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:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Saturday, March 30, 2013

Biking1 stroke rehab - 2013

Its going to occur. I picked up my bike from the shop on Wed. That night as I'm reading a loud boom occurs  in my apartment. The front tire inner tube gave out.  This morning I get the  tire off the rim using my bike tire levers.
I've changed dozens of tires so I know exactly what to do.  None of this patching for me I just go straight to a new inner tube.  Since this is my first tire change post stroke I found out that tire levers can also be used to snap the tire back onto the rim. That was the easy part. I spent the next 15 minutes wrestling  the tire onto the front fork. With two useable hands I could have gotten it done in 10 seconds. But success was going to occur. That effort knocked the front brake pad out of alignment so the left pad was preventing the wheel from turning. And since this was the new SlidePad system it took me another 15 minutes to get it adjusted. Finally got it outside in the 58 degree weather and while I only rode around in the parking lot, it felt great. The seat was no longer twisting underneath me, the left foot was prevented from sliding off due to the toe clip. The new braking system allowed me to get going fast enough so I was no longer wobbling. The rear view mirror meant I didn't need to try looking over my shoulder. The only problem to be corrected is my left wrist curls and will not stay straight.  But its happening and I am happy, happy, happy.

Ill. Fire Dept. Medics Sued For Misdiagnosed Stroke

How many more of these will it take before the stroke associations and the Joint Commission step up to the plate and do their job of pushing objective diagnosis of stroke? Like these sixteen. They don't even have to expend any intellectual energy, I've done that for them. Even so there is a misunderstanding that strokes can be resolved if they are just diagnosed fast enough. That's a direct failure/result of the F.A.S.T. campaign.
http://www.firehouse.com/news/10912331/ill-fire-dept-medics-sued-for-misdiagnosed-stroke
An Aurora woman has sued the city and fire department, arguing three paramedics thought she was drunk when she called for emergency help last year when in reality she was having a stroke.
Susan Miller's lawsuit, filed in Kane County this week, argues that paramedics only treated her for six minutes and failed to provide proper care after arriving at her house at 2:04 a.m. May 28, 2012, after she complained of numbness in her arm and that she had fallen and could not get up.
Miller told the paramedics she had drank alcohol earlier in the day and the paramedics, instead of treating her and performing other tests, told her son to have his mother "sleep it off," according to the lawsuit.
Less than three hours later, the woman's ex-husband took her to the Provena Mercy Medical Center in Aurora and doctors determined she suffered a stroke.
"As a result in the delay in receiving the proper medical treatment for her stroke, Miller suffered and continues to suffer from various injuries including but not limited to permanent facial paralysis, vision loss and one-sided paralysis," read part of the lawsuit. "The defendant's utter indifferent or conscious disregard for the safety of Miller is evident from defendant's failure to discover a danger through recklessness or carelessness and which could have been discovered with the exercise of ordinary care."
A message left at the Aurora Fire Department's main station was not returned.
Aurora city spokesman Clay Muhammad said the city had not yet been served with the lawsuit and would not comment. Miller's attorney, Dennis Stefanowicz, did not return messages.
Both sides are due in court June 13. Miller seeks a jury trial and unspecified damages, according to the lawsuit.

Walking in the dark

After Michigan state lost I went for a walk in the woods, this time with a headband flashlight. It took me 15 minutes to get it on one-handed. Great therapy because your foot placement is unknown so your ankle muscles need to immediately compensate for any deviations  in flatness. I'll have to go sometime in daylight with my pruning saw to get the hanging branches trimmed.  Then I walked around the apartment pond and listened to the mallards swimming and splashing around while watching the moon rise. Its great to be alive.

Cerebral vasospasm following subarachnoid hemorrhage: time for a new world of thought

A good explanation of what follows after a hemorrhage.  I'm sure your doctor explained all this since this is only 3.5 years old.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706525/

INTRODUCTION

When persons in good health are suddenly seized with pains in the head, and straightway are laid down speechless, and breathe with stertor, they die in seven days.
Hippocrates 460–370 BC, Aphorisms on Apoplexy1
Hippocrates’ 2400-year-old description of delayed death probably caused by a ruptured intracranial aneurysm with subsequent vasospasm is still valid today. Aneurysmal subarachnoid hemorrhage (SAH) affects about 10 out of 100,000 adults annually, and up to half of those affected die soon after2; most of the rest are successfully treated surgically and/or endovascularly. Despite obliterating the offending aneurysm and removing the risk of rebleeding, up to half of the treated patients develop a syndrome of focal and/or cognitive deficits due to cerebral vasospasm (delayed ischemic neurological deficit, symptomatic vasospasm) between the fourth and ninth day after the SAH3. As a result, many die or suffer permanent morbidity2, and it has been described as the single most important cause of morbidity and mortality in patients whose ruptured aneurysm is successfully treated4.
Patients require vigilant monitoring and treatment for up to 2 weeks, including invasive monitoring of blood pressure, cerebral blood flow and metabolism and often complex treatment with calcium antagonists, hypertensive drugs, hemodilution and hypervolemia (triple H therapy), plus risky and often only temporarily effective intra-arterial administration of vasodilator drugs or balloon angioplasty5. These treatments have been documented in nine international conferences on cerebral vasospasm (Table 1).
Table 1
Summary of international conferences on cerebral vasospasm, 1972–2006
Since the demonstration of arterial narrowing in the syndrome of cerebral vasospasm in 19516 and the further emphasis in 1978 by Weir et al.3, it has been proven that SAH gives rise to arterial narrowing and in turn ischemia, causing infarction and poor outcome. Most research into delayed deterioration after SAH has been conducted in concordance with this axiom, with the goal of interrupting this perceived chain of events. There have been many clinical trials, but until the arrival of clazosentan, a selective endothelin 1A receptor antagonist, it has not been possible to reproducibly break this chain. Clazosentan did, however, effectively prevent and reverse arterial narrowing in one work7, providing what was thought may at last be an effective treatment. However, the subsequent multi-center CONSCIOUS trial, despite significant reductions in angiographic vasospasm, failed to show any effect on long-term outcome.
The axiom has thus been challenged in such a fashion that it amounts to a paradigm shift.
Accumulated evidence suggests that (1) arterial narrowing is not the only cause of delayed clinical deterioration, (2) arterial narrowing is not necessarily multifactorial but (3) may actually be an effect of a single factor and finally (4) the entire picture of delayed clinical deterioration may be multifactorial. These facts should lead to a search for a more comprehensive and adequate theory that not only can explain observed discrepancies but also will lead to development of a specific and effective treatment strategy.
In recent years, two major concepts in pre-vasospasm research have developed: early brain injury and cortical spreading depression. Basic animal works and some clinical observations have long pointed to the importance of the pre-vasospasm period, with recognition of the importance of transitory ischemia at the onset of SAH 8, the opening of the blood–brain barrier9,10, the existence of early arterial narrowing in clinical settings11 and the detection of cortical spreading ischemia after SAH12. One or more of these events may replace arterial narrowing as important causes of poor outcomes after SAH13.

PATHOPHYSIOLOGY OF ARTERIAL NARROWING: NEW DEVELOPMENTS

The idea of arterial narrowing has previously been central to understanding the syndrome of cerebral vasospasm, but as outlined above, a paradigm shift is underway. Even so, the association of arterial narrowing with delayed ischemic deficits and the fact that reversal of narrowing by angioplasty can reverse deficits make consideration of pathophysiological events in cerebral arteries still very relevant, as shown in several reviews. Highlights of recent developments are presented below.

