Recombinant human thioredoxin-1 promotes neurogenesis and facilitates cognitive recovery following cerebral ischemia in mice

What research is your doctor going to do based on this? Nothing is a fireable offense.
http://www.sciencedirect.com/science/article/pii/S0028390813005030

• Li Tian^{a, 1},
• Huang Nie^{a, 1},
• Yang Zhang^{b, 1},
• Yu Chen^a,
• Zhengwu Peng^c,
• Min Cai^a,
• Haidong Wei^a,
• Pei Qin^a,
• Hailong Dong^{a, ,} ,
• Lize Xiong^{a, , ,}

• ^a Department of Anesthesiology, Xijing Hospital, The Fourth Military Medical University, 127th Changle West Road, Xi'an 710032, China
• ^b Department of Orthopedic Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China
• ^c Department of Psychosomatic Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China

  Open Access

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Highlights

•

rhTrx-1 ameliorated spatial learning and memory deficits induced by ischemia.

•

rhTrx-1 promoted ischemia-induced neurogenesis in DG.

•

rhTrx-1 enhanced proliferation and neuronal differentiation of cultured NSCs.

•

Neurogenesis enhanced by rhTrx-1 was inhibited by U0126 – inhibitor of ERK signaling pathway.

---

Abstract

Cerebral ischemia (CI) can induce loss of hippocampal neurons, causing cognitive dysfunction such as learning and memory deficits. In adult mammals, the hippocampal dentate gyrus contains neural stem cells (NSCs) that continuously generate newborn neurons and integrate into the pre-existing networks throughout life, which may ameliorate cognitive dysfunction following CI. Recent studies have demonstrated that recombinant human thioredoxin-1 (rhTrx-1) could promote proliferation of human adipose tissue-derived mesenchymal stem cells and angiogenesis. To investigate whether rhTrx-1 also regulates hippocampal neurogenesis following CI and its underlying mechanisms, adult mice were subjected to bilateral common carotid arteries occlusion (BCCAO) to induce CI and treated with rhTrx-1 before reperfusion. Mice treated with rhTrx-1 showed shortened escape latencies in Morris water maze by 30 days and improvements in spatial memory demonstrated by probe trial test. Enhanced NSCs proliferation was observed at day 14, indicated by BrdU and Ki67 immunostaining. Doublecortin (DCX)⁺ cells were also significantly increased following rhTrx-1 treatment. Despite increases in BrdU⁺/NeuN⁺ cells by day 30, the double-labeling to total BrdU⁺ ratio was not affected by rhTrx-1 treatment. The promotive effects of rhTrx-1 on NSCs proliferation and differentiation were further confirmed in in vitro assays. Western blot revealed increased ERK1/2 phosphorylation after rhTrx-1 treatment, and the ERK inhibitor U0126 abrogated the effects of rhTrx-1 on NSCs proliferation. These results provide initial evidence that rhTrx-1 effects neurogenesis through the ERK signaling pathway and are beneficial for improving spatial learning and memory in adult mice following global CI.

2013 Thomas Willis Award Lecture Causation and Collaboration for Stroke Research

This is pathetic that we can't read the whole Willis lecture. We need to know this because our doctors won't.
http://stroke.ahajournals.org/content/early/2013/11/06/STROKEAHA.113.001269.short

1. Eng H. Lo, PhD

+ Author Affiliations

1. From the Departments of Neurology and Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown.

1. Correspondence to Eng H. Lo, PhD, Massachusetts General Hospital, Harvard Medical School, MGH E 149-2401, 13th St, Charlestown, MA 02129. E-mail Lo@helix.mgh.harvard.edu

Abstract

The pathophysiology of stroke is complex. Adaptive and maladaptive signalling occurs between multiple cell types in the brain. There is crosstalk between central and systemic responses. And there are overlapping pathways during initial injury and subsequent repair. These numerous feed-forward and feed-back interactions have made it difficult to translate experimental discoveries into clinical applications. An emerging hypothesis in biomedical research now suggests that contrary to a traditional model, translation may not be efficiently obtained without a rigorous understanding of mechanisms. Hence, to optimize diagnostics and therapeutics for stroke patients, it is necessary to identify and define causal mechanisms. Mirroring the multi-compartment interactions in stroke pathophysiology, bench-to-bedside, and bedside-back-to-bench advances in stroke may be best achieved with inter-disciplinary collaborations between basic research, neuroimaging, and broadly based clinical science. Causation can then be two-fold, ie, dissecting mechanisms and targets, as well as developing future scientists who can blur the boundaries between basic, translational, and clinical research. In systems theory, a critical goal is to distinguish causation from correlation. In stroke research, causation may perhaps be found through a collaborative search for mechanisms.

