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, July 31, 2015

pants clip fastener

Trying to close this style of pants fastener one-handed is a chore in swearing. I have just enough of a belly that I can't directly see how to line up the tab piece with the bar. So I do hit and miss sometimes for ten minutes. I'll stick to studs or buttons from now on.

Local rehab hospital earns Gold Seal of Approval - Rehabilitation Hospital of Southwest Virginia

There is absolutely nothing in here that tells me that the RESULTS are better in this hospital than other hospitals. I don't give a crap about how well you do processes. Call that hospital CEO(Georgeanne Cole, CEO) and demand to know what the RESULTS are; tPA efficacy, 30 day deaths, 100% recovery.
Big f*cking whoopee.
You can check out Joint Commission standards here:
 I saw absolutely nothing about what should be done the first week or anything about measuring 30-day deaths and 100% recovery.  God, these people are worse than worthless. Complacent good-for-nothings.

The puffery piece here:

he Rehabilitation Hospital of Southwest Virginia has earned certification for Disease-Specific Care in stroke rehabilitation. The Joint Commission’s Gold Seal of Approva was awarded to the hospital for its compliance with the organization’s national standards for healthcare quality and safety for stroke rehabilitation.
“By choosing to have The Joint Commission evaluate our stroke program, we are making a significant investment in the quality of patient care. The Joint Commission certification provides us a framework to take our hospital to the next level and helps create a culture of excellence,” said Georgeanne Cole, CEO of the Rehabilitation Hospital of Southwest Virginia. “This is a major step toward continually improving the care we provide and offering patients peace of mind knowing they are getting quality care at the industry’s highest standard.”
To earn the certification, the Rehabilitation Hospital of Southwest Virginia underwent a rigorous on-site survey on June 6, 2015. A surveyor with expertise in the care of patients with neurological issues from the Joint Commission evaluated the hospital’s stroke rehabilitation program for compliance with standards of care specific to the needs of patients and families, including the provision and quality of care, medical staff, leadership and medication management.
"In achieving Joint Commission certification, the Rehabilitation Hospital of Southwest Virginia has demonstrated its commitment to the highest level of care for its patients that suffered from a stroke," says Jean Range, M.S., R.N., C.P.H.Q., executive director, Disease-Specific Care Certification, The Joint Commission. “Certification is a voluntary process and I commend them for successfully undertaking this challenge to elevate its standard of care and instill confidence in the community it serves.”
Studies indicate that 60 percent of stroke survivors can benefit from comprehensive rehabilitation. Eighty percent of patients receiving this level of therapy return to their homes, work, schools or active retirement, according to the National Rehabilitation Caucus. The Joint Commission’s acknowledgement of the Rehabilitation Hospital of Southwest Virginia’s continuum of care for stroke offers patients and families peace of mind in knowing they are getting quality stroke care for maximized results. (But they don't say how many of their patients return to their former lives)

Stroke Care Path Primes Patients for Successful Rehabilitation - Cleveland Clinic

This really is worthless because they don't mention what the results are; tPA efficacy, 30 day deaths, 100% recovery. Cleveland Clinic should know better than to suggest that this shows how good they are.
Medium f*cking whoopee.
In 2010, Cleveland Clinic’s Neurological Institute debuted its care path for acute ischemic stroke. This guide provides comprehensive protocols for evaluation and management of patients during the acute stroke phase to help optimize patient outcomes(What are those outcomes?). It streamlines care, helps reduce hospital length of stay and ensures that every patient receives the same standard of care. Since its implementation, we have seen the Stroke Care Path benefit patients not only during the acute phases of care, but throughout their rehabilitation.
In the past few years, Cleveland Clinic has developed more than 25 care paths for other diseases and conditions, including congestive heart failure, knee and hip replacement, spine care, and dementia. All the guides are based on medical research, clinical guidelines, clinician experience and evidence collected via our Knowledge Program — a health information data collection system that gives physicians a comprehensive view of a patient’s medical status and enables researchers to broadly and quantitatively assess the effectiveness of medical decisions and processes. The Knowledge Program includes information obtained from patients by electronic questionnaires as well as clinical data extracted from Cleveland Clinic’s electronic medical record.
As we treat more patients and as medical technology advances, information in the Knowledge Program constantly evolves. So, too, must our care paths. We recently completed a revision of our Stroke Care Path to ensure that it reflects the latest evidence-based care, in addition to standards of care provided by The Joint Commission and the American Heart Association/American Stroke Association in their certification program for Primary Stroke Centers and Comprehensive Stroke Centers.

Priming Patients for Rehabilitation

Our Stroke Care Path focuses on the period from initial presentation at the emergency department or hospital with acute stroke symptoms to 90 days after hospital discharge.  The care provided during that time is paramount to successful rehabilitation. It is critically important that, as soon as patients enter the hospital, we are not only thinking about their diagnosis and treatment, but their rehabilitation. Evidence indicates that the sooner patients begin rehabilitation, the better their outcome.
Figure. Cleveland Clinic’s Neurological Institute has developed a care path for acute ischemic stroke that standardizes inpatient treatment (including for venous thromboembolism, as shown here) and rehabilitation to improve patient outcomes. ICS = Intermittent Compression Stockings EX = Enoxaparin 40mg subcutaneous daily UFH = Unfractionated Heparin 5000 units TID tPA = Tissue plasminogen activator.