Nerve Growth Factor, Brain-Derived Neurotrophic Factor, Neurotrophin-3 and Glial-Derived Neurotrophic Factor Enhance Angiogenesis in a Tissue-Engineered In Vitro Model

We need angiogenesis to support stem cells and migrating neurons to the damaged area. Ask your doctor to apply this to your recovery. Its going to take some intellect to transfer this knowledge from skin to the brain.
http://online.liebertpub.com/doi/abs/10.1089/ten.tea.2012.0745

ABSTRACT

Skin is a major source of secretion of the neurotrophic factors nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and glial-derived neurotrophic factor (GDNF) controlling cutaneous sensory innervation. Beside their neuronal contribution, we hypothesized that neurotrophic factors also modulate the cutaneous microvascular network. First, we showed that NGF, BDNF, NT-3, and GDNF were all expressed in the epidermis, while only NGF and NT-3 were expressed by cultured fibroblasts, and BDNF by human endothelial cells. We demonstrated that these peptides are highly potent angiogenic factors using a human tissue-engineered angiogenesis model. A 40% to 80% increase in the number of capillary-like tubes was observed after the addition of 10 ng/mL of NGF, 0.1 ng/mL of BDNF, 15 ng/mL of NT-3, and 50 ng/mL of GDNF. This is the first characterization of the direct angiogenic effect of NT-3 and GDNF. This angiogenic effect was mediated directly through binding with the neurotrophic factor receptors tropomyosin-receptor kinase A (TrkA), TrkB, GFRα-1 and c-ret that were all expressed by human endothelial cells, while this effect was blocked by addition of the Trk inhibitor K252a. Thus, if NGF, BDNF, NT-3, and GDNF may only moderately regulate the microvascular network in normal skin, they might have the potential to greatly increase angiogenesis in pathological situations.

Watching object related movements modulates mirror-like activity in parietal brain regions

More proof of action observation. See how long before your doctor and therapists give you stroke protocols based upon this. 10-20 years I bet. No self-prescribing, you know how dangerous it is watching videos of muscle movement.
http://www.clinph-journal.com/article/S1388-2457%2813%2900120-X/abstract

Highlights 


The observation of goal-directed movements leads to stronger event-related desynchronization (ERD) in alpha, beta and gamma frequency bands over parietal compared to central brain regions.

Both the type of grasping and the type of object induced an ERS over sensorimotor areas in the upper alpha and lower beta band, respectively.

Beside the often cited MNS linked mu rhythm there is further cortical rhythmicity over parietal sites, which might be part of an “extended” human MNS.

Abstract 

Objective

We studied the activation of cortical motor and parietal areas during the observation of object related grasping movements. By manipulating the type of an object (realistic versus abstract) and the type of grasping (correct versus incorrect), we addressed the question how observing such object related movements influences cortical rhythmicity, especially the mu-rhythm, in the context of an “extended” human mirror neuron system (MNS).

Methods

Multichannel electroencephalogram (EEG) was recorded during the observation of different object-related grasping actions in twenty healthy subjects. Different movies were presented, showing sequences of correct or incorrect hand grasping actions related to an abstract or realistic (daily life) object.

Results

Event-related de/synchronization (ERD/ERS) analyses revealed a larger ERD in the upper alpha (10–12Hz), beta (16–20Hz) and gamma (36–40Hz) frequency bands over parietal brain regions depending on the type of grasping. The type of object only influenced ERD patterns in the gamma band range (36–40Hz) at parietal sites suggesting a strong relation of gamma band activity and cortical object representation. Abstract and realistic objects produced lower beta band synchronization at central sites only, whereas depending on the type of grasping an ERS in the upper alpha band (10–12Hz) was observed.

Conclusion

Depending on the type of the grasped object and the type of grasping stronger parietal cortical activation occurred during movement observation.

Significance

Discussing the results in terms of an “extended” human mirror neuron system (MNS), it could be concluded that beside sensorimotor areas a stronger involvement of parietal brain regions was found depending on the type of object and grasping movement observed.

Acute Microvascular Changes after Subarachnoid Hemorrhage and Transient Global Cerebral Ischemia

Yeah, another paper on hemorrhage.
http://scholar.google.com/scholar_url?hl=en&q=http://downloads.hindawi.com/journals/srt/2013/425281.pdf&sa=X&scisig=AAGBfm0CNg2J04M7tLmWYuYh11Fbfm-72w&oi=scholaralrt
1. Introduction
Subarachnoid hemorrhage (SAH) is a type of hemorrhagic
stroke, most commonly caused by a ruptured intracranial
aneurysm. At the time of aneurysm rupture, blood pours
into the subarachnoid space, and the intracranial pressure
(ICP) inside the rigid calvarium increases sharply, causing
a corresponding decrease in cerebral blood flow (CBF). The
patient’s clinical presentation on arrival to the hospital can
depend on the degree and duration of this initial global
cerebral ischemia.
Patients with aneurysmal SAHmay develop angiographic
vasospasm and delayed cerebral ischemia (DCI) with onset
3–12 days after the initial rupture [1]. DCI may or may
not be accompanied by large artery vasospasm as seen with
vascular imaging [2]. A multicenter randomized clinical trial
has not shown improvement in neurologic outcome despite
ameliorating the delayed large artery vasospasm [3].Whether
this is due to efficacy of rescue therapy in the placebo
groups or drug toxicity abrogating beneficial effects in the
clazosentan groups has not been resolved. Nevertheless, as
a result of these results, research in SAH has also investigated
early brain injury and acute microvascular changes
[4]. Nimodipine, an L-type calcium channel antagonist, is
the only pharmacologic agent that has been shown to consistently
improve neurologic outcomes in clinical trials of
patients with SAH
[5].
Similarly, cardiac arrest (CA) results in global cerebral
ischemia that is transient in clinically relevant cases, since
if cardiac function is not restored, the situation is of pathological
interest only. Other causes of transient global cerebral
ischemia (tGCI) include asphyxia, shock, and complex
cardiac surgery [6]. The clinical presentation depends on the
duration of cardiac arrest and time to initiating cardiopulmonary
resuscitation. After global cerebral ischemia from
SAH or tGCI, a cascade of molecular events occurs, resulting
in variable degrees of brain injury and cerebrovascular
changes.
Global cerebral ischemia in postcardiac arrest has also
been studied extensively for many decades in various animal
models. Other than early induced mild hypothermia [7, 8],
clinical translation of neuroprotective strategies and therapeutics
has largely been unsuccessful.
The study of the microcirculation after tGCI and SAH
remains a difficult undertaking, but this strategy of study
may reveal potential therapeutic targets and new insights
into disease pathophysiology.The purpose of this paper is to
look at relevant animal and preclinical studies investigating
2 Stroke Research and Treatment
acute microvascular changes (within the first 48 hours)
occurring after either SAH or tGCI. Cerebral microvessels
may be defined as vessels less than or equal to 100 micrometers
in diameter [9]. Animal studies of focal ischemia or
studies focused on the large cerebral vessels (i.e., circle of
Willis arteries, basilar artery, etc.) are not included in this
paper. While we acknowledge that tGCI may occur in a
large heterogeneous group of disorders (i.e., traumatic brain
injury, intracerebral hemorrhage, etc.), we have chosen to
focus solely on tGCI secondary to cardiac arrest or mechanisms
mimicking cardiac arrest, such as extracranial arterial
occlusion. After providing an overview of various animal
models and general trends in cerebral hemodynamics after
SAH and tGCI, we provide an in-depth review of studies
investigating specific microvascular changes that occur in
these two conditions: (1) microvascular constriction; (2)
increased leukocyte-endothelial cell interactions; (3) blood
brain barrier (BBB) breakdown; and (4) platelet aggregation
and microthrombosis.

9 pages in total.

Agomelatine, a novel intriguing antidepressant option enhancing neuroplasticity: A critical review

Have your doctor and researcher compare this one to the previous research on anti-depressants to see which one is better. You do expect your medical staff to know the answer to such simple questions, don't you?
http://informahealthcare.com/doi/abs/10.3109/15622975.2013.765593
Objectives. The treatment of major affective disorders, commonly associated with high disability and elevated social costs may be still considered unsatisfactory. Among all antidepressant drugs, predominantly acting through monoaminergic mechanisms, agomelatine is of particular interest due to another alternative mechanism of action. Targeting melatonergic receptors, agomelatine play a crucial role in synchronizing circadian rhythms, known to be altered in depressed subjects. Methods. A critical review of the literature focusing on efficacy, safety and tolerability of agomelatine in major affective disorders was performed. Additionally, we focused on the potential of agomelatine in enhancing neuroplasticity mechanisms and promote neurogenesis. A total of 136 articles from peer-reviewed journals were identified, of which 50 were assessed for eligibility and 21 were included. Results. Agomelatine, a melatonergic analogue drug acting as MT1/MT2 agonist and 5-HT2C antagonist, has been reported to be effective as antidepressant drug. Studies confirmed not only clinical efficacy but also safety and tolerability of agomelatine. Also, it enhances neuroplasticity mechanisms and adult neurogenesis in brain areas such as hippocampus and prefrontal cortex. Conclusions. Agomelatine actually represents an intriguing option in the treatment of affective disorders.