Cordocytes-Stem Cells Cooperation in the Human Brain with Emphasis on Pivotal Role of Cordocytes in Perivascular Areas of Broken and Thrombosed Vessels

Your doctor can figure out how rebuilding blood vessels in the damaged area may help your recovery.
http://informahealthcare.com/doi/abs/10.3109/01913123.2013.846449

December 2013, Vol. 37, No. 6 , Pages 425-432 (doi:10.3109/01913123.2013.846449)

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Viorel Pais, PhD¹, Leon Danaila, MD, PhD¹, and Emil Pais, DDS, MS²

¹Department of Neurosurgery, National Institute of Neurology and Neurovascular Diseases,

Bucharest

, Romania and

²Spectral Molecular Imaging,

Los Angeles, CA

, USA

Correspondence:

Viorel Pais, PhD, Collaborator

, Department of Neurosurgery, National Institute of Neurology and Neurovascular Diseases,

10-12 Soseaua Berceni, Sector 4, 41914 Bucharest

, Romania. Tel: (40)31-409-7790. Fax: (40)21-334-6463. E-mail: viorelpais@hotmail.com

Abstract

This study is based on data analysis by light and transmission electron microscopy of the surgical cases in cerebral tumors, cerebrovascular malformations, thromboses in the carotid system, and other injuries such as perivascular hemorrhage. We examined cortical arteries and veins, perivascular areas with old hematic masses, vasculogenic foci, and broken large vessels. We identified, characterized, and compared both undifferentiated cells and well-differentiated cordocytes within periadventitial areas where these cells cooperate very well with precursor/stem cells to perform vital functions for cerebral vasculature with immediate effect on brain parenchyma. This useful cellular cooperation was observed by serial sections pointing out the main role of cordocytes during the entire process of collateral vessel formation after thrombosis and, respectively, in vascular wall repair after ruptures. This is the first cytohistopathological study which illustrates and explains some facets of cordocytes-stem cells cooperation around the vessels of human brain with emphasis on the fundamental role of cordocytes in response to vascular injuries. Our pioneering study will be completed for both basic science and modern medical care by further studies.

Read More: http://informahealthcare.com/doi/abs/10.3109/01913123.2013.846449

Noninvasive Brain Stimulation for Treatment of Right- and Left-Handed Poststroke Aphasics

Is this enough to have as a protocol for aphasia?
http://www.karger.com/Article/FullText/355499
Noninvasive Brain Stimulation for Treatment of Right- and Left-Handed Poststroke Aphasics
Heiss W.-D. · Hartmann A. · Rubi-Fessen I. · Anglade C. · Kracht L. · Kessler J. · Weiduschat N. · Rommel T. · Thiel A.
Cerebrovasc Dis 2013;36:363-372 (DOI: 10.1159/000355499)

Abstract

Background: Accumulating evidence from single case studies, small case series and randomized controlled trials seems to suggest that inhibitory noninvasive brain stimulation (NIBS) over the contralesional inferior frontal gyrus (IFG) of right-handers in conjunction with speech and language therapy (SLT) improves recovery from poststroke aphasia. Application of inhibitory NIBS to improve recovery in left-handed patients has not yet been reported. Methods: A total of 29 right-handed subacute poststroke aphasics were randomized to receive either 10 sessions of SLT following 20 min of inhibitory repetitive transcranial magnetic stimulation (rTMS) over the contralesional IFG or 10 sessions of SLT following sham stimulation; 2 left-handers were treated according to the same protocol with real rTMS. Language activation patterns were assessed with positron emission tomography prior to and after the treatment; 95% confidence intervals for changes in language performance scores and the activated brain volumes in both hemispheres were derived from TMS- and sham-treated right-handed patients and compared to the same parameters in left-handers. Results: Right-handed patients treated with rTMS showed better recovery of language function in global aphasia test scores (t test, p < 0.002) as well as in picture-naming performance (ANOVA, p = 0.03) than sham-treated right-handers. In treated right-handers, a shift of activation to the ipsilesional hemisphere was observed, while sham-treated patients consolidated network activity in the contralesional hemisphere (repeated-measures ANOVA, p = 0.009). Both left-handed patients also improved, with 1 patient within the confidence limits of TMS-treated right-handers (23 points, 15.9-28.9) and the other patient within the limits of sham-treated subjects (8 points, 2.8-14.5). Both patients exhibited only a very small interhemispheric shift, much less than expected in TMS-treated right-handers, and more or less consolidated initially active networks in both hemispheres. Conclusion: Inhibitory rTMS over the nondominant IFG appears to be a safe and effective treatment for right-handed poststroke aphasics. In the 2 cases of left-handed aphasics no deterioration of language performance was observed with this protocol. However, therapeutic efficiency is less obvious and seems to be more related to the dominance pattern prior to the stroke than to the TMS intervention.

