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 438 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:

Monday, September 1, 2014

Does functional MRI detect activation in white matter? A review of emerging evidence, issues, and future directions

Right now your doctor has no clue as to how much damage is in your white matter. With no diagnosis of damage there can be no idea of what stroke protocols work in correcting such damage. You doctor is totally flying blind when trying to determine what needs to be done. But then that is no different that what occurs today in any therapy given to help survivors recover. Everything in stroke is flying blind, no wonder only 10% fully recover. Would you want a blind doctor operating on clipping your aneurysm in your brain? 
  • 1Division of Medical Sciences, Department of Psychology, University of Victoria, Victoria, BC, Canada
  • 2Department of Radiology, Faculty of Medicine, University of Calgary, Calgary, AB, Canada
  • 3Applied Sciences, Simon Fraser University, Burnaby, BC, Canada
  • 4Fraser Health Authority, Surrey Memorial Hospital, Surrey, BC, Canada
Functional magnetic resonance imaging (fMRI) is a non-invasive technique that allows for visualization of activated brain regions. Until recently, fMRI studies have focused on gray matter. There are two main reasons white matter fMRI remains controversial: (1) the blood oxygen level dependent (BOLD) fMRI signal depends on cerebral blood flow and volume, which are lower in white matter than gray matter and (2) fMRI signal has been associated with post-synaptic potentials (mainly localized in gray matter) as opposed to action potentials (the primary type of neural activity in white matter). Despite these observations, there is no direct evidence against measuring fMRI activation in white matter and reports of fMRI activation in white matter continue to increase. The questions underlying white matter fMRI activation are important. White matter fMRI activation has the potential to greatly expand the breadth of brain connectivity research, as well as improve the assessment and diagnosis of white matter and connectivity disorders. The current review provides an overview of the motivation to investigate white matter fMRI activation, as well as the published evidence of this phenomenon. We speculate on possible neurophysiologic bases of white matter fMRI signals, and discuss potential explanations for why reports of white matter fMRI activation are relatively scarce. We end with a discussion of future basic and clinical research directions in the study of white matter fMRI.

Motivation to Investigate White Matter fMRI

Functional magnetic resonance imaging (fMRI) is used to visualize the neuroanatomical regions associated with brain function. The most commonly used technique for fMRI, blood oxygenation level dependent (BOLD) contrast, was first demonstrated in the early 1990s (Ogawa et al., 1992). Since then, fMRI has broadened our understanding of how the brain functions under both healthy and diseased conditions (e.g., Rosen et al., 1998; Dolan, 2008; Haller and Bartsch, 2009; Rosen and Savoy, 2012). Although fMRI continues to grow in popularity in both research and clinical settings, the full potential of this technique remains untapped because fMRI activity has historically not been considered to be detectable in white matter tissue (Logothetis and Wandell, 2004). In spite of this, fMRI studies often produce activation in white matter and consequently there has been much debate over whether this activation is a true or false representation of underlying neural activity. There are two main reasons that white matter fMRI is controversial. First, BOLD signal relies on cerebral blood volume and flow, which are three to seven times lower in white matter (Rostrup et al., 2000; Preibisch and Haase, 2001; Helenius et al., 2003). However, the vasculature and perfusion of white matter (Figure 1) are capable of supporting hemodynamic changes that are detectable with BOLD fMRI [see Section White Matter Vasculature, Cerebral Blood Flow (CBF), and Cerebral Blood Volume (CBV)]. Second, the primary source of fMRI signal is thought to arise from post-synaptic potentials (which occur mainly in gray matter) as opposed to action potentials (e.g., Logothetis et al., 2001; but see e.g., Smith et al., 2002). However, neither of these statements exclude the possibility, and there is no direct evidence against the possibility of measuring fMRI activation in white matter.

More at link.

Lipid dynamics at dendritic spines

We probably need dendritic branching to recover. What is your doctor doing to accomplish that? Look at the last bolded sentence, this is what makes me think cholesterol reduction is not necessarily good for our recovery. But I'm stupid because I'm not medically trained and thus should never be listened to.
  • Centro Biología Molecular Severo Ochoa, CSIC-UAM, Madrid, Spain
Dynamic changes in the structure and composition of the membrane protrusions forming dendritic spines underlie memory and learning processes. In recent years a great effort has been made to characterize in detail the protein machinery that controls spine plasticity. However, we know much less about the involvement of lipids, despite being major membrane components and structure determinants. Moreover, protein complexes that regulate spine plasticity depend on specific interactions with membrane lipids for proper function and accurate intracellular signaling. In this review we gather information available on the lipid composition at dendritic spine membranes and on its dynamics. We pay particular attention to the influence that spine lipid dynamism has on glutamate receptors, which are key regulators of synaptic plasticity.