Friday, March 29, 2013

Why I survived my stroke

This is all speculation on my part. Your doctor should know a hell of a lot more than I do.
My brain reserve was built up.
by
1. bilingualism
2. new musical instruments,
piano, My daughter taught me 3 years prior but I never got beyond one-handed playing
saxophone, 3 years prior I started this but never got good enough to remember the finger positions after stroke. Its one of my goals now.
3. sudoku, I would do this every night before going to bed, worked my way up to doing the hardest ones in each book.  Immediately post-stroke I tried this and couldn't juggle that many numbers in my mind, even the easy ones were off limits.
4. new outdoor activity, 10 years of whitewater canoeing. Providing both a cognitive challenge and exercise created neurogenesis.

My physical condition was great. Three years after the event during a physical my resting heart rate was 54 at age 53. The doctor asked what cardio exercises I was doing. 'None for the last three years'.

I received tPA within 90 minutes of onset of the stroke.
I wrote about this earlier here but this is a little more fleshed out.  Video of Denison Falls there.
http://oc1dean.blogspot.com/2010/09/3-reasons-i-survived.html

I have to build up my reserve again to prepare for dementia or Alzheimers.

Inflammation In Atherosclerotic Plaque Formation

4 min. 36 seconds of explanation. This is what happened to my right carotid artery. My doctor should have explained this but no, he didn't say anything.
The accent is a bit hard to understand and needs to be  rerecorded to a laypersons understanding.
http://www.youtube.com/watch?v=Na6-kP9VYCU

picture from here:
 http://mycardiacwebsite.com/Coronary%20Artery%20Disease/heart_attacks.html
plaque buid up

Doctors and patients could decide who gets medical marijuana under draft Mass. rules

You can check out my 3 posts on canabinoids or 17 on marijuana to decide how you want to respond to requests for comments. You have until April 10 to respond.
You could try the prevention route - a marijuana bud a day reduces stroke risk by50%.
or
the spasticity route
or neurogenesis
or neuropathic pain
or prevention as better than statins.
Whatever, tell them you need the ability to use it for whatever scientific proof comes along rather than limit it to current knowledge.
http://www.boston.com/whitecoatnotes/2013/03/29/doctors-and-patients-could-decide-who-gets-medical-marijuana-under-draft-mass-rules/BGIADLbsh9BA45LUGFqB3M/story.html
Draft rules for medical use of marijuana in Massachusetts, issued Friday by the state Department of Public Health, largely leave it up to doctors to decide which patients will qualify for treatment with the drug.
Patients must have a debilitating condition -- defined as causing weakness, wasting syndrome, intractable pain or nausea, or impairing strength or ability and limiting major life activities -- and the regulations list qualifying conditions, including cancer, glaucoma, HIV/AIDS, hepatitis C, and ALS(you need to get stroke in here at least). But the rules also would allow doctors and their patients to decide what other conditions would qualify patients for treatment. Poorly written - nothing on preventing disability or use for rehabilitation.
Pay it forward, you must respond for future survivors. Get off your ass and do something.
more at link.

Ebselen Alters Mitochondrial Physiology and Reduces Viability of Rat Hippocampal Astrocytes

We really don't want to reduce astrocyte viability so get your researcher looking into this.
A 1998 article suggested that ebselen might be a good neuroprotective drug.  Your doctor needs to reconcile the deleterious contradictions between these 2 articles.
http://online.liebertpub.com/doi/abs/10.1089/dna.2012.1939

ABSTRACT

The seleno-organic compound and radical scavenger ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one) have been extensively employed as an anti-inflammatory and neuroprotective compound. However, its glutathione peroxidase activity at the expense of cellular thiols groups could underlie certain deleterious actions of the compound on cell physiology. In this study, we have analyzed the effect of ebselen on rat hippocampal astrocytes in culture. Cellular viability, the intracellular free-Ca2+ concentration ([Ca2+]c), the mitochondrial free-Ca2+ concentration ([Ca2+]m), and mitochondrial membrane potential (ψm) were analyzed. The caspase-3 activity was also assayed. Our results show that cell viability was reduced by treatment of cells with ebselen, depending on the concentration employed. In the presence of ebselen, we observed an initial transient increase in [Ca2+]c that was then followed by a progressive increase to an elevated plateau. We also observed a transient increase in [Ca2+]m in the presence of ebselen that returned toward a value over the prestimulation level. The compound induced depolarization of ψm and altered the permeability of the mitochondrial membrane. Additionally, a disruption of the mitochondrial network was observed. Finally, we did not detect changes in caspase-3 activation in response to ebselen treatment. Collectively, these data support the likelihood of ebselen, depending on the concentration employed, reduces viability of rat hippocampal astrocytes via its action on the mitochondrial activity. These may be early effects that do not involve caspase-3 activation. We conclude that, depending on the concentration used, ebselen might exert deleterious actions on astrocyte physiology that could compromise cell function.

Bilingualism - neuroprotection and cognitive ability

Some consider learning programming languages in the same category. In my career I have learned Assembler, Cobol, Java, C, Smalltalk, DB2, MQSeries.  I can probably add this to my reasons for surviving my stroke. I may have to learn another language to prevent possible dementia.
The blogger discussing it here:
http://brainblogger.com/2013/03/29/bilingualism-may-be-neuroprotective/
The original articles here:
Lifelong bilingualism maintains neural efficiency for cognitive control in aging.
Lifelong bilingualism maintains white matter integrity in older adults.

Traumatic Brain Injury

A great poster explaining TBI. We need something similar for stroke because no one  seems to be cognizant of all the neurons dying secondarily due to:
1.  Excitotoxicity
2.  Glutamate poisoning
3.  Capillaries that don't open due to pericytes
4.  Inflammatory action leaking through the blood brain barrier
 My doctor could have just handed me a poster like this since he didn't tell me anything about my stroke at all. And maybe I wouldn't be such an asshole pointing out all the failures in the stroke world.
http://knowingneurons.com/2013/03/27/traumatic-brain-injury/

Thursday, March 28, 2013

Mitchell, SD chiropractor denies causing Gunkel's stroke

This is so simple to prevent something like this. Never get your neck adjusted.
http://www.mitchellrepublic.com/event/article/id/77150/group/homepage/
A local chiropractor has denied accusations from a local woman who claims a neck adjustment caused her to suffer a stroke.
In a two-page answer filed Monday, Gary Hendrix, a chiropractor with an office located at 310 N. Lawler St. in Mitchell, denies that a neck adjustment he performed on Christie Gunkel caused her to have a stroke.
Gunkel, who recently became treasurer of Davison County, filed a lawsuit in January claiming a neck adjustment she received from Hendrix on Aug. 8 caused a “dissection,” or tear, in an artery in her neck, resulting in a stroke. Hendrix admits to treating Gunkel, and admits she “had problems following treatment,” but denies he did anything to cause the stroke, court documents say.
Gunkel also claims Hendrix breached the standard of care and failed to inform Gunkel of all the risks involved in a neck adjustment, a claim that Hendrix denies in his response.
Gunkel is represented by Renee H. Christensen, of Sioux Falls. Hendrix is represented by J. Crisman Palmer, of Rapid City.
In an interview with The Daily Republic in January, Gunkel said she went to Hendrix’s office Aug. 8 because of soreness in her neck, and Hendrix treated her with a neck adjustment.
Later that day, Gunkel went to the emergency room at Avera Queen of Peace Hospital in Mitchell, where she suffered a stroke, she said. From there, Gunkel was taken by ambulance to Avera McKennan Hospital in Sioux Falls, where she spent four days undergoing CT scans and MRIs, as well as physical and occupational therapy.
Gunkel claims she suffered permanent injury, experienced and will continue to experience “great pain, discomfort, mental anguish and loss of enjoyment of life,” and has “been unable to perform several normal functions of life,” her complaint says.