Parental longevity is associated with cognition and brain ageing in middle-aged offspring

So since my Mom at 95 still living at home and doing good, dad died at 91 with Parkinsons dementia, at least Parkinsons is not genetic, Maybe my  dementia chances are not that great.
But after your stroke how much is your doctor working on preventing dementia in you? They've done nothing for your recovery, are they at least working on preventing your dementia?
Parental longevity is associated with cognition and brain ageing in middle-aged offspring

1. Joanne M. Murabito1,2⇑,
2. Alexa S. Beiser2,3,4,
3. Charles DeCarli5,
4. Sudha Seshadri2,4,
5. Philip A. Wolf2,4 and
6. Rhoda Au2,4

+ Author Affiliations

1. ¹Section of General Internal Medicine, Department of Medicine, Boston University School of Medicine, Boston, MA, USA
2. ²NHLBI's Framingham Heart Study, 73 Mount Wayte Avenue, Suite 2, Framingham, MA, USA
3. ³Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA
4. ⁴Department of Neurology, Boston University School of Medicine, Boston, MA, USA
5. ⁵University of California at Davis, Sacramento, CA, USA

1. Address correspondence to: J. M. Murabito. Tel: (+1) 5089353461; Fax: (+1) 5086261262. Email: murabito@bu.edu

• Received April 17, 2013.
• Accepted August 16, 2013.

Abstract

Background: offspring of long-lived individuals have lower risk for dementia. We examined the relation between parental longevity and cognition and subclinical markers of brain ageing in community-dwelling adult offspring.

Methods: offspring participants with both parents in the Framingham Heart Study, aged ≥55 years and dementia-free underwent baseline and repeat neuropsychological (NP) testing and brain magnetic resonance imaging (MRI). Parental longevity was defined as having at least one parent survive to age ≥85 years. To test the association between parental longevity and measures of cognition and brain volumes, we used multivariable linear and logistic regression adjusting for age, sex, education and time to NP testing or brain MRI.

Results: of 728 offspring (mean age 66 years, 54% women), 407 (56%) had ≥1 parent achieve longevity. In cross-sectional analysis, parental longevity was associated with better scores on attention (beta 0.21 ± 0.08, P = 0.006) and a lower odds of extensive white matter hyperintensity on brain MRI (odds ratio 0.59, 95% CI: 0.38, 0.92, P = 0.019). The association with white matter hyperintensity was no longer significant in models adjusted for cardiovascular risk factors and disease. In longitudinal analysis (6.7 ± 1.7 years later), offspring with parental longevity had slower decline in attention (0.18 ± 0.08, P = 0.038), executive function (beta 0.19 ± 0.09, P = 0.031) and visual memory (beta −0.18 ± 0.08, P = 0.023), and less increase in temporal horn volume (beta −0.25 ± 0.09, P = 0.005). The associations persisted in fully adjusted models.

Conclusion: parental longevity is associated with better brain ageing in middle-aged offspring.

 

Resting state interhemispheric motor connectivity and white matter integrity correlate with motor impairment in chronic stroke

This is so blasted obvious, you need to look at the damage to the brain, that will correlate to impairments.
http://www.frontiersin.org/Journal/10.3389/fneur.2013.00178/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neurology-w46-2013
Joyce L. Chen^1,2,3 and Gottfried Schlaug¹*

• ¹Neuroimaging and Stroke Recovery Laboratories, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
• ²Heart and Stroke Foundation Canadian Partnership in Stroke Recovery, Sunnybrook Research Institute, Toronto, ON, Canada
• ³Department of Physical Therapy, University of Toronto, Toronto, ON, Canada

Functional and structural reorganization in the brain occurs after stroke. The ability to predict motor outcomes may depend on patterns of brain functional and structural connectivity. We tested the hypothesis that alterations in motor transcallosal and corticospinal connections correlate with motor impairment in patients with chronic stroke. Eleven ischemic stroke patients underwent the Upper Extremity Fugl-Meyer (UE-FM) assessment, resting state functional magnetic resonance imaging, and diffusion tensor imaging (DTI). Twelve healthy control subjects underwent DTI. We assessed the temporal coupling in neural activity between interhemispheric motor cortex, and white matter integrity by means of fractional anisotropy (FA), in the transcallosal motor fibers and corticospinal tract. Partial correlation analyses were performed to determine whether these connectivity measures correlate with Upper UE-FM scores. Patients compared to controls had reduced FA in common voxels of transcallosal motor and ipsilesional corticospinal fibers. Within the patient group those with higher interhemispheric motor cortex connectivity and higher FA in the transcallosal motor fibers were less impaired. The results show that markers of functional and structural motor cortex connectivity correlate with motor impairment in the chronic stage of stroke.