By utilizing the treatment guidelines in our Stroke Care Path, physicians prepare patients for rehabilitation. The following are some of the steps we take:
  • Patients admitted with a stroke diagnosis are evaluated by a physical therapist and an occupational therapist as soon as they are medically able. This often occurs the day after admission. Patients with National Institutes of Health stroke scale scores between 4 and 20 receive a full evaluation by a physical medicine and rehabilitation physician.
  •  Nurses administer a dysphagia screen to all patients immediately upon admission unless they first require advanced procedures such as hyperacute MRI. If patients fail the swallow screening, they automatically are evaluated by a speech-language pathologist.
  •  We encourage early mobility. In the past, stroke patients often remained in bed. Now we urge them to ambulate and spend more time in a chair. We have incorporated lift devices and lift teams to help patients with limited mobility move to chairs. Early mobility has several advantages: It helps prevent urinary retention, constipation, pressure ulcers, pneumonia and deep vein thrombosis. It also is an important component of physical and occupational therapy.
  •  Patients undergo a comprehensive evaluation by a case manager within 24 hours of admission. The case manager examines all aspects of the patient’s plan of care, including finances, insurance and family/social situations. They look for anything that might prevent or limit patients’ early rehabilitation. Case managers also provide a list of rehab facilities that meet each patient’s needs and work closely with families to help select the ideal one.
  •  Each patient receives a mood screening prior to discharge and during follow-up outpatient visits. If patients suffer from poststroke depression, they are less likely to participate in their own care, thereby hindering rehabilitation efforts. Cleveland Clinic uses the Patient Health Questionnaire for Depression and Anxiety (PHQ-4) to assess mood. If patients score high, a social worker or therapist intervenes and treatment is initiated.
  •  Prior to discharge, all medications are reviewed and coordinated to reduce the risk of recurrent stroke. In addition, the discharge summary includes advice on managing personal stroke risk factors (such as blood pressure, weight and cholesterol) and a description of stroke warning signs and symptoms.

 Examining Early Urinary Catheter Removal

One recommendation in the Stroke Care Path that facilitates rehabilitation and prevents infection is removal of urinary catheters as soon as possible. However, it is important to note that the guide also cautions physicians against early removal in certain situations. They may delay removal if:
  • Patients are intermittently drowsy and unable to communicate their need to urinate
  • Patients are taking opiates, anticholinergic medications or other medications that cause obtundation or urinary retention
  • Patients are diabetic and have a history of outlet obstruction or urinary retention that predict a failed early catheter removal
  • Patients are unable to speak
In short, catheter removal requires that patients are adequately alert and physically able to say when they need to use the bathroom.

Guiding Informed Decisions

The Stroke Care Path is an invaluable tool for our physicians to provide evidence-based poststroke care(Not Results) and prepare patients for successful rehabilitation. It is used not only within Cleveland Clinic hospitals, but in ambulatory therapy centers and subacute and rehabilitation facilities. This allows us to implement best practices and a high standard of care through the entire course of our patients’ medical and rehabilitative treatment.

Curing cancer in 10 years: Is it hype? And is that hype OK?

We've got goals for cancer and Alzheimers but nothing for stroke. Leadership failure of our stroke associations on every level. With no goal or plan for stroke solutions we will continue to flounder and trillions upon trillions of neurons will needlessly die.
Once again, we have jackshit leaders, WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM
The problem is; 'How do you get to 100% recovery?' It's a simple question. Solve the hard answer.

Curing cancer in 10 years: Is it hype? And is that hype OK?

The goal of National Alzheimer's Plan to prevent and effectively treat Alzheimer's by 2025.

My high blood pressure

Yesterday I was planning on giving blood again. Got there, took my blood pressure,186/98. Never been higher than 140/88. The cutoff for donating is 180 so I'll have to do it another time.
I will not be taking any blood pressure medications. If I need to I'll use beet juice and watermelon juice to lower it. DO NOT follow my ideas, you can ask your doctor but I'll guarantee they will know nothing about more natural ways to reduce blood pressure.

Bach1 Represses Wnt/β-Catenin Signaling and Angiogenesis

Since we would like to have angiogenesis what is your doctor doing to reduce Bach1?

  1. Dan Meng
+ Author Affiliations
  1. From the Department of Physiology and Pathophysiology (L.J., Xiangxiang Wei, J.L., Xinhong Wang, C.N., X.K., J.X., Z.Z., R.Q., N.S., A.C., R.W., S.C., D.M.) and Department of Biochemistry and Molecular Biology (S.S., Xu Wang), School of Basic Medical Sciences, Fudan University, Shanghai, China; Department of Cardiothoracic Surgery, Shanghai Children’s Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China (M.Y.); Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China (X.Z., S.D.); Department of Cardiology, Shanghai Institute of Cardiovascular Disease, ZhongShan Hospital, Fudan University, Shanghai, China (K.Y.); Center for Vascular Disease and Translational Medicine, Xiangya Third Hospital, Central South University, Changsha, China (A.C.); Department of Biology, Laurentian University, Sudbury, Ontario, Canada (R.W.); and Division of Cardiology, Department of Medicine, Stem Cell Institute, University of Minnesota Medical School, Minneapolis (J.Z.).
  1. Correspondence to Dan Meng, MD, or Sifeng Chen, MD, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, 138 Yixueyuan Rd, PO Box 224, Shanghai 200032, China. E-mails or
  1. * These authors contributed equally to this article.