Stroke’s Quantum Jump: The Interprofessional Team

A department heads' blog at Queens University. Its pathetic that the last quantum leap for stroke was back in 1996 for tPA. And tPA has poor efficacy so it was more like a high jump.
http://deptmed.queensu.ca/blog/?p=220

My reply in the comments section, no response.
When are we going to get to the next quantum jump and start identifying interventions that are neuroprotective or stop the neuronal cascade of death? I know Dr. Michael Tymianski has noted that 1000+ drugs that worked in preventing damage in rodents did not work in humans. That might be explained by rodent inflammation is not the same as human inflammation. For my next stroke I will demand my doctor give me ibuprofen, levodopa, anti-depressants,minocycline, fish oil, amantadine or tell me why not.

More Dietary Fiber Might Help Thwart Stroke

What more can you ask for? An open-ended stroke-risk reduction. Your doctor can translate how many grams of fiber you need to have a zero risk of stroke. Note the word initial. No self prescribing, you know how dangerous doing things without your doctors knowledge is.
http://www.webmd.com/stroke/news/20130328/more-dietary-fiber-might-help-thwart-stroke-study
For every 7-gram bump in daily fiber consumption, an individual's risk for experiencing an initial stroke appears to plummet 7 percent, the investigators concluded after analyzing 20-plus years of research.
More research would be needed to come up with an ideal stroke-prevention grocery list.
More at link.

Aviir MIRISK VP test

A coronary risk test your doctor will have to weigh in on.  Your doctor will know if this is suitable for predicting stroke also and what needs to be done to prevent adverse events. You hope.
http://www.aviir.com/patients/mirisk_vp_patient_faqs

Stroke Awareness and Education Toolkit for Healthcare Providers

From The Delta States Stroke Network (DSSN) is a partnership of southeastern states in the Delta
region, including, Alabama, Arkansas, Louisiana, Mississippi, and Tennessee.
You can see what training the medical world has on our condition,
No mention of neuroprotection or cascade of death.
Nothing on hypothermia.
No protocols on recovery.
http://msdh.ms.gov/msdhsite/_static/resources/3904.pdf
71 pages of not very useful stuff.

Up-regulation of the canonical Wnt-3 A and Sonic hedgehog signaling underlies melanocortin-induced neurogenesis after cerebral ischemia

More hedgehogs, get your researcher involved.
http://www.sciencedirect.com/science/article/pii/S0014299913002203

Abstract

In experimental cerebral ischemia, melanocortin MC4 receptor agonists induce neuroprotection and neurogenesis with subsequent long-lasting functional recovery. Here we investigated the molecular mechanisms underlying melanocortin-induced neurogenesis. Gerbils were subjected to transient global cerebral ischemia, then they were treated every 12 h, and until sacrifice, with 5-bromo-2’-deoxyuridine (BrdU; to label proliferating cells), and the melanocortin analog [Nle4,D-Phe7]α-melanocyte-stimulating hormone (NDP-α-MSH) or saline. NDP-α-MSH increased hippocampus dentate gyrus (DG) expression of Wnt-3 A, β-catenin, Sonic hedgehog (Shh), Zif268, interleukin-10 (IL-10) and doublecortin (DCX), as detected at days 3, 6 and 10 after the ischemic insult. Further, an elevated number of BrdU immunoreactive cells was found at days 3 and 10, and an improved histological picture with reduced neuronal loss at day 10, associated with learning and memory recovery. Pharmacological blockade of the Wnt-3 A/β-catenin and Shh pathways, as well as of melanocortin MC4 receptors, prevented all effects of NDP-α-MSH. These data indicate that, in experimental brain ischemia, treatment with melanocortins acting at MC4 receptors induces neural stem/progenitor cell proliferation in the DG by promptly and effectively triggering the canonical Wnt-3 A/β-catenin and Shh signaling pathways. Activation of these pathways is associated with up-regulation of the repair factor Zif268 and the neurogenesis facilitating factor IL-10, and it seems to address mainly towards a neuronal fate, as indicated by the increase in DCX positive cells.

Wednesday, March 27, 2013

Researchers form new nerve cells – directly in the brain

Come on, lets speed this up, 10 million persons a year could use this.
You can use this to watch the cells to see how they are doing.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=129731&CultureCode=en
The field of cell therapy, which aims to form new cells in the body in order to cure disease, has taken another important step in the development towards new treatments. A new report from researchers at Lund University in Sweden shows that it is possible to re-programme other cells to become nerve cells, directly in the brain.
Two years ago, researchers in Lund were the first in the world to re-programme human skin cells, known as fibroblasts, to dopamine-producing nerve cells – without taking a detour via the stem cell stage. The research group has now gone a step further and shown that it is possible to re-programme both skin cells and support cells directly to nerve cells, in place in the brain.
“The findings are the first important evidence that it is possible to re-programme other cells to become nerve cells inside the brain”, said Malin Parmar, research group leader and Reader in Neurobiology.
The researchers used genes designed to be activated or de-activated using a drug. The genes were inserted into two types of human cells: fibroblasts and glia cells – support cells that are naturally present in the brain. Once the researchers had transplanted the cells into the brains of rats, the genes were activated using a drug in the animals’ drinking water. The cells then began their transformation into nerve cells.
In a separate experiment on mice, where similar genes were injected into the mice’s brains, the research group also succeeded in re-programming the mice’s own glia cells to become nerve cells.
“The research findings have the potential to open the way for alternatives to cell transplants in the future, which would remove previous obstacles to research, such as the difficulty of getting the brain to accept foreign cells, and the risk of tumour development”, said Malin Parmar.
All in all, the new technique of direct re-programming in the brain could open up new possibilities to more effectively replace dying brain cells in conditions such as Parkinson’s disease.
“We are now developing the technique so that it can be used to create new nerve cells that replace the function of damaged cells. Being able to carry out the re-programming in vivo makes it possible to imagine a future in which we form new cells directly in the human brain, without taking a detour via cell cultures and transplants”, concluded Malin Parmar.
http://www.lunduniversity.lu.se/o.o.i.s?id=24890&news_item=6030

Better treatment for hemorrhagic stroke patients on horizon

A breakthrough that a Great Stroke Association would follow thru with hypothesis, theories and clinical studies.
http://medicalxpress.com/news/2013-03-treatment-patients-horizon.html
Two molecules may provide, for the first time, an indication of which stroke patients will suffer a further, long-term neurological deficit, allowing doctors to tailor treatment more effectively.

Read more at: http://medicalxpress.com/news/2013-03-treatment-patients-horizon.html#jCp
 Two molecules may provide, for the first time, an indication of which stroke patients will suffer a further, long-term neurological deficit, allowing doctors to tailor treatment more effectively.

Subarachnoid haemorrhage (SAH), a form of stroke, affects around half a million people worldwide each year. Nearly 50 per cent of patients who survive the initial haemorrhage die within 30 days, with survivors likely to suffer permanent disability. A study by Dr Sanjaya Kuruppu and Professor Ian Smith of Monash University and clinicians at Harvard Medical School, Dr Mingming Ning and Dr Sherry Chou, has shown that there may be a way to predict the sub-group of SAH patients that will suffer severe long-term disability. By assessing the cerebrospinal fluid of SAH patients, the researchers discovered that in the three days immediately following the stroke, an enzyme, endothelin converting enzyme-1 (ECE-1) and its substrate big endothelin-1 (BigET-1) were elevated in patients that suffered a disability that severely impacted on their capacity to self-care. Dr Sanjaya Kuruppu, of the Monash Department of Biochemistry and Molecular Biology said the discovery was a breakthrough in treating a deadly and unpredictable condition. "This is the first time doctors have had an early and accurate indication that disability will occur, giving them time to focus appropriate and aggressive therapies on this group of patients," Dr Kuruppu said. "More importantly, it provides families with information required to make crucial decisions about subsequent long-term care." As cerebrospinal fluid is routinely monitored following SAH, testing for elevated levels of ECE-1 and BigET-1 would have no negative impact on patients. Professor Ian Smith, Pro Vice-Chancellor (Research and Research Infrastructure) was the lead researcher on the project at Monash. "The next step in bringing this breakthrough to a clinical setting is to develop the technology to enable rapid diagnosis in a hospital setting and we're currently making progress on this," Professor Smith said. The Monash researchers, again in collaboration with Harvard, are planning a larger clinical study in the near future. They aim to determine the exact threshold level of the molecules required to classify a patient as being at high risk of developing long-term disability.