More at link.

Automated decision-support system for prediction of treatment responders in acute ischemic stroke

You will need to find out how your hospital uses such a system to relegate you to a treatment protocol. This will be needed to be done in advance since if you are locked in and the lockedin protocol leads to minimal supportive treatment you are screwed. You can't allow the medical staff to determine this.
http://www.frontiersin.org/Journal/10.3389/fneur.2013.00140/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neurology-w46-2013

Kartheeban Nagenthiraja^1,2*, Brian P. Walcott^3,4, Mikkel B. Hansen¹, Leif Østergaard¹ and Kim Mouridsen¹

• ¹Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark
• ²Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
• ³Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
• ⁴Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA

MRI is widely used in the assessment of acute ischemic stroke. In particular, it identifies the mismatch between hypoperfused and the permanently damaged tissue, the PWI-DWI mismatch volume. It is used to help triage patients into active or supportive treatment pathways. COMBAT Stroke is an automated software tool for estimating the mismatch volume and ratio based on MRI. Herein, we validate the decision made by the software with actual clinical decision rendered. Furthermore, we evaluate the association between treatment decisions (both automated and actual) and outcomes. COMBAT Stroke was used to determine PWI-DWI mismatch volume and ratio in 228 patients from two European multi-center stroke databases. We performed confusion matrix analysis to summarize the agreement between the automated selection and the clinical decision. Finally, we evaluated the clinical and imaging outcomes of the patients in the four entries of the confusion matrix (true positive, true negative, false negative, and false positive). About 186 of 228 patients with acute stroke underwent thrombolytic treatment, with the remaining 42 receiving supportive treatment only. Selection based on radiographic criteria using COMBAT Stroke classified 142 patients as potential candidates for thrombolytic treatment and 86 for supportive treatment; 60% sensitivity and 29% specificity. The patients deemed eligible for thrombolytic treatment by COMBAT Stroke demonstrated significantly higher rates of compromised tissue salvage, less neurological deficit, and were more likely to experience thrombus dissolving and reestablishment of normal blood flow at 24 h follow-up compared to those who were treated without substantial PWI-DWI mismatch. These results provide evidence that COMBAT Stroke, in addition to clinical assessment, may offer an optimal framework for a fast, efficient, and standardized clinical support tool to select patients for thrombolysis in acute ischemic stroke. (Once again proving that tPA is truly a goldilocks question)

More at link.

The goldilocks dilemma in acute ischemic stroke

They miss the point that tPA is basically a failure since only the 'right candidates' benefit. Not until we publicly call it a failure will there be a concerted effort to find something better and maybe go down the route of stopping the neuronal cascade of death.
http://www.frontiersin.org/Journal/10.3389/fneur.2013.00164/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neurology-w46-2013
Aaron P. Tansy and David S. Liebeskind*

• Department of Neurology, UCLA Stroke Center, University of California, Los Angeles, CA, USA

Despite the advent of and exciting advances in novel endovascular therapies, t-PA remains the only proven treatment for acute ischemic stroke to date. Although a variety of reasons likely underlie why past trials of endovascular strategies have been unsuccessful, we address in this perspective piece one critical unknown for which a solution is undoubtedly necessary if future ones are to meet with success: determination and selection of patients that are “just right” for endovascular treatments, or the Goldilocks dilemma. Key clinical criteria highlighted in past trials may help provide a solution to this critical problem. However, for them to do so, we propose that they must be applied in service of a model that accounts for the nuanced, dynamic nature of acute ischemic stroke better than the prevailing “time is brain” model. We provide and examine three clinical cases to illustrate this proposal towards solving the Goldilocks dilemma and advancing treatment in acute ischemic stroke. Further, we address our field’s ongoing challenge and mission in the meantime to best care for the “not-so-right” patients, by far the majority of the affected stroke population.

The introduction of intravenous tissue plasminogen activator (t-PA) heralded a sea change in the management of acute ischemic stroke (AIS). For the first time ever, a medical therapy for acute stroke was proven effective in reducing long-term impairment (1). Since that landmark event nearly two decades ago, the AIS field has witnessed the exciting development of novel endovascular strategies and heightened hopes of potentially improving upon t-PA’s clinical efficacy (2–7). The Goldilocks dilemma, or finding the ideal patient who is “just right,” remains the most formidable challenge in establishing new therapies for AIS.