Rationale: Wnt/β-catenin signaling has an important role in the angiogenic activity of endothelial cells (ECs). Bach1 is a transcription factor and is expressed in ECs, but whether Bach1 regulates angiogenesis is unknown.
Objective: This study evaluated the role of Bach1 in angiogenesis and Wnt/β-catenin signaling.
Methods and Results: Hind-limb ischemia was surgically induced in Bach1–/– mice and their wild-type littermates and in C57BL/6J mice treated with adenoviruses coding for Bach1 or GFP. Lack of Bach1 expression was associated with significant increases in perfusion and vascular density and in the expression of proangiogenic cytokines in the ischemic hindlimb of mice, with enhancement of the angiogenic activity of ECs (eg, tube formation, migration, and proliferation). Bach1 overexpression impaired angiogenesis in mice with hind-limb ischemia and inhibited Wnt3a-stimulated angiogenic response and the expression of Wnt/β-catenin target genes, such as interleukin-8 and vascular endothelial growth factor, in human umbilical vein ECs. Interleukin-8 and vascular endothelial growth factor were responsible for the antiangiogenic response of Bach1. Immunoprecipitation and GST pull-down assessments indicated that Bach1 binds directly to TCF4 and reduces the interaction of β-catenin with TCF4. Bach1 overexpression reduces the interaction between p300/CBP and β-catenin, as well as β-catenin acetylation, and chromatin immunoprecipitation experiments confirmed that Bach1 occupies the TCF4-binding site of the interleukin-8 promoter and recruits histone deacetylase 1 to the interleukin-8 promoter in human umbilical vein ECs.
Conclusions: Bach1 suppresses angiogenesis after ischemic injury and impairs Wnt/β-catenin signaling by disrupting the interaction between β-catenin and TCF4 and by recruiting histone deacetylase 1 to the promoter of TCF4-targeted genes.

Stroke services at James Cook highly rated by national audit - Middlesbrough, United Kingdom

This means absolutely nothing. Getting assessed and seem by staff in a particular time means nothing. You have to look at the results - tPA efficacy, 30 day deaths, 100% recovery.  People who tout this really shouldn't even consider themselves a stroke unit.

EIGHT out of ten patients are reaching the stroke unit at James Cook University Hospital, Middlesbrough, within four hours of arrival, compared to five out of ten nationally.
The data, released by the Royal Collage of Physicians’ Sentinel Stroke National Audit Programme, also reveals that the average patient arrives on the stroke ward within 90 minutes following initial assessments and routine scans.
Figures show South Tees Hospitals NHS Foundation Trust was the only service in the country to achieve more than 90 per cent of patients seeing a stroke nurse and stroke therapist within 24 hours - and all relevant therapists within 72 hours.
The proportion of applicable patients receiving six month reviews at 89 per cent - is also well above the national average of 21 per cent.
Stroke consultant Dr Adrian Bergin said: “What these statistics show is that we get patients to the right place quickly and assessed by the right people.”
The figures are expected to improve even further in the future following the opening of the specialist stroke rehabilitation unit at Redcar Primary Care Hospital in April and the launch of the early supported discharge (ESD) team, which now enables up to 40 per cent of South Tees patients to receive stroke rehabilitation therapy in their own home.
Dr Ali Tahmassebi, South Tees Clinical Commissioning Group GP and lead for the IMProVE programme (Integrated Management and Proactive Care for the Vulnerable and Elderly) behind the positive changes to stroke services, said: “We are delighted to receive further confirmation that James Cook continues to improve stroke care.” (Not results)

Thursday, July 30, 2015

Blood test predicts prognosis for traumatic brain injuries

Another possibility that needs more followup research to see if this would work for stroke. Who the hell do we talk to to get this accomplished? Or do we just sit and wait 50 years because we have no stroke leaders or any strategy to fix stroke problems?