At most excitatory synapses in the Central Nervous System, presynaptic boutons synapse onto small membrane protrusions that emerge from the dendritic shaft: the dendritic spines. Changes in dendritic spine number, size and shape contribute to determine the strength of excitatory synaptic transmission (Yuste and Bonhoeffer, 2001; Carlisle and Kennedy, 2005). The remodeling of these membrane protrusions in response to stimuli depends on lipids, which are major components of the membrane with the ability to shape it and modify protein activities within. However, only recently the contribution of spine lipids has attracted similar attention to that of spine proteins. Pioneer work showing the requirement of glial cholesterol for synapse formation (Mauch et al., 2001) and the elimination of spines upon reduction of cholesterol or sphingolipids (Hering et al., 2003) triggered research in this field. Technical progress facilitates today the not so long ago impossible analysis of the subtle changes in lipid composition and of the topographical distribution of individual lipid species in cellular compartments. Probes have been developed to label lipid molecules such as new generation fluorescent tags (Eggeling et al., 2009) or modified toxins with specific lipid binding abilities such as the theta-toxin or lysenin, which bind cholesterol or sphingomyelin, respectively (Abe et al., 2012). These probes together with advanced microscopy techniques that achieve sub-diffraction optical resolution (i.e., near-field scanning optical microscopy (NSOM), photoactivated localization microscopy (PALM) stochastic optical reconstruction microscopy (STORM) or stimulated depletion (STED) fluorescent microscopy) allow the direct observation of the nanoscale dynamics of membrane lipids in a living cell (Eggeling et al., 2009; van Zanten et al., 2010; Castro et al., 2013). As we gain insight on how lipids and their metabolic enzymes regulate dendritic spine shape and protein function their importance is confirmed and strengthened. We aim here to review this knowledge focusing the attention on the dynamic lipidomics of dendritic spines. We will also discuss about how this influences synaptic plasticity through the modulation of glutamate receptors of the AMPA and NMDA-type (AMPARc and NMDARc). These receptors are instrumental to elicit Long Term Potentiation (LTP) and Long Term Depression (LTD), which are considered the molecular mechanisms underlying learning and memory (Neves et al., 2008; Collingridge et al., 2010).

Lipid Composition at Dendritic Spines

A relevant question about spine physiology is whether spine membrane lipid composition and organization is different to that of the dendritic shaft membranes from which these protrusions emerge. A systematic analysis of spine lipid composition is lacking due to technical limitations. However, accumulating evidence indicates it differs from that of the shaft. This raises questions such as why this specificity is necessary and how it is achieved, maintained or modulated upon stimuli. Until now, most of the information on synaptic lipid composition comes from the biochemical analysis of synaptosomal preparations. Functional studies have also highlighted the relevant contribution of certain lipids to spine physiology. From these two types of approaches we now know that cholesterol and sphingolipids are enriched in spines. Because of their chemical affinity these lipids form highly dynamic and heterogeneous membrane nanodomains, the so called rafts, which can be stabilized to form larger platforms by protein-protein or protein-lipid interactions (Pike, 2006). Rafts compartmentalize cellular processes contributing to the accurate spatial and temporal organization of molecules required at dendritic spines (Allen et al., 2007). Neurotrophin and neurotransmitter receptors (NTRcs) are recruited from extrasynaptic to synaptic sites through association to lipid rafts, which reduce receptor lateral mobility at the synaptic space (Nagappan and Lu, 2005; Fernandes et al., 2010). In fact, the post synapse has been proposed as a lipid raft-enriched territory and certain key structural proteins such as the postsynaptic density protein 95 (PSD95) as well as AMPARc dynamically associate to these domains (Perez and Bredt, 1998; Suzuki, 2002; Hering et al., 2003; Suzuki et al., 2011). The tight control of the turnover of phosphoinositides and their derivatives plays also a central role in spine plasticity. We next describe data available on the presence of the aforementioned lipids in spines and on their contribution to spine physiology. Hopefully, the already mentioned imaging techniques based on advanced lipid probes and super-resolution microscopy together with most sensitive quantitative measurements (i.e., liquid chromatography coupled with tandem mass spectrometry) would contribute to more precisely define the lipid composition of spines and its changes in real time in living cells.