Read more at: http://medicalxpress.com/news/2013-03-treatment-patients-horizon.html#jCp
 Subarachnoid haemorrhage (SAH), a form of stroke, affects around half a million people worldwide each year. Nearly 50 per cent of patients who survive the initial haemorrhage die within 30 days, with survivors likely to suffer permanent disability. A study by Dr Sanjaya Kuruppu and Professor Ian Smith of Monash University and clinicians at Harvard Medical School, Dr Mingming Ning and Dr Sherry Chou, has shown that there may be a way to predict the sub-group of SAH patients that will suffer severe long-term disability. By assessing the cerebrospinal fluid of SAH patients, the researchers discovered that in the three days immediately following the stroke, an enzyme, endothelin converting enzyme-1 (ECE-1) and its substrate big endothelin-1 (BigET-1) were elevated in patients that suffered a disability that severely impacted on their capacity to self-care. Dr Sanjaya Kuruppu, of the Monash Department of Biochemistry and Molecular Biology said the discovery was a breakthrough in treating a deadly and unpredictable condition. "This is the first time doctors have had an early and accurate indication that disability will occur, giving them time to focus appropriate and aggressive therapies on this group of patients," Dr Kuruppu said. "More importantly, it provides families with information required to make crucial decisions about subsequent long-term care." As cerebrospinal fluid is routinely monitored following SAH, testing for elevated levels of ECE-1 and BigET-1 would have no negative impact on patients. Professor Ian Smith, Pro Vice-Chancellor (Research and Research Infrastructure) was the lead researcher on the project at Monash. "The next step in bringing this breakthrough to a clinical setting is to develop the technology to enable rapid diagnosis in a hospital setting and we're currently making progress on this," Professor Smith said. The Monash researchers, again in collaboration with Harvard, are planning a larger clinical study in the near future. They aim to determine the exact threshold level of the molecules required to classify a patient as being at high risk of developing long-term disability.
Subarachnoid haemorrhage (SAH), a form of stroke, affects around half a million people worldwide each year. Nearly 50 per cent of patients who survive the initial haemorrhage die within 30 days, with survivors likely to suffer permanent disability. A study by Dr Sanjaya Kuruppu and Professor Ian Smith of Monash University and clinicians at Harvard Medical School, Dr Mingming Ning and Dr Sherry Chou, has shown that there may be a way to predict the sub-group of SAH patients that will suffer severe long-term disability. By assessing the cerebrospinal fluid of SAH patients, the researchers discovered that in the three days immediately following the stroke, an enzyme, endothelin converting enzyme-1 (ECE-1) and its substrate big endothelin-1 (BigET-1) were elevated in patients that suffered a disability that severely impacted on their capacity to self-care. Dr Sanjaya Kuruppu, of the Monash Department of Biochemistry and Molecular Biology said the discovery was a breakthrough in treating a deadly and unpredictable condition. "This is the first time doctors have had an early and accurate indication that disability will occur, giving them time to focus appropriate and aggressive therapies on this group of patients," Dr Kuruppu said. "More importantly, it provides families with information required to make crucial decisions about subsequent long-term care." As cerebrospinal fluid is routinely monitored following SAH, testing for elevated levels of ECE-1 and BigET-1 would have no negative impact on patients. Professor Ian Smith, Pro Vice-Chancellor (Research and Research Infrastructure) was the lead researcher on the project at Monash. "The next step in bringing this breakthrough to a clinical setting is to develop the technology to enable rapid diagnosis in a hospital setting and we're currently making progress on this," Professor Smith said. The Monash researchers, again in collaboration with Harvard, are planning a larger clinical study in the near future. They aim to determine the exact threshold level of the molecules required to classify a patient as being at high risk of developing long-term disability.

Read more at: http://medicalxpress.com/news/2013-03-treatment-patients-horizon.html#jCp
Subarachnoid haemorrhage (SAH), a form of stroke, affects around half a million people worldwide each year. Nearly 50 per cent of patients who survive the initial haemorrhage die within 30 days, with survivors likely to suffer permanent disability. A study by Dr Sanjaya Kuruppu and Professor Ian Smith of Monash University and clinicians at Harvard Medical School, Dr Mingming Ning and Dr Sherry Chou, has shown that there may be a way to predict the sub-group of SAH patients that will suffer severe long-term disability. By assessing the cerebrospinal fluid of SAH patients, the researchers discovered that in the three days immediately following the stroke, an enzyme, endothelin converting enzyme-1 (ECE-1) and its substrate big endothelin-1 (BigET-1) were elevated in patients that suffered a disability that severely impacted on their capacity to self-care. Dr Sanjaya Kuruppu, of the Monash Department of Biochemistry and Molecular Biology said the discovery was a breakthrough in treating a deadly and unpredictable condition. "This is the first time doctors have had an early and accurate indication that disability will occur, giving them time to focus appropriate and aggressive therapies on this group of patients," Dr Kuruppu said. "More importantly, it provides families with information required to make crucial decisions about subsequent long-term care." As cerebrospinal fluid is routinely monitored following SAH, testing for elevated levels of ECE-1 and BigET-1 would have no negative impact on patients. Professor Ian Smith, Pro Vice-Chancellor (Research and Research Infrastructure) was the lead researcher on the project at Monash. "The next step in bringing this breakthrough to a clinical setting is to develop the technology to enable rapid diagnosis in a hospital setting and we're currently making progress on this," Professor Smith said. The Monash researchers, again in collaboration with Harvard, are planning a larger clinical study in the near future. They aim to determine the exact threshold level of the molecules required to classify a patient as being at high risk of developing long-term disability.

Read more at: http://medicalxpress.com/news/2013-03-treatment-patients-horizon.html#jCp
Subarachnoid haemorrhage (SAH), a form of stroke, affects around half a million people worldwide each year. Nearly 50 per cent of patients who survive the initial haemorrhage die within 30 days, with survivors likely to suffer permanent disability. A study by Dr Sanjaya Kuruppu and Professor Ian Smith of Monash University and clinicians at Harvard Medical School, Dr Mingming Ning and Dr Sherry Chou, has shown that there may be a way to predict the sub-group of SAH patients that will suffer severe long-term disability. By assessing the cerebrospinal fluid of SAH patients, the researchers discovered that in the three days immediately following the stroke, an enzyme, endothelin converting enzyme-1 (ECE-1) and its substrate big endothelin-1 (BigET-1) were elevated in patients that suffered a disability that severely impacted on their capacity to self-care. Dr Sanjaya Kuruppu, of the Monash Department of Biochemistry and Molecular Biology said the discovery was a breakthrough in treating a deadly and unpredictable condition. "This is the first time doctors have had an early and accurate indication that disability will occur, giving them time to focus appropriate and aggressive therapies on this group of patients," Dr Kuruppu said. "More importantly, it provides families with information required to make crucial decisions about subsequent long-term care." As cerebrospinal fluid is routinely monitored following SAH, testing for elevated levels of ECE-1 and BigET-1 would have no negative impact on patients. Professor Ian Smith, Pro Vice-Chancellor (Research and Research Infrastructure) was the lead researcher on the project at Monash. "The next step in bringing this breakthrough to a clinical setting is to develop the technology to enable rapid diagnosis in a hospital setting and we're currently making progress on this," Professor Smith said. The Monash researchers, again in collaboration with Harvard, are planning a larger clinical study in the near future. They aim to determine the exact threshold level of the molecules required to classify a patient as being at high risk of developing long-term disability.