A new blood test could help emergency room doctors quickly diagnose traumatic brain injury and determine its severity. The findings, published July 10 in the Journal of Neurotrauma, could help identify patients who might benefit from extra therapy or experimental treatments.
"Compared to other proteins that have been measured in , BDNF does a much better job of predicting outcomes," says Frederick Korley, M.D., Ph.D., an assistant professor of emergency medicine at the Johns Hopkins University School of Medicine and first author of the new paper.
After a hit to the head or rapid whiplash, whether from a car crash, athletic event or other accident, millions of Americans develop traumatic brain injuries (TBIs) each year. TBIs can range from mild concussions—causing only a headache or temporary blurred vision—to much more severe injuries—causing seizures, confusion, memory and attention problems, muscle weakness, or coma for many months. These symptoms, whether mild or more severe, are generally caused by damaged brain cells.
Until now, most physicians have relied on CT scans and patients' symptoms to determine whether to send them home and have them resume their usual activities or take extra precautions. However, CT scans can only detect bleeding in the brain, not damage to brain cells, which can happen without bleeding.
"A typical situation is that someone comes to the emergency department with a suspected TBI, we get a CT scan, and if the scan shows no bleeding, we send the patient home," says Korley. "However, these patients go home and continue having headaches, difficulty concentrating and memory problems, and they can't figure out why they are having these symptoms after doctors told them everything was fine."
Korley and collaborators around the country wanted to know if a blood test could better predict which patients would have ongoing brain injury-related problems, to provide better treatment for them. So they measured the levels of three proteins that they suspected play a role in brain cell activity in more than 300 patients with a TBI and 150 patients without brain injuries. Then, they followed those with a TBI for the next six months.
Levels of one protein, called brain-derived neurotrophic factor (BDNF), taken within 24 hours of someone's head injury, could predict the severity of a TBI and how a patient would fare, they found. While healthy people averaged 60 nanograms per milliliter of BDNF in their bloodstreams, patients with brain injuries had less than one-third of that amount, averaging less than 20 nanograms per milliliter, and those with the most severe TBIs had even lower levels, around 4 nanograms per milliliter. Moreover, patients with high levels of BDNF had mostly recovered from their injuries six months later. But in patients with the lowest levels of BDNF, symptoms still lingered at follow-up. The results suggest that a test for BDNF levels, administered in the emergency room, could help stratify patients.
"The advantage of being able to predict prognosis early on is that you can advise patients on what to do, recommend whether they need to take time off work or school, and decide whether they need to follow up with a rehab doctor or neurologist," Korley says. In addition, it could help decide which to enroll in clinical trials for new drugs or therapies targeting severe TBIs.
Korley would like to follow up with more research on why, at a molecular level, brain injuries lower levels of BDNF in the blood and whether things known to increase BDNF levels—including exercise and omega-3 fatty acids—could help treat TBIs. He also wants to know whether changes in BDNF levels over time can be a proxy for recovery and if they could be used to gauge the effectiveness of an intervention.
"We looked at that very first blood sample obtained within 24 hours of an injury," he says. "But for BDNF to be used as a surrogate outcome, we'll have to see what happens to BDNF blood levels down the line, at one, three or six months after the injury." He and his collaborators have already started collecting data for those prospective studies, he adds.
Journal reference: Journal of Neurotrauma search and more info

Experience with the “Good” Limb Induces Aberrant Synaptic Plasticity in the Perilesion Cortex after Stroke

Well if using the 'good' side impairs recovery of the 'bad' side then all survivors are totally fucking screwed in trying to get 100% recovery.  Which to me means we need to stop a lot of the damage in the first place by stopping the neuronal cascade of death.
What is your doctors solution to get around this problem? I don't know is not an ok answer.
  1. Theresa A. Jones2,3
  1. Author contributions: S.Y.K., R.P.A., D.L.A., J.A.K., and T.A.J. designed research; S.Y.K., R.P.A., D.L.A., K.A.T., N.A.D., and T.A.J. performed research; J.A.K. contributed unpublished reagents/analytic tools; S.Y.K., R.P.A., D.L.A., and T.A.J. analyzed data; S.Y.K. and T.A.J. wrote the paper.
  2. *R.P.A. and D.L.A. contributed equally to this work.
  1. The Journal of Neuroscience, 35(22): 8604-8610; doi: 10.1523/JNEUROSCI.0829-15.2015


Following unilateral stroke, the contralateral (paretic) body side is often severely impaired, and individuals naturally learn to rely more on the nonparetic body side, which involves learning new skills with it. Such compensatory hyper-reliance on the “good” body side, however, can limit functional improvements of the paretic side. In rats, motor skill training with the nonparetic forelimb (NPT) following a unilateral infarct lessens the efficacy of rehabilitative training, and reduces neuronal activation in perilesion motor cortex. However, the underlying mechanisms remain unclear. In the present study, we investigated how forelimb movement representations and synaptic restructuring in perilesion motor cortex respond to NPT and their relationship with behavioral outcomes. Forelimb representations were diminished as a result of NPT, as revealed with intracortical microstimulation mapping. Using transmission electron microscopy and stereological analyses, we found that densities of axodendritic synapses, especially axo-spinous synapses, as well as multiple synaptic boutons were increased in the perilesion cortex by NPT. The synaptic density was negatively correlated with the functional outcome of the paretic limb, as revealed in reaching performance. Furthermore, in animals with NPT, there was dissociation between astrocytic morphological features and axo-spinous synaptic density in perilesion motor cortex, compared with controls. These findings demonstrate that skill learning with the nonparetic limb following unilateral brain damage results in aberrant synaptogenesis, potentially of transcallosal projections, and this seems to hamper the functionality of the perilesion motor cortex and the paretic forelimb.

Augmentation of M-Type (KCNQ) Potassium Channels as a Novel Strategy to Reduce Stroke-Induced Brain Injury

Another possibility that needs more followup research. Who the hell do we talk to to get this accomplished? Or do we just sit and wait 50 years because we have no stroke leaders or any strategy to fix stroke problems?
  1. Mark S. Shapiro1
  1. Author contributions: S.M.B., J.D.L., and M.S.S. designed research; S.M.B. performed research; S.M.B., F.S.C., J.D.L., and M.S.S. contributed unpublished reagents/analytic tools; S.M.B. and F.S.C. analyzed data; S.M.B. and M.S.S. wrote the paper.
  1. The Journal of Neuroscience, 35(5): 2101-2111; doi: 10.1523/JNEUROSCI.3805-14.2015