Unfortunately, as of yet, no endovascular method has demonstrated itself more clinically effective than t-PA either in head-to-head comparison or in combination with it (5–7). Why is this? This question is an undoubtedly challenging and complex one, but also an undoubtedly necessary one to answer. Indeed, continued progress in AIS treatment and any potential role that endovascular methods may play in it rests in the balance. We address the Goldilocks dilemma as a key unsolved piece of this larger problem that has already received a great deal of attention in the stroke community: identifying the ideal patients and enrolling them in clinical trials seeking to prove efficacy of endovascular treatments.

The recent disappointing outcomes in related trials are a reflection not necessarily of flawed endovascular therapies, but, rather, of flawed selection of candidates likely to benefit from them. We also propose that improvement of the theoretical framework of ischemic stroke on which the criteria for determination of “just right” trial-eligibility is based may allow future trials to finally achieve success. Finally, we emphasize that, although our Goldilocks search for the “just right” acute stroke patient is necessary for future improvement in care, we must not be distracted and neglect our primary mission to care for all stroke patients including those “not-so-right” – by far, the vast majority for whom we neurointensivists and neurohospitalists currently provide acute stroke care.

More at link.

Prospects of levetiracetam as a neuroprotective drug against status epilepticus, traumatic brain injury, and stroke

Get those clinical trials going.

Prospects of levetiracetam as a neuroprotective drug against status epilepticus, traumatic brain injury, and stroke

Ashok K. Shetty^1,2,3*

• ¹Institute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine at Scott & White, Temple, TX, USA
• ²Research Service, Olin E. Teague Veterans Affairs Medical Center, Central Texas Veterans Health Care System, Temple, TX, USA
• ³Department of Molecular and Cellular Medicine, Texas A&M Health Science Center College of Medicine, College Station, TX, USA

Levetiracetam (LEV) is an anti-epileptic drug commonly used for the treatment of partial onset and generalized seizures. In addition to its neuromodulatory and neuroinhibitory effects via its binding to the synaptic vesicle protein SV2A, multiple studies have suggested neuroprotective properties for LEV in both epileptic and non-epileptic conditions. The purpose of this review is to discuss the extent of LEV-mediated protection seen in different neurological conditions, the potential of LEV for easing epileptogenesis, and the possible mechanisms that underlie the protective properties of LEV. LEV has been found to be particularly beneficial for restraining seizures in animal models of spontaneous epilepsy, acute seizures, and status epilepticus (SE). However, its ability for easing epileptogenesis and cognitive dysfunction following SE remains controversial with some studies implying favorable outcomes and others reporting no beneficial effects. Efficacy of LEV as a neuroprotective drug against traumatic brain injury (TBI) has received much attention. While animal studies in TBI models have showed significant neuroprotection and improvements in motor and memory performance with LEV treatment, clinical studies suggest that LEV has similar efficacy as phenytoin in terms of its ability to prevent post-traumatic epilepsy. LEV treatment for TBI is also reported to have fewer adverse effects and monitoring considerations but electroencephalographic recordings suggest the presence of increased seizure tendency. Studies on stroke imply that LEV is a useful alternative to carbamazepine for preventing post-stroke seizures in terms of efficacy and safety. Thus, LEV treatment has promise for restraining SE-, TBI-, or stroke-induced chronic epilepsy. Nevertheless, additional studies are needed to ascertain the most apt dose, timing of intervention, and duration of treatment after the initial precipitating injury and the mechanisms underlying LEV-mediated beneficial effects.

Introduction

Levetiracetam [LEV; 2S-(oxo-1-pyrrolidinyl) butanamide] is an anti-epileptic drug (AED) often utilized for the treatment of partial onset and generalized seizures (1, 2). LEV has both anti-seizure and anti-epileptogenic properties. It has been also proposed that LEV is an attractive AED for managing post-traumatic seizures (PTSs) owing to its beneficial pharmacokinetic attributes, including excellent bioavailability, linear kinetics, minimal plasma protein binding, and rapid achievement of steady state concentrations (2–4). The underlying mechanisms by which LEV facilitates anti-epileptic and anti-epileptogenic effects are different from classic AEDs. Studies insinuate that LEV bestows its effects mainly through the inhibition of the synaptic vesicle protein 2A (1). Additional investigations have also revealed that LEV can inhibit HVA-Ca² channels (N-type), negate the inhibition of negative allosteric modulators such as zinc and β-carbolines of γ-aminobutyric acid (GABA)- and glycine-gated currents, and diminish the calcium release from intraneuronal stores (1, 5).