Read more at: http://medicalxpress.com/news/2013-03-treatment-patients-horizon.html#jCp
Subarachnoid haemorrhage (SAH), a form of stroke, affects around half a million people worldwide each year. Nearly 50 per cent of patients who survive the initial haemorrhage die within 30 days, with survivors likely to suffer permanent disability. A study by Dr Sanjaya Kuruppu and Professor Ian Smith of Monash University and clinicians at Harvard Medical School, Dr Mingming Ning and Dr Sherry Chou, has shown that there may be a way to predict the sub-group of SAH patients that will suffer severe long-term disability. By assessing the cerebrospinal fluid of SAH patients, the researchers discovered that in the three days immediately following the stroke, an enzyme, endothelin converting enzyme-1 (ECE-1) and its substrate big endothelin-1 (BigET-1) were elevated in patients that suffered a disability that severely impacted on their capacity to self-care. Dr Sanjaya Kuruppu, of the Monash Department of Biochemistry and Molecular Biology said the discovery was a breakthrough in treating a deadly and unpredictable condition. "This is the first time doctors have had an early and accurate indication that disability will occur, giving them time to focus appropriate and aggressive therapies on this group of patients," Dr Kuruppu said. "More importantly, it provides families with information required to make crucial decisions about subsequent long-term care." As cerebrospinal fluid is routinely monitored following SAH, testing for elevated levels of ECE-1 and BigET-1 would have no negative impact on patients. Professor Ian Smith, Pro Vice-Chancellor (Research and Research Infrastructure) was the lead researcher on the project at Monash. "The next step in bringing this breakthrough to a clinical setting is to develop the technology to enable rapid diagnosis in a hospital setting and we're currently making progress on this," Professor Smith said. The Monash researchers, again in collaboration with Harvard, are planning a larger clinical study in the near future. They aim to determine the exact threshold level of the molecules required to classify a patient as being at high risk of developing long-term disability.

Read more at: http://medicalxpress.com/news/2013-03-treatment-patients-horizon.html#jCp

Effects of constraint induced movement therapy technique using wedge on weight bearing symmetry and functional balance in chronic hemiparesis patients

One of my readers had this wedge to help walking. Your therapist better know about this. Not to be done without your therapists blessing.
http://www.koomeshjournal.ir/browse.php?a_id=1822&sid=1&slc_lang=en
Article abstract:  
Introduction: Weight bearing asymmetry is one of the basic causes of disturbance in maintaining balance of hemiparesis patients that could complicate standing and participation in activities of daily living in these patients. The purpose of this study was to investigate the immediate effects of constraint induced movement therapy technique using wedge on symmetry index as well as the short-term effects of this technique on functional balance of chronic hemiparesis patients.
 
Materials and Methods: In this quasi-experimental study, twenty-one hemiparesis patients by mean age of 54.28 (±10.06) and the mean passed duration of injury 50.14 (±36.48) months were selected by simple non-probability method. The symmetry index was measured in three conditions: non-wedge, wedge 5ºand wedge 7.5º. Also, functional balance of patients was measured with Functional Reach (FR) and Timed Up and Go (TUG) tests before and after using of short-term constraint induced movement therapy technique.
 
Results: According to the results of this study, symmetry index difference was significant in both wedge 5º and wedge 7.5º conditions compared with no-wedge condition (p&lt0.001), while it was not significant between wedge 5º and wedge 7.5º conditions. The mean scores of FR (P=0.012) and TUG (P=0.006) showed significant changes after using the constraint induced movement therapy technique
 Conclusion: Constraint induced movement therapy technique caused immediate improvement of weight bearing symmetry and improvement of functional balance in short-term interval.

Cerebrospinal fluid leak secondary to chiropractic manipulation

My opinion is to never get your neck adjusted. This person was lucky.
http://www.surgicalneurologyint.com/article.asp?issn=2152-7806;year=2013;volume=4;issue=3;spage=118;epage=120;aulast=Kusnezov
Abstract 
Background: There is a paucity of quality data on the incidence of adverse outcomes of chiropractic manipulation. Spontaneous intracranial hypotension (SIH) subsequent to cervical spinal manipulation has been documented. However, no imaging correlates have previously been presented demonstrating a clear causal relationship to manipulation with follow-up and correlating with clinical symptomatology.
Case Description: We present a case of subacute cervical cerebrospinal fluid (CSF) leak resulting from chiropractic manipulation of the cervical spine. The patient is a 29-year-old female who received manipulation one week prior to developing symptoms of severe orthostatic headache, nausea, and vomiting. Magnetic resonance imaging (MRI) revealed a new C5-C6 ventral CSF collection. Symptomatic onset corresponded with the recent cervical chiropractic adjustment. We present serial imaging correlating with her symptomatology and review the pertinent literature on complications of chiropractic manipulation.
Conclusion: Our case of ventral CSF leak with symptoms of intracranial hypotension demonstrated spontaneous symptomatic resolution without permanent neurological sequelae.

Early growth hormone (GH) treatment promotes relevant motor functional improvement after severe frontal cortex lesion in adult rats

For your doctor and researcher to answer how this might help your recovery. No self-precribing.
Lucky rats.
http://www.sciencedirect.com/science/article/pii/S0166432813001459

Abstract

A number of studies, in animals and humans, describe the positive effects of the growth hormone (GH) treatment combined with rehabilitation on brain reparation after brain injury. We examined the effect of GH treatment and rehabilitation in adult rats with severe frontal motor cortex ablation. Thirty-five male rats were trained in the paw-reaching-for-food task and the preferred forelimb was recorded. Under anesthesia, the motor cortex contralateral to the preferred forelimb was aspirated or sham-operated. Animals were then treated with GH (0.15 mg/kg/day, s.c) or vehicle during 5 days, commencing immediately or 6 days post-lesion. Rehabilitation was applied at short- and long-term after GH treatment. Behavioral data were analized by ANOVA following Bonferroni post hoc test. After sacrifice, immunohistochemical detection of glial fibrillary acid protein (GFAP) and nestin were undertaken in the brain of all groups.
Animal group treated with GH immediately after the lesion, but not any other group, showed a significant improvement of the motor impairment induced by the motor lesion, and their performances in the motor test were no different from sham-operated controls.
GFAP immunolabeling and nestin immunoreactivity were observed in the perilesional area in all injured animals; nestin immunoreactivity was higher in GH-treated injured rats (mainly in animals GH-treated 6 days post-lesion). GFAP immunoreactivity was similar among injured rats. Interestingly, nestin re-expression was detected in the contralateral undamaged motor cortex only in GH-treated injured rats, being higher in animals GH-treated immediately after the lesion than in animals GH-treated 6 days post-lesion.
Early GH treatment induces significant recovery of the motor impairment produced by frontal cortical ablation. GH effects include increased neurogenesis for reparation (perilesional area) and for increased brain plasticity (contralateral motor area).

Increased neuroplasticity may protect against cardiovascular disease

A good question for your doctor. How do you use this to prevent your next stroke.
http://informahealthcare.com/doi/abs/10.3109/00207454.2013.785949

ABSTRACT

Neuroplasticity refers to the capacity of the nervous system to modify its organization, and the brain can be shaped by environmental input. Individuals exhibit different degrees of neuroplasticity because of their different courses of growth. Neuroplasticity may thus play a role in individual differences in the treatment of neuropsychiatric diseases. Since the nervous system is the leading system in the human body, neuroplasticity may also play role in the treatment of other diseases. The cardiovascular system is controlled by the nervous system, mainly by the autonomic nervous system. Stress may lead to depression and cardiovascular disease (CVD). CVD always coexists with depression, which is a disorder of decreased neuroplasticity. And the mechanisms of depression and CVD are related. So we conclude that decreased neuroplasticity causes the coexistence of depression with CVD, and increased neuroplasticity may be beneficial against the development of CVD. This theory provides another angle that can explain some of the reported phenomena related to CVD and neuropsychiatry.



Read More: http://informahealthcare.com/doi/abs/10.3109/00207454.2013.785949

Is Impaired Control of Reactive Stepping Related to Falls During Inpatient Stroke Rehabilitation?