Cerebral ischemic stroke is a worldwide cause of mortality/morbidity and thus an important focus of research to decrease the severity of brain injury. Therapeutic options for acute stroke are still limited. In neurons throughout the brain, “M-type” K+ currents, underlain by KCNQ subunits 2–5, play dominant roles in control over excitability, and are thus implicated in myriad neurological and psychiatric disorders. Although KCNQ channel openers, such as retigabine, have emerged as anti-epilepsy drugs, their effects on ischemic injury remain unknown. Here, we investigated the protective effects of M-channel openers on stroke-induced brain injury in mouse photothrombotic and middle cerebral artery occlusion (MCAo) models. Both photothrombosis and MCAo led to rapid, predictable, and consistently sized necrotic brain lesions, inflammatory responses, and behavioral deficits. Administration of three distinct M-channel openers at 0–6 h after ischemic injury significantly decreased brain infarct size and inflammation, and prevented neurological dysfunction, although they were more effective when administered 0–3 h poststroke. Thus, we show beneficial effects against stroke-induced brain injury and neuronal death through pharmacological regulation of ion channels that control neuronal excitability.

B-Lymphocyte-Mediated Delayed Cognitive Impairment following Stroke

With double the risk of dementia post-stroke your doctor better have a protocol to prevent that. But I bet s/he does not have anything at all. You're screwed.
  1. Marion S. Buckwalter1,6
  1. Author contributions: K.P.D., L.N.Q., M.S., R.C.A., T.V.V.N., GJ..S.-L., S.J., J.H., L.S., F.M.L., J.A.S., R.C.M., and M.S.B. designed research; K.P.D., L.N.Q., M.S., R.C.A., T.V.V.N., G.J.S.-L., S.J., and J.H. performed research; J.A.S. contributed unpublished reagents/analytic tools; K.P.D., R.C.M., and M.S.B. analyzed data; K.P.D., J.A.S., and M.S.B. wrote the paper.
  1. The Journal of Neuroscience, 35(5): 2133-2145; doi: 10.1523/JNEUROSCI.4098-14.2015


Each year, 10 million people worldwide survive the neurologic injury associated with a stroke. Importantly, stroke survivors have more than twice the risk of subsequently developing dementia compared with people who have never had a stroke. The link between stroke and the later development of dementia is not understood. There are reports of oligoclonal bands in the CSF of stroke patients, suggesting that in some people a B-lymphocyte response to stroke may occur in the CNS. Therefore, we tested the hypothesis that a B-lymphocyte response to stroke could contribute to the onset of dementia. We discovered that, in mouse models, activated B-lymphocytes infiltrate infarcted tissue in the weeks after stroke. B-lymphocytes undergo isotype switching, and IgM, IgG, and IgA antibodies are found in the neuropil adjacent to the lesion. Concurrently, mice develop delayed deficits in LTP and cognition. Genetic deficiency, and the pharmacologic ablation of B-lymphocytes using an anti-CD20 antibody, prevents the appearance of delayed cognitive deficits. Furthermore, immunostaining of human postmortem tissue revealed that a B-lymphocyte response to stroke also occurs in the brain of some people with stroke and dementia. These data suggest that some stroke patients may develop a B-lymphocyte response to stroke that contributes to dementia, and is potentially treatable with FDA-approved drugs that target B cells.

Reduced Intracranial Pressure After Severe Traumatic Brain Injury Achieved With Therapeutic Hypothermia

Would this help for hemorrhagic strokes? Whom is going to answer that question? You'll have to ask your doctor that question when you present to the ER with a hemorrhagic stroke.
Results from a European clinical trial comparing therapeutic hypothermia to standard treatment for patients with elevated intracranial pressure (ICP) as a result of severe traumatic brain injury demonstrate a significant mean decrease in ICP with body cooling to 32-35 degrees Celsius , which did not occur in the absence of therapeutic hypothermia. The study design and preliminary data are reported in Therapeutic Hypothermia and Temperature Management.
Liam Flynn, BMBS, Jonathan Rhodes, MBChB, PhD, and Peter Andrews, MBChB, MD, University of Edinburgh and Western General Hospital, Edinburgh, United Kingdom, use a strategy of lowering the body temperature to affect increases in pressure and blood flow in and around the brain that cause much of the damage associated with traumatic brain injury. Among the patients with increased ICP in this study, who did not respond to initial therapy, a mean reduction in ICP of 4.3 + 1.6 mmHg was recorded at the first hour the target body temperature was reached, and the decrease in pressure continued throughout the 6 hours of hypothermia therapy.
"These preliminary findings from an ongoing clinical trial are important to the field and support the beneficial effects of therapeutic hypothermia on controlling ICP elevations in severe TBI patients," says W. Dalton Dietrich, PhD, University of Miami Leonard M. Miller School of Medicine, Miami, Florida.
SOURCE: Therapeutic Hypothermia and Temperature Management

hiking preikestolen: pulpit rock in Norway

This will occur sometime for me, even if I have to do it alone. Getting down to sit on the edge like that might be quite entertaining for me, getting up again could be death.
This writeup has great pictures and how to do it.
Looks much easier than my Yosemite failure.

Intra-Arterial Immunoselected CD34+ Stem Cells for Acute Ischemic Stroke

Using the Rankin scale to prove that stem cells works is way too crude  to have any predictive ability. This also fails because they are testing this in the first 6 months, prime time for spontaneous recovery.  This research proved nothing except that it didn't seem to make anyone worse.