Moreover, a multitude of studies have proposed that LEV has considerable neuroprotective properties in both epileptic and non-epileptic disorders (2, 6–9). The capability of LEV to augment the manifestation of glial glutamate transporters EAAT1/GLAST and EAAT2/GLT-1 has been proposed as one of the foremost mechanisms through which LEV mediates its neuroprotective properties (2, 10). This hypothesis fits well with one of the conspicuous changes detected following most brain insults, which is increased concentration of glutamate in the extracellular areas causing enhanced activation of N-methyl-d-aspartate (NMDA) receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors on neurons and culminating in significant neurodegeneration (2, 11, 12). The efficacy of LEV as a neuroprotective compound has been examined in several brain injury and neurodegenerative disease prototypes. These include brain damage resulting from status epilepticus (SE) or acute seizures, spontaneous epilepsy, closed head trauma, subarachnoid hemorrhage (SAH), hypoxic-ischemia, and stroke. The goal of this review is to confer the extent of LEV-mediated neuroprotection observed in different brain injury models, the potential of LEV for easing epileptogenesis, and the possible mechanisms that underlie neuroprotective properties of LEV in different neurological conditions.

Much more at link.

How to inte­grate neuroplasticity-based inter­ven­tions with exist­ing stan­dards of care

Your doctor will have a real challenge with that because there are no standards of care for stroke recovery that anyone can point to.
http://www.slideshare.net/fullscreen/AlvaroF/integrate-neuroplasticity-basedinterventions/1

Sleep ADLs

While lying on my back I try to place my left arm fully extended on my left side. In order to get it there there has to be no sheets or blankets in the way. I have to do this at least 6 times a night because of the poor sleep I get. This means I've done it  6 x 365 x 7years = 15,330 repetitions. At that rate it will take another 449 years to get to 1 million reps. I guess I'll have to wake up a lot more often in the middle of the night in order to accomplish this before I die. This should be already established as some kind of protocol  in the stroke rehab database your stroke association has for all survivors to use.

Joint Commission names 1,099 hospitals top performers

This is totally worthless for stroke. You don't measure processes, you measure lower 30 day deaths and 100% recovery. God the stupidity burns.
http://www.cardiovascularbusiness.com/topics/practice-management/joint-commission-names-1099-hospitals-top-performers

Tungsten ‘could raise health risk’

I can't tell if this is worth worrying about or how to worry about it.
http://www.thisisguernsey.com/news/uk-news/2013/11/11/tungsten-could-raise-health-risk/

Snow - Yes

Its lightly snowing today. Maybe this winter will actually be a decent winter for stroke rehab. You need fairly deep snow so you have to post hole your steps requiring you to lift your foot high enough to clear the snow and stay balanced. Last year was pathetic, about 5 snowfalls of 4-5 inches each time, the snow would completely melt between each snowfall and the ground never froze. My trail clearing just needs two more limbs cut out. I hate daylight savings time, it doesn't allow me any walking time in daylight after work.

Bilingualism delays age at onset of dementia, independent of education and immigration status

So is your therapy protocol going to include language training to offset your  33% chance of developing Dementia/Alzheimers after a stroke.?  

http://www.ncbi.nlm.nih.gov/pubmed/24198291

Alladi S, Bak TH, Duggirala V, Surampudi B, Shailaja M, Shukla AK, Chaudhuri JR, Kaul S.

Source

From the Department of Neurology (S.A., M.S., A.K.S., S.K.), Nizam's Institute of Medical Sciences, Hyderabad, India; Department of Psychology (T.H.B.), Centre for Cognitive Aging and Cognitive Epidemiology and Centre for Clinical Brain Sciences, University of Edinburgh, UK; Department of Linguistics (V.D.), Osmania University, Hyderabad; Centre for Neural and Cognitive Sciences (B.S.), University of Hyderabad; and Department of Neurology (J.R.C.), Yashoda Hospitals, Hyderabad, India.

Abstract

OBJECTIVES:

The purpose of the study was to determine the association between bilingualism and age at onset of dementia and its subtypes, taking into account potential confounding factors.

METHODS:

Case records of 648 patients with dementia (391 of them bilingual) diagnosed in a specialist clinic were reviewed. The age at onset of first symptoms was compared between monolingual and bilingual groups. The influence of number of languages spoken, education, occupation, and other potentially interacting variables was examined.

RESULTS:

Overall, bilingual patients developed dementia 4.5 years later than the monolingual ones. A significant difference in age at onset was found across Alzheimer disease dementia as well as frontotemporal dementia and vascular dementia, and was also observed in illiterate patients. There was no additional benefit to speaking more than 2 languages. The bilingual effect on age at dementia onset was shown independently of other potential confounding factors such as education, sex, occupation, and urban vs rural dwelling of subjects.

CONCLUSIONS:

This is the largest study so far documenting a delayed onset of dementia in bilingual patients and the first one to show it separately in different dementia subtypes. It is the first study reporting a bilingual advantage in those who are illiterate, suggesting that education is not a sufficient explanation for the observed difference. The findings are interpreted in the context of the bilingual advantages in attention and executive functions.