Use this to assist your therapist in preventing your falls.
http://nnr.sagepub.com/content/early/2013/03/15/1545968313478486.abstract

Abstract

Background. Individuals with stroke fall more often than age-matched controls. Although many focus on the multifactorial nature of falls, the fundamental problem is likely the ability for an individual to generate reactions to recover from a loss of balance. Stepping reactions to recover balance are particularly important to balance recovery, and individuals with stroke have difficulty executing these responses to prevent a fall following a loss of balance. Objective. The purpose of this study is to determine if characteristics of balance recovery steps are related to falls during inpatient stroke rehabilitation. Methods. We conducted a retrospective review of individuals with stroke attending inpatient rehabilitation (n = 136). Details of falls experienced during inpatient rehabilitation were obtained from incident reports, nursing notes, and patient interviews. Stepping reactions were evoked using a “release-from-lean” postural perturbation. Poisson regression was used to determine characteristics of stepping reactions that were related to increased fall frequency relative to length of stay. Results. In all, 20 individuals experienced 29 falls during inpatient rehabilitation. The characteristics of stepping reactions significantly related to increased fall rates were increased frequency of external assistance to prevent a fall to the floor, increased frequency of no-step responses, increased frequency of step responses with inadequate foot clearance, and delayed time to initiate stepping responses. Conclusions. Impaired control of balance recovery steps is related to increased fall rates during inpatient stroke rehabilitation. This study informs the specific features of stepping reactions that can be targeted with physiotherapy intervention during inpatient rehabilitation to improve dynamic stability control and potentially prevent falls.

Tuesday, March 26, 2013

Changing seasons for stroke rehab

Ten days ago I probably went for my last cross-country ski of the year. 2 hours worth with no cardio exertion at all. It was a pathetic winter, I wanted feet of snow for extra therapy. Two days later I took my bike to the local bike shop for a tuneup and to get the one-handed braking system SlidePad installed and a mirror attached. The coming weekend is supposed to hit 50F. This year is going to be the year I bike all over town. It took 2.5 years after my first analysis of how to accomplish this. I will start with a dedicated bike path 6 blocks away on side streets.


Previous posts;

Analysis to riding a two-wheeled bike

Biking and sex—avoid the vicious cycle

 

http://oc1dean.blogspot.com/2012/11/study-biking-restores-brain.html

http://oc1dean.blogspot.com/2010/11/triking-and-dangerous-stroke-rehab.html

http://oc1dean.blogspot.com/2012/10/preparation-for-biking-saebo-flex.html

http://oc1dean.blogspot.com/2011/08/epic-failure-at-bike-stroke-therapy.html 

 http://oc1dean.blogspot.com/2012/09/baby-steps-in-biking-stroke-rehab.html

http://oc1dean.blogspot.com/2012/09/baby-steps-in-biking-2-stroke-rehab.html

http://oc1dean.blogspot.com/2012/09/baby-steps-in-biking3-stroke-rehab.html

http://oc1dean.blogspot.com/2012/10/baby-steps-in-biking4-stroke-rehab.html

http://oc1dean.blogspot.com/2012/11/baby-steps-in-biking5-stroke-rehab.html

http://oc1dean.blogspot.com/2012/11/adventures-in-biking6-stroke-rehab.html 

Don't follow my steps, your doctor and therapists control your recovery.

Discovery could help scientists stop the ‘death cascade’ of neurons after a stroke

So I guess I'm just popularizing the term, neuronal cascade of death, I first started using it in 2011. What do you prefer?
Death cascade
Neuronal cascade of death
apoptosis
Necrosis
Neuroprotection - boring, boring, boring
This is from

Distressed swimmers often panic, sapping the strength they need to keep their heads above water until help arrives. When desperate for oxygen, neurons behave in a similar way. They freak out, stupidly discharging energy until they drown in a sea of their own extruded salts. Every year, millions of victims of stroke or brain trauma suffer permanent brain damage because of this mad rush to oblivion that begins once a part of the brain is deprived of blood.

Saving neurons. When normal neurons (top) are subjected to stroke-like damage, they quickly deteriorate and die (center). New research shows that a small portion of the cell’s glutamate receptors, the KA1 subunit, is responsible for this damage. Cells treated with an antibody that blocks this subunit are largely protected (bottom).
It is well known that a ubiquitous cell receptor drives these oxygen-starved neurons’ lemming-like behavior. But this particular receptor, for the neurotransmitter glutamate, is also responsible for the rapid transmission of information between neurons required for all cognition, among other things. Shutting it off has serious consequences, like coma. Now, a team of scientists at The Rockefeller University has identified a single subunit of this receptor that drives neuronal death. This new discovery suggests that drugs targeting a specific subunit of the complex glutamate receptor might be able to slow brain damage without disrupting other crucial brain functions.
“We have found that you can make mice resistant to this kind of cell death by blocking one piece of the receptor without the terrible side effects you get by blocking the whole thing,” says Sidney Strickland, head of the Laboratory of Neurobiology and Genetics, who directed the research. “Now we can start exploring potential drugs to do that in humans.”
The neuronal panic that occurs when a clot or other insult blocks the flow of blood to part of the brain is called excitotoxic neurodegeneration. It results in the brain cells spitting out glutamate, which then accumulates in the synapses between neurons and stimulates the release of more glutamate. It’s a vicious cycle that kills the cells quickly and continues until blood flow is restored. Doctors often treat stroke victims by administering a heavy dose of a clot-buster called tissue plasminogen activator (tPA), a protein that can stimulate the dissolution of clots. Ironically, however, the same drug that does this crucial clot-busting also accelerates the panicky process that kills neurons, research by Strickland and others has shown. Investigating exactly how tPA does that is what led Strickland’s team to the recent discovery.
Neurons are typically couched in laminin, an extracellular matrix protein known to be involved with tPA in the neuronal “death cascade.” The Strickland lab’s experiments, published in The Journal of Cell Biology, show that tPA produces an enzyme that degrades laminin into toxic products that kill the neurons in their midst, specifically by stimulating the production of one of five subunits for a particular kind of glutamate receptor. The overproduction of this specific subunit, KA1, makes the cells hypersensitive to glutamate, which fans the glutamate frenzy leading to their death.
To better understand the process, Zu-Lin Chen and other colleagues at Rockefeller in the Strickland lab and at the University of Leicester in England designed lines of genetically modified mice that lacked either tPA or laminin specifically in the hippocampus, a region of the brain often damaged by stroke. To their surprise, they found that mice without laminin were protected from the typical neural degeneration that follows a simulated stroke in regular mice. They also found that mice with laminin but not tPA were relatively protected.
But when they injected degraded laminin into mouse brains without laminin or tPA they found a similar overproduction of the subunit of the glutamate receptor that they measured when inducing stroke in normal mice. The problem: Laminin, once degraded by tPA, prompts the proliferation of the receptor subunit that makes the cells suicidally sensitive to glutamate. By preventively injecting a molecule that disables that particular subunit, they were able to dramatically reduce the cell death following a stroke. A big plus: The treated mice did not suffer the severe side effects that come with blocking the entire glutamate receptor.
Whether this will turn into a therapy that can be applied after a stroke is uncertain.
“Can you do it after the fact? That will be a question,” Strickland says. “Cell death happens pretty quickly. But it’s an interesting avenue to pursue.”

Programmed Cell Death (Apoptosis)

With a Stroke, Discerning 'Mimic' from 'Chameleon' Can Save a Life

This is so stunningly simple, you get one of these sixteen objective diagnosis possibilities working in your hospital.
http://www.empr.com/with-a-stroke-discerning-mimic-from-chameleon-can-save-a-life/article/286143/#
The presentation of stroke can be complex, characterized by both false positives and false negatives. In the article "Strokes: Mimics and Chameleons" Fernandes et al address stroke-related diagnostic challenges.1 "Mimics" (false positives)—ie, non-stroke conditions that present with symptoms similar to stroke—account for up to 25% of suspected stroke presentations. A "chameleon" is a stroke that masquerades as a different disease state (false negative);1 indeed, a "seemingly infinite number" of ostensibly different clinical syndromes can turn out to be stroke.2
Despite the availability of measurement scales such as the Face, Arm, Speech, Time (FAST) score,3 or the Recognition of Stroke in the Emergency Room (ROSIER),4 diagnosis can remain elusive.1 Moreover, sophisticated imaging techniques—eg, magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) and brain computed tomography (CT)—are sensitive and specific for diagnosing stroke, but their utility declines with time following stroke onset. Therefore, the authors recommend clinical history and examination as the "reference standard," supported by brain imaging for avoiding both mimics and chameleons.