Treatment with CD34+ hematopoietic stem/progenitor cells has been shown to improve functional recovery in nonhuman models of ischemic stroke via promotion of angiogenesis and neurogenesis. We aimed to determine the safety and feasibility of treatment with CD34+ cells delivered intra-arterially in patients with acute ischemic stroke. This was the first study in human subjects. We performed a prospective, nonrandomized, open-label, phase I study of autologous, immunoselected CD34+ stem/progenitor cell therapy in patients presenting within 7 days of onset with severe anterior circulation ischemic stroke (National Institutes of Health Stroke Scale [NIHSS] score ≥8). CD34+ cells were collected from the bone marrow of the subjects before being delivered by catheter angiography into the ipsilesional middle cerebral artery. Eighty-two patients with severe anterior circulation ischemic stroke were screened, of whom five proceeded to treatment. The common reasons for exclusion were age >80 years (n = 19); medical instability (n = 17), and significant carotid stenosis (n = 13). The procedure was well tolerated in all patients, and no significant treatment-related adverse effects occurred. All patients showed improvements in clinical functional scores (Modified Rankin Score and NIHSS score) and reductions in lesion volume during a 6-month follow-up period. Autologous CD34+ selected stem/progenitor cell therapy delivered intra-arterially into the infarct territory can be achieved safely in patients with acute ischemic stroke. Future studies that address eligibility criteria, dosage, delivery site, and timing and that use surrogate imaging markers of outcome are desirable before larger scale clinical trials.

Study of the neuroprotective effects of memantine in patients with mild to moderate ischemic stroke

I bet memantine is not being agressively followed up to create a translational stroke protocol for its use. I'll bet 50 years before it gets used, allowing trillions of neurons to die in the meantime. How can the ASA, NSA and WSO live with themselves for allowing such needless neuron deaths to occur?


Ischemic stroke is amongst the top four causes of mortality and the leading cause of disability in the world. The aim of this study was to evaluate the efficacy of a high dose memantine on neurological function of patients with ischemic stroke. In a randomized, 2 armed, open-label study, patients with mild to moderate cerebral thromboembolic event (CTEE) who admitted to Imam Hossein Hospital, Tehran, Iran, during preceding 24 hours, entered the study. Patients allocated in two study groups of memantine (as add-on therapy) and control. All patients were managed based on the American Heart Association and American Stroke Association (AHA/ASA) guidelines. Patients in memantine group received conventional treatment plus memantine 20 mg TID. The National Institute of Health Stroke Scale (NIHSS) was determined and recorded daily. The primary objective was comparison of the changes in NIHSS in the study groups at day 1 and day 5 of intervention. Significance level of p<0.05 was considered for statistical analysis. Patients were randomly allocated in control (15 women and 14 men, age 70.78 ± 10.92 years) and memantine (16 women and 8 men, age 73.33 ± 9.35 years) groups. There were no significant differences in age and sex distribution of two study groups as well as in comorbidities and concurrent drugs. NIHSS changes were significantly different between control (1.24 ± 0.96) and memantine group (2.96 ± 0.1), (p < 0.0001). Our results reveal that memantine added to standard treatment of CTEE could result in a remarkable decrease in the NIHSS confirming improvement of the neurological function of the patients.

The dichotomy of memantine treatment for ischemic stroke: dose-dependent protective and detrimental effects

You're going to have to know when you are having your stroke so you can get proper pretreatment. Good luck with that.


Excitotoxicity is a major contributor to cell death during the acute phase of ischemic stroke but aggressive pharmacological targeting of excitotoxicity has failed clinically. Here we investigated whether pretreatment with low doses of memantine, within the range currently used and well tolerated for the treatment of Alzheimer's disease, produce a protective effect in stroke. A coculture preparation exposed to modeled ischemia showed cell death associated with rapid glutamate rises and cytotoxic Ca(2+) influx. Cell death was significantly enhanced in the presence of high memantine concentrations. However, low memantine concentrations significantly protected neurons and glia via excitotoxic cascade interruption. Mice were systemically administered a range of memantine doses (0.02, 0.2, 2, 10, and 20 mg/kg/day) starting 24 hours before 60 minutes reversible focal cerebral ischemia and continuing for a 48-hour recovery period. Low dose (0.2 mg/kg/day) memantine treatment significantly reduced lesion volume (by 30% to 50%) and improved behavioral outcomes in stroke lesions that had been separated into either small/striatal or large/striatocortical infarcts. However, higher doses of memantine (20 mg/kg/day) significantly increased injury. These results show that clinically established low doses of memantine should be considered for patients 'at risk' of stroke, while higher doses are contraindicated.

Memantine enhances recovery from stroke

Whom is following up on this? Who has updated the stroke strategy? Who has the stroke strategy? I somehow missed this when it came out a year ago.

Erratum in

  • Stroke. 2014 Nov;45(11):e238.



Stroke treatment is constrained by limited treatment windows and the clinical inefficacy of agents that showed preclinical promise. Yet animal and clinical data suggest considerable poststroke plasticity, which could allow treatment with recovery-modulating agents. Memantine is a well-tolerated N-methyl-D-aspartate glutamate receptor antagonist in common use for Alzheimer disease.