Pharmacological extraction of cholesterol or inhibition of its synthesis led to the disappearance of dendritic spines in cultured hippocampal neurons, probably mediated by disruption of the actin cytoskeleton (Hering et al., 2003). This finding defined cholesterol as a core component of spines.

Much more at link.

Protection after stroke: cellular effectors of neurovascular unit integrity

Now if we just had a great stroke association that would take this information and create translational stroke protocols to stop parts of the neuronal cascade of death. But we have crap for stroke associations and thus future survivors will continue to not have any useful stroke protocols in the first week.
  • 1Cellular and Molecular Neurobiology Area, Group of Neuroscience of Antioquia, Faculty of Medicine, Sede de Investigación Universitaria (SIU), University of Antioquia UdeA, Medellín, Colombia
  • 2Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá D.C., Colombia
Neurological disorders are prevalent worldwide. Cerebrovascular diseases (CVDs), which account for 55% of all neurological diseases, are the leading cause of permanent disability, cognitive and motor disorders and dementia. Stroke affects the function and structure of blood-brain barrier, the loss of cerebral blood flow regulation, oxidative stress, inflammation and the loss of neural connections. Currently, no gold standard treatments are available outside the acute therapeutic window to improve outcome in stroke patients. Some promising candidate targets have been identified for the improvement of long-term recovery after stroke, such as Rho GTPases, cell adhesion proteins, kinases, and phosphatases. Previous studies by our lab indicated that Rho GTPases (Rac and RhoA) are involved in both tissue damage and survival, as these proteins are essential for the morphology and movement of neurons, astrocytes and endothelial cells, thus playing a critical role in the balance between cell survival and death. Treatment with a pharmacological inhibitor of RhoA/ROCK blocks the activation of the neurodegeneration cascade. In addition, Rac and synaptic adhesion proteins (p120 catenin and N-catenin) play critical roles in protection against cerebral infarction and in recovery by supporting the neurovascular unit and cytoskeletal remodeling activity to maintain the integrity of the brain parenchyma. Interestingly, neuroprotective agents, such as atorvastatin, and CDK5 silencing after cerebral ischemia and in a glutamate-induced excitotoxicity model may act on the same cellular effectors to recover neurovascular unit integrity. Therefore, future efforts must focus on individually targeting the structural and functional roles of each effector of neurovascular unit and the interactions in neural and non-neural cells in the post-ischemic brain and address how to promote the recovery or prevent the loss of homeostasis in the short, medium and long term.