The flexDrive: an ultra-light implant for optical control and highly parallel chronic recording of neuronal ensembles in freely moving mice

By following this to its logical conclusion we would be able to implant these into human subjects and listen in to the signals that neurons send to each other to enable neuroplasticity. With that knowledge we can make neuroplasticity repeatable and assured. And close to 100% recovery can be acheived. If you don't have big goals you will never get there. Or you can be like the pathetic stroke associations that just send out press releases and their board of directors that will not take a chance.  Bah humbug.
http://www.ncbi.nlm.nih.gov/pubmed/23717267

Voigts J, Siegle JH, Pritchett DL, Moore CI.

Source

Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology Cambridge, MA, USA ; Department of Neuroscience, Brown University Providence, RI, USA.

Abstract

Electrophysiological recordings from ensembles of neurons in behaving mice are a central tool in the study of neural circuits. Despite the widespread use of chronic electrophysiology, the precise positioning of recording electrodes required for high-quality recordings remains a challenge, especially in behaving mice. The complexity of available drive mechanisms, combined with restrictions on implant weight tolerated by mice, limits current methods to recordings from no more than 4-8 electrodes in a single target area. We developed a highly miniaturized yet simple drive design that can be used to independently position 16 electrodes with up to 64 channels in a package that weighs ~2 g. This advance over current designs is achieved by a novel spring-based drive mechanism that reduces implant weight and complexity. The device is easy to build and accommodates arbitrary spatial arrangements of electrodes. Multiple optical fibers can be integrated into the recording array and independently manipulated in depth. Thus, our novel design enables precise optogenetic control and highly parallel chronic recordings of identified single neurons throughout neural circuits in mice.

Images at link.

World-first therapy puts dad in touch again so he can cradle daughter - SENSE

The article talking about it here;
http://www.heraldsun.com.au/news/victoria/worldfirst-therapy-puts-dad-in-touch-again-so-he-can-cradle-daughter/story-fni0fit3-1226756537760
The actual research described here:
SENSe: Study of the Effectiveness of Neurorehabilitation on Sensation
This really seems no different than what Margaret Yekutiel wrote in the book, Sensory Re-Education of the Hand After Stroke in 2001.

Forum: Stroke victim senator is anti-ObamaCare: Why?

Good question, ask him directly. I would suggest instead of the national standards he is proposing he push a National Stroke Plan, similar to the National Alzheimers Plan. That way everything in stroke can be studied - prevention, diagnosis, hyperacute therapy, acute therapy, chronic therapy, cause of death, database of stroke, ambulance care.
http://www.pjstar.com/article/20131109/OPINION/131109329/10950/OPINION

From past experiences to future perspectives: some major points still open in adult neurogenesis

What is your doctor going to learn from this to create a stroke protocol to generate new neurons in your brain?
http://www.frontiersin.org/Journal/abstract/72191

Paolo Peretto^{1, 2*} and Luca Bonfanti^{1, 3*}

• ¹Neuroscience Institute Cavalieri Ottolenghi (NICO), University of Turin, Italy
• ² Dept. of Life Sciences and Systems Biology, Italy
• ³ Dept. of Veterinary Sciences, Italy

Two decades of investigation on adult neurogenesis yielded an utterly new vision of brain plasticity in mammals. Nevertheless, the ultimate goal of exploiting neurogenic processes for brain repair is still far from being achieved. Starting from this antinomy, the big question is: should be the research field of adult neurogenesis considered as a dead end in the perspective of brain repair, or, alternatively, do we need further efforts directed to better understand this biological process in order to solve the problem? Though neurobiologists do not share the same answer, it is evident that the huge knowledge gathered up to now in the field is not sufficient for granting translation of basic neurobiological research to reparative strategies. In this opinion article we suggest that failure in developing efficacious therapeutic approaches is linked to several unresolved issues in both domains of physiological and lesion-induced neurogenesis. We focus on the role of some aspects (e.g., stem/progenitor cell availability, regenerative capacity, glial cell activation, inflammatory reactions) which can determine the potential for neurogenic plasticity, yet depending on different variables which influence the tissue environment (ages, anatomical regions, homeostatic/pathologic states) and in turn depend on evolutionary constraints linked to the animal species. In our opinion, further investment/investigation directed at filling such existing gaps of knowledge in brain plasticity are needed before a new era for brain repair might be opened.