More at link.

Latest Advancements in Acute Stroke Management Sparrow Hospital April 17, 2013

This is all in preparation for a night session held by Sparrow hospital.
Latest Advancements in Acute Stroke Management April 17, 2013
I want to ask  appropriate questions without having them dismiss my questions just because I know more than they do on the subject.  Medical persons are touchy that way. You aren't important because you haven't the training to  understand this complexity.  My questions are going to be on what they are specifically doing to stop apoptosis or necrosis of brain cells.

You didn't mention any hypothermia in either the ambulance or the ER. Is hypothermia not yet considered ready for prime time?

The only ischemic treatment you specified in the first week is tPA. Are there no treatments in the first week that research has identified as neuroprotective or that can stop the neuronal cascade of death?
Maybe ibuprofen?, Viagra?, amantadine?, minocycline?, levodopa?, statins?, fish oil?, anti-depressants?, Paeoniflorin?, Inhalation of nitric oxide?, Melatonin?, Glibenclamide?, Etazolate?, linagliptin?, edaravone used in Japan since 2001, Enzogenol from New Zealand, Draculin?,


How Cold Sores Could Hamper Memory

Ask your doctor if your memory problems post-stroke are because of
1.  Older Brains Actually Become ‘Full’
2.  Mem­ory Loss Could Be The Fault Of Your Meds, Not Your Age
3.  How marijuana makes you forget   You older women have to share that weed with me.
4.   Passing through a doorway causes frustrating memory lapses
5.  Blood Test May Show Memory Loss in Older Women
6. The effect of acute increase in urge to void on cognitive function in healthy adults

or this latest. You don't have to accept the Occams' Razor cause.
http://news.yahoo.com/cold-sores-could-hamper-memory-094500696.html

Etanercept(Enbrel) and IBMs' Watson

This is from a technology site so take what they are saying with a grain of salt. Video training on how to apply it. Still seems more like a puff piece.
Patented by Amgen.
http://www.hpcwire.com/hpcwire/2013-03-26/ibm_s_watson_making_diagnosis_and_treatment_recommendations.html
According to an article in the March 2013 edition of Atlantic magazine titled “The Robot Will See You Now," IBM’s super computer Watson has teamed up with Memorial Sloan/Kettering Hospital to make diagnosis and treatment recommendations. IBM Watson has been programmed with 600,000 pieces of medical evidence from over two million pages of medical text as well as the entire English version of Wikipedia all stored in 15 terabytes of RAM (15 trillion bytes of memory). This is roughly equivalent to the information contained on a bookshelf that is 19 miles long.

“Computer-driven, evidence-based advice like that provided by IBM’s Watson gives validity to the off label use of prescription drugs” states Rolando Rodriguez, M.D., Neurosurgeon at Neurological Wellness Center. “The perispinal administration of the drug etanercept (Enbrel) to patients diagnosed with Alzheimer’s, stroke or traumatic brain injury (TBI) has the potential to enable a significant recovery in memory, mood, speech and physical function,” stated Dr. Rodriguez. “Doctors and nurses are drowning in information with new research popping up daily. They often don’t know what to do and are guessing as well as they can,” said Samuel Nussbaum, WellPoint’s Chief Medical Officer.

A general consensus is emerging among healthcare professionals that to effectively address the many problems in the present healthcare system in America will require a fundamental redesign, a transformation in which existing modalities are replaced by new care delivery paradigms. The expansion of computer medical decision support systems like that provided by IBM's Watson has emerged as one of the areas where there is broad support among the medical community. The proliferation of biomedical information will continue to accelerate taxing the cognitive abilities of physicians as they struggle with the weight of new research findings, clinical guidelines, and recommendations of best practices. Computerized medical decision support systems certainly have the potential to produce better outcomes, increase productivity, lower costs and reduce the occurrence of adverse events.

Perispinal injections of the drug Enbrel are an excellent example. “The medical research is clear: a single injection has the potential to produce a life-changing recovery in persons afflicted with stroke or traumatic brain injury with little to no risk to health, yet the procedure is only slowly starting to gain traction with mainstream medicine,” states Dr. Rodriguez. IBM’s Watson has the potential to be a major game changer in the field of medicine. When physicians’ diagnoses and treatment decisions are evaluated with computer-assisted 20/20 hindsight WellPoint’s Samuel Nussbaum said that “health care professionals make accurate treatment decisions in lung cancer cases only 50% of the time.” “The dictates of a capitalistic healthcare system preclude a drug like Enbrel from ever gaining FDA approval for the treatment of stroke or TBI. The estimated cost for repurposing Enbrel for treating stroke and TBI is $100 million. Considering just one to eight doses are required for the complete treatment, I can be confident this drug will never be approved for stroke or TBI” said Augusto Ramirez, M.D., of Neurological Wellness Center. Neurological Wellness Center offers a complete two-hour course on Alzheimer's treatment, stroke treatment and traumatic brain injury treatment covering all aspects of perispinal injection technique at their center in Managua Nicaragua.

For many, flying to Managua Nicaragua to receive this personalized training is an enormous expense and inconvenience. To overcome this problem, Neurological Wellness Center, under the direction of Augusto Ramirez, M.D., created Perispinal Enbrel Step-By-Step Instructional Video and accompanying e-book.

Neurological Wellness Center’s perispinal Enbrel is profoundly effective as an Alzheimer’s treatment, stroke treatment and TBI treatment. The complete treatment recommendation: for stroke is one 25mg injection of Enbrel every four days for a total of four doses over 16 days; for TBI is one 25mg injection of Enbrel every four days for a total of eight doses. This compares with Amgen/Pfizer’s FDA-approved dose schedule for moderate plaque psoriasis of 50mg twice weekly for three months followed by 50mg weekly for life. The Neurological Wellness Center’s maximum recommended dose for Alzheimer’s disease is 25mg/week for life.

The drug Enbrel is available now. Enbrel received FDA approval in 1998. Its safety profile is well understood. For Enbrel to effectively treat Alzheimer’s, stroke and TBI, it must be administered to the back of the neck precisely between the cervical vertebrae C-5 and C-6. (I wouldn't allow just any doctor to inject me at this location)This perispinal injection allows Enbrel to enter the brain by lymph drainage assisted by gravity. Fortunately for the millions of people now afflicted with Alzheimer’s, stroke and TBI, a video is now available online detailing in step-by-step fashion how to administer a perispinal injection of Enbrel,” said Dr. Rolando Rodrigues.

Obesity and Your Brain

Can a steady diet of cheeseburgers change your brain? It might just be possible, according to a 2012 study from Nature Neuroscience that linked high fat diets to neurogenesis and obesity in mice.

Ask your doctor if we want this initiated kind of neurogenesis
http://www.lumosity.com/blog/obesit/

High fat diets change the brain
The study put mice into two groups: those fed a normal diet and those who feasted regularly on high fat foods. After 1 month of chowing down, adult mice on high fat diets had quadruple the rate of new brain cell growth in the hypothalamus, a part of the brain responsible for regulating many metabolic processes.
But did neurogenesis also cause obesity? To answer this question, researchers irradiated the newly created portions of rats’ brains. Not only did radiation inhibit 85% of neurogenesis, but irradiated mice gained significantly less weight and fat mass compared to the group that kept their new neural growth—even though all of them stayed on the same high fat diet. Furthermore, irradiated mice used more energy and were more active despite their unhealthy diet.
Fighting obesity: current methods
The link between diet, obesity, and the brain is thought-provoking. But take it with a grain of salt: the connection has yet to be confirmed in humans. As we wait for more research, consider some current methods that could help change your eating habits.
Many scientists have pointed out that obesity often functions like an addiction to food in the brain. And a 2012 study from the University of Amsterdam found that challenging cognitive training lowered addiction symptoms in individuals with a drinking problem. People who trained not only drank less—they actually improved memory capacity as well.
As research continues to show that your behaviors change your brain, cognitive training becomes ever more important. Try strengthening your willpower today: exercises similar to Lumosity’s Memory Matrix and Monster Garden were used in the University of Amsterdam study to great effect. Unlock full access today to try out all 40+ games and promote positive change in your brain!