Neurological disorders are highly prevalent around the globe. In 2008, neurodegenerative disorders were responsible for 1% of disabilities worldwide (W.H.O., 2003). Strokes account for 55% of all neurological diseases and are considered the leading cause of permanent physical and mental disability (OMS, 2013). The primary risk factors of stroke include hyperlipidemia, hypertension, diabetes mellitus, and harmful habits, such as smoking and excessive alcohol consumption. The high incidence of strokes is related to an increased number of dementia cases and other emotional and cognitive disorders, such as depression and memory loss (Ovbiagele and Nguyen-Huynh, 2011). Death, physical deterioration, and altered quality of life are consequences of the natural history of strokes among patients who survive an ischemic event (Sacco, 1997, 1998; Feigin et al., 2003; Silva et al., 2006). Interestingly, the coexistence of cerebral ischemia and neurodegenerative pathologies profoundly impacts the development of dementia, suggesting a reciprocal interaction between ischemia and neurodegeneration (Nagy et al., 1997; Snowdon et al., 1997). These observations, along with the results of epidemiological studies that have indicated that Alzheimer’s disease (AD) and cerebrovascular diseases share similar risk factors (Breteler, 2000), have shifted interest to vascular factors as fundamental contributors to the pathogenesis of neurodegenerative diseases (de la Torre and Mussivand, 1993; Kalaria, 2000; Iadecola and Gorelick, 2003). This hypothesis has been supported by the experimental findings that showed that amyloid-beta (Aβ) peptide, which is commonly detected in AD patients, exhibits strong cerebrovascular effects and that ischemia-induced responses to hypoxia are potent modulators of cerebral amyloidogenesis (Iadecola, 2004). Both Aβ peptide and vascular risk factors deteriorate the structure and function of the neurovascular unit (NVU, consisting of the endothelium, glia, neurons, pericytes, and the basal lamina) (Mirra and Gearing, 1997; Snowdon et al., 1997; Breteler, 2000; Kalaria, 2000; Iadecola and Gorelick, 2003; Iadecola, 2004).
The NVU acts as a guardian of cerebral homeostasis. Neurons, glia, the perivascular space, and the endothelium are closely interrelated to maintain the homeostasis of the brain microenvironment (Iadecola, 2010), regulate blood flow, modulate the exchange across the blood-brain barrier (BBB), contribute to immune vigilance and provide trophic support to the brain (Iadecola, 2010). Substantial evidence has shown that cerebrovascular dysfunction is implicated in not only cognitive impairment (such as that of cognitive origin) but also neurodegenerative diseases, such as AD (Chui et al., 1992; Alavi et al., 1998; Kalaria, 2000; Iadecola, 2004; Simpkins et al., 2005; Hachinski et al., 2006; Pendlebury et al., 2012). Ischemic stroke is exacerbated by several risk factors that affect the function and structure of blood vessels in the brain and cells associated with the NVU, reducing the ability of the brain parenchyma to repair due to the rupture of the BBB, the loss of brain blood flow regulation, oxidative stress, inflammation, and the loss of neuronal connections, ultimately increasing brain dysfunction (Deane et al., 2003; Ohab et al., 2006; Konsman et al., 2007; Weber et al., 2007; Bell et al., 2009; Wolburg et al., 2009). The study of stroke has focused on understanding the molecular and pathophysiological mechanisms of neuronal death, recovery and pharmacological intervention strategies, as well as clinical and epidemiological characteristics (Silva et al., 2006). In addition, several molecular targets associated with endothelial dysfunction and cardio-cerebrovascular risk, including CDK5, Rho GTPases, and cell adhesion proteins, are described below and presented in a hypothetical schematic in Figure 1 to explain and propose a potential neuroprotective approach for stroke.

Much more at link.

Obesity is a risk factor for significant carotid atherosclerosis in patients aged 39 to 55 years

At age 50 when I had my stroke my right carotid artery dissected due to trauma and probably 80% atherosclerosis blockage. I was in fantastic shape, my cardiovascular fitness level was as an athlete. But since I'm an outlier no one will analyze why my plaque was so bad and maybe save others from a stroke. It is much easier to just put out f*cking lazy press releases and relegate the problem solving to someone else.
da Silva ES, et al. – Authors compared the prevalence of risk factors between young and old individuals with significant carotid atherosclerosis. Obesity and smoking were significant risk factors for young patients in this sample.
  • They retrospectively reviewed the records of patients aged 39 to 55 years (group I) and aged >=60 years (group II) with significant atherosclerotic stenosis at the carotid bifurcation.
  • Group I patients had significantly higher values for the following factors: weight, height, body mass index, diastolic pressure, prevalence of current smoking, total and low–density lipoprotein cholesterol and significant lower values for systolic pressure, creatinine, and prevalence of coronary artery disease.
  • Group I patients were more symptomatic and showed higher rates of carotid occlusion and near occlusion.
  • Atherosclerosis of the carotid bifurcation was more aggressive in the younger group, with a higher rate of occlusion and near occlusion.

Mayo Clinic - Cholesterol: Top 5 foods to lower your numbers

If you think the Mayo Clinic knows what they are talking about with cholesterol. Read it all here:

1. Oatmeal, oat bran and high-fiber foods

2. Fish and omega-3 fatty acids

  • Mackerel
  • Lake trout
  • Herring
  • Sardines
  • Albacore tuna
  • Salmon
  • Halibut

3. Walnuts, almonds and other nuts

4. Olive oil

5. Foods with added plant sterols or stanols


And from Harvard Medical School;

CHAPTER 1: Understanding Cholesterol: The Good, the Bad, and the Necessary

Cholesterol performs three main functions:
  1. It helps make the outer coating of cells.
  2. It makes up the bile acids that work to digest food in the intestine.
  3. It allows the body to make Vitamin D and hormones, like estrogen in women and testosterone in men.
Without cholesterol, none of these functions would take place, and without these functions, human beings wouldn't exist.

