus. Infusion of 10μg/d IGF-1 produced detectable levels of hIGF-1 in the cortex and hippocampus and a concomitant increase in Akt activation in the hippocampus. Both motor function and cognition were improved over 7 days following injury in IGF-1 treated cohorts. Vehicle treated brain-injured mice showed reduced hippocampal immature neuron density relative to sham controls at 7 days post-injury. In contrast, the density of hippocampal immature neurons in brain-injured mice receiving acute onset IGF-1 infusion was significantly higher than in injured mice receiving vehicle and equivalent to that in sham-injured control mice. Importantly, the neurogenic effect of IGF-1 was maintained with as much as a 6 hr delay in the initiation of infusion. These data suggest that central infusion of IGF-1 enhances the generation of immature neurons in the hippocampus, with a therapeutic window of at least 6 hrs post-injury, and promotes neurobehavioral recovery after TBI.


The Challenges of Implementing Functional Electrical Stimulation Cycling in a Patient with Hemiparesis following Stroke: A Case Report

I don't care about your minor challenges, your patient has much bigger challenges, mainly you with your 'can't do it attitude'

The Challenges of Implementing Functional Electrical Stimulation Cycling in a Patient with Hemiparesis following Stroke: A Case Report

Sarah Briggs
DPT Class of 2017 Department of Physical Therapy & Rehabilitation Science The University of Iowa Abstract Background: Strokes are the most common cause of severe disability in the United States. Functional electrical stimulation (FES) cycling may be used as an intervention to decrease disability post-stroke, though there is conflicting evidence among the existing studies exploring its use. The purpose of this case study is to describe the use of FES cycling in order to decrease residual disability post-stroke, as well as the challenges of implementing this intervention in the inpatient rehabilitation setting. Case Description: The patient was a 75 year -old female who presented to inpatient rehabilitation with a sub- acute ischemic right posterior cerebral artery stroke. The patient demons trated severe left hemiparesis, left homonymous hemianopsia resulting in left neglect, as well as impairments in sensation, balance, and functional mobility. Interventions consisted of use of an FES bicycle at a low dosage, balance activities, left attenti on tasks, sensory reeducation, strengthening, and education. Outcomes: The patient’s length of stay was 24 days. During this period, she demonstrated a 22-point increase in the Functional Independence Measure score from initial evaluation to discharge. The patient also demonstrated an increase in postural control as demonstrated by a five-point increase in her Postural Assessment Scale for Stroke score. Discussion: Though the patient made significant improvements in postural control and required much less assistance with mobility, she continued to demonstrate severe deficits at discharge that prevented her from returning home independently. Patient complexity, time constraints, scheduling difficulties, and reimbursement issues represented challenges of regular implementation of FES cycling, resulting in dosage at a level lower than is recommended. While current research is conflicting, FES cycling at an appropriate volume may be beneficial in reducing disability in sub-acute stroke survivors.  

Physical Barriers to Mobility of Stroke Patients in Rehabilitation Clinics

Do you really think your stroke hospital will follow these recommendations?  As far as I was concerned wheelchairs were the complete problem, Try operating one with one good hand and one good leg. The solution is out there, lever powered wheelchairs, or rowing wheelchairs, but I bet your hospital knows nothing about them. More stroke hospital incompetency in action.
  1. 1.Technische Universität DresdenDresdenGermany
Conference paper


Regaining independent mobility and general independence is the main goal of physical rehabilitation in stroke patients. The patients requiring rehabilitation stay as inpatients in rehabilitation clinics for a period of several weeks to several months. During this time, mobile patients are required to go to therapies and other scheduled appointments on their own. The aim of this study is to provide evidence that specific architectural design features of rehabilitation clinics hinder the independent mobility of stroke patients and to identify the main issues caused by the building design. Patients (n = 50) and staff members (n = 46) from five large German rehabilitation clinics participated in the study. Three methods were used to collect the data: patient questionnaire, staff questionnaire and patient shadowing (observation). Both staff and patients identified the major issues that stroke patients encounter in the built environment of rehabilitation clinics: wayfinding problems, insufficient dimensions of spaces (corridors), physical obstacles, uneven floor surfaces and large distances between patient rooms and therapy rooms. Shadowing data showed that the patients in the earlier stages of rehabilitation, mainly using a wheelchair, encounter the most barriers related to the built environment. Design recommendations for more mobility supportive rehabilitation clinics are made based on the study findings.

Controlling your weight is key to lowering stroke risk

This comes from Harvard Medical School. I've lost 20 of the 35 pounds I gained post stroke, mainly from only eating two meals a day and walking a lot. (about 9% loss for me).

Controlling your weight is key to lowering stroke risk

Controlling your weight is key to lowering stroke risk
Image: iStock
There is a lot you can do to lower your chances of having a stroke. Even if you've already had a stroke or TIA ("mini-stroke"), you can take steps to prevent another.
Controlling your weight is an important way to lower stroke risk. Excess pounds strain the entire circulatory system and can lead to other health conditions, including high blood pressure, diabetes, high cholesterol, and obstructive sleep apnea. But losing as little as 5% to 10% of your starting weight can lower your blood pressure and other stroke risk factors.
Get your copy of Stroke

Protect your brain: That’s the strategy that Harvard doctors recommend in this report on preventing and treating stroke. Whether you’ve already had a mini-stroke or a major stroke, or have been warned that your high blood pressure might cause a future stroke, Stroke: Diagnosing, treating, and recovering from a "brain attack" provides help and advice.

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Of course, you'll need to keep the weight off for good, not just while you're on a diet. The tips below can help you shed pounds and keep them off:
Move more. Exercise is one obvious way to burn off calories. But another approach is to increase your everyday activity wherever you can — walking, fidgeting, pacing while on the phone, taking stairs instead of the elevator.
Skip the sipped calories. Sodas, lattes, sports drinks, energy drinks, and even fruit juices are packed with unnecessary calories. Worse, your body doesn't account for them the way it registers solid calories, so you can keep chugging them before your internal "fullness" mechanism tells you to stop. Instead, try unsweetened coffee or tea, or flavor your own sparkling water with a slice of lemon or lime, a sprig of fresh mint, or a few raspberries.
Eat more whole foods. If you eat more unprocessed foods — such as fruits, vegetables, and whole grains — you'll fill yourself up on meals that take a long time to digest. Plus, whole foods are full of vitamins, minerals, and fiber and tend to be lower in salt — which is better for your blood pressure, too.
Find healthier snacks. Snack time is many people's downfall — but you don't have to skip it as long as you snack wisely. Try carrot sticks as a sweet, crunchy alternative to crackers or potato chips, or air-popped popcorn (provided you skip the butter and salt and season it with your favorite spices instead). For a satisfying blend of carbs and protein, try a dollop of sunflower seed butter on apple slices.
For more information on lifestyle changes you can make to help prevent a stroke, buy Stroke: Diagnosing, treating, and recovering from a "brain attack," a Special Health Report from Harvard Medical School.