Memantine, 30 mg/kg per day, or vehicle, was delivered chronically in drinking water beginning >2 hours after photothrombotic stroke.


Although there was no difference in infarct size, behavior, or optical intrinsic signal maps in the first 7 days after stroke, mice treated chronically with memantine showed significant improvements in motor control, measured by cylinder test and grid-walking performance, compared with vehicle-treated animals. Optical intrinsic signal revealed an increased area of forepaw sensory maps at 28 days after stroke. There was decreased reactive astrogliosis and increased vascular density around the infarcted cortex. Peri-infarct Western blots revealed increased brain-derived neurotrophic factor and phosphorylated-tropomyosin-related kinase-B receptor expression.


Our results suggest that memantine improves stroke outcomes in an apparently non-neuroprotective manner involving increased brain-derived neurotrophic factor signaling, reduced reactive astrogliosis, and improved vascularization, associated with improved recovery of sensory and motor cortical function. The clinical availability and tolerability of memantine make it an attractive candidate for clinical translation.

Quiz: Which Deadly Warrior Are You?

 You're the battle-crazed warrior who terrorized Europe! You are tough, determined and outgoing. You are known to be impulsive and tend to take what you want without considering the repercussions. You are headstrong and when you have your heart set on something, nothing will get in your way. You can be utterly ferocious - your enemies better watch their backs!

Wednesday, July 29, 2015

Governor Raimondo Signs Rhode Island Stroke Bill Into Law

It may be a national model for stroke care but it doesn't say one damn thing about RESULTS!
Governor Gina Raimondo has signed our stroke bill into law – ensuring the best possible care for stroke patients in the Ocean State!  The bill had been unanimously approved by the Rhode Island House and Senate. 
The new law makes some important updates to the Stroke Prevention and Treatment Act of 2009. While the changes in the stroke bill are fairly minor, they are important and will allow the Rhode Island Stroke Task Force to continue its charge of improving the system of care for stroke patients in the Ocean State.  Revisions include: 
  • Relaxing the stroke registry reporting requirement by allowing hospitals flexibility to use different data platforms; 
  • Adding a Comprehensive Stroke Center designation.  This is a level above the Primary Stroke Centers created by the original law - there is already one hospital in Rhode Island that has achieved this high level designation; and,
  • Requiring an annual review of the EMS Pre-Hospital Care Protocol for stroke.  
When the Stroke Prevention and Treatment Act was enacted nearly six years ago, there were just two Primary Stroke Centers in Rhode Island.  We now have seven Primary Stroke Centers and one Comprehensive Stroke Center.  Thanks to the work of the Stroke Task Force and dedicated You’re the Cure advocates, Rhode Island is considered a national model for stroke care. (Not results)

The coming Alzheimer’s crisis in America for Medicare

Are our stroke associations warning of the same crisis for stroke and have they created a strategy to address it? FUCKING UNLIKELY.
From the ASA; By 2030, 3.88% of the US population >18 years of age is projected to have had a stroke. Between 2012 and 2030, real (2010$) total direct annual stroke-related medical costs are expected to increase from $71.55 billion to $183.13 billion. Not as bad as Alzheimers but still substantial.
Current quibbling over what Jeb Bush meant when he said it’s time to phase out and replace Medicare — as opposed to “attacking the seniors,” as one woman at a recent event bellowed out — will soon seem quaint against the realities of our future.
Never mind projections that the program will be able to finance only 86 percent of its obligations by 2030. Or that by 2050, the number declines to 80 percent, according to a recently released Social Security and Medicare Boards of Trustees report.
Kathleen Parker writes a twice-weekly column on politics and culture. She received the Pulitzer Prize for Commentary In 2010.  
These are relatively comforting numbers compared with new projections from the Alzheimer’s Association. By 2050, the group says, 13.8 million Americans may have Alzheimer’s disease, at a cost of $1.1 trillion per year, mostly to Medicare and Medicaid.
Today, by comparison, 5.3 million have the disease.
“Basically, it will bankrupt Medicare,” said Robert Egge, the Alzheimer’s Association’s chief public policy officer. I met with Egge and chief science officer Maria Carrillo during the association’s recent international conference in Washington.
The 2015 cost of care for Alzheimer’s and all other dementias is estimated at $226 billion, with 68 percent being paid by Medicare and Medicaid, Egge said.
This total includes only direct costs for the care of Alzheimer’s sufferers — there currently is no treatment — and doesn’t take into consideration unpaid care by families. Within the next 10 years, 19 states will see at least a 40 percent increase in the number of people affected.
Lest you feel overwhelmed by numbers — and demoralized by the reduction of human suffering to numerical values — suffice it to say that we are in a state of emergency. Yet, even with this obvious urgency, relatively few resources have been dedicated to research for prevention and treatment compared with other chronic diseases. This, despite the fact that Alzheimer’s is the sixth leading cause of death in the United States, according to the Centers for Disease Control and Prevention.
Current federal research funding is less than $600 million annually, while top scientists say they’ll need $2 billion a year to meet the association’s 2025 goal of prevention and effective treatment. There’s cause for some hope. Last month, bipartisan House and Senate subcommittees approved increasing funding to the National Institutes of Health for Alzheimer’s research by 50 percent and 60 percent, respectively.
If this funding becomes law — and the association’s goals are met — costs could be reduced by $220 billion over the first five years and $367 billion in 2050 alone, according to an association report. Sixty percent of those savings would accrue to Medicare and Medicaid.
Among other scientific developments reported this week, researchers have isolated a “common ancestor” among all forms of dementia, including Alzheimer’s, Parkinson’s and Lewy body.
“All are caused by misfolding proteins,” Carrillo explained to me. Two different “misfolded” proteins — amyloid beta and tau — are toxic to brain cells.
I am sad to report these proteins cannot be corrected with daily doses of a sturdy zinfandel. There is, however, a new drug that delivers a molecule scientists have created to “chaperone” these proteins so that they fold correctly.
Carrillo doesn’t want to overstate the value of this one-target-one-molecule approach, though it is promising. She suggests that eventually we’ll treat Alzheimer’s with a “cocktail” that will be created based on an individual’s genetic makeup and other factors.
Other hope-inspiring developments include six diagnostic tools that, in combination, can be useful in predicting Alzheimer’s. They include memory and thinking tests, as well as MRI scans that can measure the thickness of the brain’s right entorhinal cortex and the volume of the hippocampus, both of which are important to memory.
It is reassuring that both policymakers and scientists are committed to tackling these diseases. But women especially should be interested in the progress of dementia research. For reasons unknown, women suffer Alzheimer’s at a higher rate — two-thirds of today’s sufferers are women. And women’s function declines twice as fast as men’s. This fall, the association will issue an international call for research on why this is so.
In the meantime, Congress should waste no time in correcting the travesty of too-little funding for a devastating disease that demands our urgent attention. Otherwise, what to do about Medicare will be rendered irrelevant.