For more information or to purchase this book, follow this link:

And from   David Perlmutter MD Empowering neurologist

Your Brain Needs Cholesterol

Cholesterol is vitally important for brain function. While your brain represents about 2-3% of your total body weight, 25% of the cholesterol in your body is found in your brain, where it plays important roles in such things as membrane function, acts as an antioxidant, and serves as the raw material from which we are able to make things like progesterone, estrogen, cortisol, testosterone and even vitamin D.
In fact, in a recent study available on the NIH Public Access site, researchers showed that in the elderly, the best memory function was observed in those with the highest levels of cholesterol. Low cholesterol is associated with an increased risk for depression and even death.




Triglycerides and cardiovascular disease

I suppose I shouldn't comment on doctors  area of expertise, but I still think that they need to solve why inflammation occurs rather than the particles floating in the bloodstream. Have they never heard of cause and effect or root cause analysis. They wouldn't last a week in a programming environment. They would be fired within days for suggesting working on peripheral issues rather than solving the real problem.  But then this is somebody else's problem, no need to really worry about it. I'll get paid regardless.  Pay for performance would solve that problem or having business rules apply to doctors.
Nordestgaard BG, et al. – After the introduction of statins, clinical emphasis first focussed on LDL cholesterol–lowering, then on the potential for raising HDL cholesterol, with less focus on lowering triglycerides.
  • However, the understanding from genetic studies and negative results from randomised trials that low HDL cholesterol might not cause cardiovascular disease as originally thought has now generated renewed interest in raised concentrations of triglycerides.
  • This renewed interest has also been driven by epidemiological and genetic evidence supporting raised triglycerides, remnant cholesterol, or triglyceride–rich lipoproteins as an additional cause of cardiovascular disease and all–cause mortality.
  • Triglycerides can be measured in the non–fasting or fasting states, with concentrations of 2—10 mmol/L conferring increased risk of cardiovascular disease, and concentrations greater than 10 mmol/L conferring increased risk of acute pancreatitis and possibly cardiovascular disease.
  • Although randomised trials showing cardiovascular benefit of triglyceride reduction are scarce, new triglyceride–lowering drugs are being developed, and large–scale trials have been initiated that will hopefully provide conclusive evidence as to whether lowering triglycerides reduces the risk of cardiovascular disease.

Sunday, August 31, 2014

If it were not for this continuous stream of motor impulses, we would collapse like a bunch of broccoli

A direct quote from Young Frankenstein. What exactly does your doctor have to say  about why you didn't collapse like broccoli when you had your stroke?
And this series of quotes is probably more explanation of your brain than your doctor told you about.

The Option of Doing Nothing and Its Impact on Postchoice Persistence

Does your doctor understand this in figuring out how to motivate you post-stroke to do therapy that only has a 10% chance of getting you to full recovery? Does your doctor understand anything at all about recovery? What exactly are his/her written stroke protocols to do exactly that?
  1. Rom Y. Schrift1
  2. Jeffrey R. Parker2
  1. 1Wharton Business School, University of Pennsylvania
  2. 2J. Mack Robinson College of Business, Georgia State University
  1. Rom Y. Schrift, The Wharton School, 700 Jon M. Huntsman Hall, University of Pennsylvania, Philadelphia, PA 19104 E-mail:
  1. Author Contributions R. Y. Schrift and J. R. Parker jointly developed the studies’ concepts and contributed equally to the design. Both authors performed the testing and data collection, and both approved the final version of the manuscript for submission.


Individuals regularly face adversity in the pursuit of goals that require ongoing commitment. Whether or not individuals persist in the face of adversity greatly affects the likelihood that they will achieve their goals. We argue that a seemingly minor change in the individual’s original choice set—specifically, the addition of a no-choice option—will increase persistence along the chosen path. Drawing on self-perception theory, we propose that choosing from a set that includes a no-choice (do nothing) option informs individuals that they both prefer the chosen path to other paths and that they consider this path alone to be worth pursuing, an inference that cannot be made in the absence of a no-choice option. This unique information strengthens individuals’ commitment to, and increases their persistence on, their chosen path. Three studies employing incentive-compatible designs supported our predictions and ruled out several rival accounts.

Saturday, August 30, 2014

Sailing as Stroke Rehabilitation Strategy

I'm sure this will never occur. But it would make for fantastic balance training. I would volunteer for such a research study. It would be even better with no safety harness because that would require you to pay attention.