First Alzheimer's professional judgment budget reflects urgency in addressing this triple threat

IF we had anything resembling even a decent stroke association we would have stroke also doing its professional judgment budget to inform Congress of research needed to reach milestones. But we have jackshit for stroke associations because all they do is put out fucking lazy press releases.

First Alzheimer's professional judgment budget reflects urgency in addressing this triple threat

Today, the National Institutes of Health (NIH) recommended an increase of $323 million in its first professional judgment budget aimed at providing Congress with a scientific estimate of what research funding is needed and can be immediately well utilized to address Alzheimer's disease in fiscal year 2017. Under the Alzheimer's Accountability Act(Where is the stroke version?) incorporated in the 2015 funding bill, a professional judgment budget for Alzheimer's research that identifies the funding necessary to achieve annual research milestones established under the National Plan to Address Alzheimer's Disease will be submitted each year until 2025. It will reflect the state of Alzheimer's knowledge, and the effectively deployable investments in research identified by leading scientists as required to achieve the plan's first goal to prevent and effectively treat Alzheimer's by 2025.
"Congress has told us they want to hear directly from the nation's top scientists. Today, they have heard from those experts that Alzheimer's disease warrants swift and significant investment," said Harry Johns, president and CEO of the Alzheimer's Association. "Congress has shown leadership on the issue of Alzheimer's research over the last few years. This scientific budget estimate will give both a more complete picture of the funding necessary in fiscal year 2017 to build on the recent research investments and to ensure we are on track to meet the goals of the National Plan. This objective research funding estimate is critical as Congress continues their work to reverse the historic underfunding of Alzheimer's disease of the past several decades."
Alzheimer's is only the third disease to receive a professional judgment budget, also known as a "by-pass budget," following cancer and HIV/AIDS. Recognizing the role that this mechanism played in the successful investments and resulting medical advances for these diseases, Alzheimer's Association grassroots advocates and staff held thousands of congressional meetings to secure support for the Alzheimer's Accountability Act. While the Alzheimer's Association and its sister organization, the Alzheimer's Impact Movement, were the only two organizations to endorse and work to advance the Alzheimer's Accountability Act, the legislation received strong, bipartisan support in both the House and the Senate.
Last month, led by Rep. Tom Cole (R-Okla.) and Sens. Roy Blunt (R-Mo.) and Patty Murray (D-Wash.), the House and Senate Appropriations Committees approved historic funding increases for Alzheimer's disease of $300 million and approximately $350 million, respectively, for fiscal year 2016. If enacted into law, this 50-60 percent increase would be the largest increase in Alzheimer's research funding to date.
"Under NIH Director Dr. Francis Collins' leadership, this professional judgment budget for fiscal year 2017 confirms what the science community has said: we must continue to increase funding for Alzheimer's disease research at significant intervals to reach the levels necessary to accomplish the first goal of the national Alzheimer's plan," said Johns.
Alzheimer's is already the most expensive disease in the nation, and the only leading cause of death among the top 10 in the U.S. without a way to prevent, cure or even slow its progression. Because advancing age is the greatest risk factor for Alzheimer's disease and Americans are living longer than ever before, those numbers are projected to soar to as many as 16 million by 2050, costing the nation $20 trillion over the next 40 years.
Earlier this year, the Association released Changing the Trajectory of Alzheimer's Disease: How a Treatment by 2025 Saves Lives and Dollars, which calculated that a treatment introduced in 2025 that delays the onset of Alzheimer's by five years would reduce the number of individuals affected by the disease by 2.5 million people and save the nation $220 billion within the first five years of a treatment being available.
For more information on Alzheimer's disease, visit the Alzheimer's Association at