Neurovascular Mechanisms of Ischemia Tolerance Against Brain Injury

 More proof that preconditioning neuronal stressors help prevent ishemic injury. That brings up the interesting possibility that maybe TIAs should all have this preconditioning to reduce ischemic damage. Don't listen to me, no medical training.
http://link.springer.com/chapter/10.1007/978-1-4614-8690-9_10

• Kunjan R. Dave,
• John W. Thompson,
• Jake T. Neumann,
• Miguel A. Perez-Pinzon,
• Hung W. Lin

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Abstract

Traumatic brain injury (TBI) can result in secondary ischemia. This secondary ischemic insult is implicated in post-TBI pathophysiology. Pharmacological intervention to elevate cerebral blood flow can improve outcomes following TBI. The brain and other organ systems have an innate ability to induce protection against ischemic injury, limiting the severity of the ischemia-induced damage. This “self” protection can be initiated by exposing the brain to a stimulus before ischemia called “preconditioning,” such as exposure to a mild episode(s) of ischemia, hypoxia, anesthesia, or pharmacologically induced mild cell stressors. Current efforts to reduce ischemia-induced brain damage have been the focus in determining the mechanisms of preconditioning-induced ischemia tolerance as findings may help lower cerebral ischemia-induced brain damage in at-risk patients including TBI patients. Different preconditioning paradigms have been shown to lower TBI-induced damage. Although not all of the mechanisms of preconditioning are confirmed in models of TBI, basic mechanisms of preconditioning applies here as ischemia is a major part of TBI. Ischemic preconditioning, in part, confers protection by modulating regulators of cerebral blood flow, increase angiogenesis, and prevent cerebral ischemia-induced increase in blood–brain barrier permeability. This chapter highlights preconditioning-induced changes in components of the neurovascular system involved in ischemia tolerance. Understanding of these pathways may aid in the development of novel therapies to protect the brain from TBI-induced secondary ischemic insult.

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Within this Chapter

1. Introduction
2. Tolerance Against TBI
3. Basic Mechanisms of Ischemia Tolerance
4. Preconditioning and Cerebral Blood Flow
5. Regulators of Cerebral Blood Flow Following Preconditioning
6. Preconditioning and Angiogenesis
7. Ischemia Tolerance Following Controlled Restoration of CBF
8. Pre-/Postconditioning and the Blood–Brain Barrier
9. Summary
10. References
11. References

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Targeted drug delivery to the brain and brain tumors using focused ultrasound and microbubbles

The targeting piece sounds very important to position drugs in the right location whenever we do find out how to stop the neuronal cascade of death.
http://europepmc.org/abstract/MED/24181339
McDannold N

Radiology, Brigham and Women's Hospital, 75 Francis St., Boston, MAnjm@bwh.harvard.edu.

The Journal of the Acoustical Society of America [2013, 134(5):4089]

Type: Journal Article
DOI: 10.1121/1.4830934

Abstract

Highlight Terms Gene Ontology(1) Diseases(3) Species(1) Chemicals(2)

The physiology of the vasculature in the central nervous system (CNS), which includes the blood-brain barrier (BBB) and other factors, severely limits the delivery of most drugs to the brain and to brain tumors. Focused ultrasound (FUS), when combined with circulating microbubbles, is a noninvasive method to locally and transiently disrupt the BBB at discrete targets and enhance delivery across the "blood-tumor barrier." This talk aims to provide insight on the current status of this unique drug delivery technique, experience with it in preclinical models, and its potential for clinical translation. In particular, methods to monitor the procedure using acoustic receivers and the feasibility of controlling and predicting drug deposition will be reviewed. If this method, which offers a flexible means to target therapeutics to desired points or volumes in the brain, can be translated to the use in humans, it can enable the use of the whole arsenal of drugs in the CNS that are currently prevented by the BBB

Neurodegenerative disease: Neurodegeneration halted with oral therapy in mice

This sounds incredibly important especially with our 33% chance of getting dementia.
http://www.nature.com/nrneurol/journal/vaop/ncurrent/full/nrneurol.2013.226.html

Bryony Jones

Abstract

An oral therapy that targets the unfolded protein response (UPR) has been shown to prevent neurodegeneration in a mouse model of prion disease. The treatment abrogated the behavioural, clinical and pathological characteristics associated with accumulation of misfolded prion protein.

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Design and control of a 2 degree of freedom upper limb robotic rehabilitation device

Have your doctor see if this is better than the Saeboflex. It seems to include wrist movement also. Another great thesis.
http://iris.lib.neu.edu/cgi/viewcontent.cgi?article=1079&context=mech_eng_theses&sei-redir=1&referer=http%3A%2F%2Fscholar.google.com%2Fscholar_url%3Fhl%3Den%26q%3Dhttp%3A%2F%2Firis.lib.neu.edu%2Fcgi%2Fviewcontent.cgi%253Farticle%253D1079%2526context%253Dmech_eng_theses%26sa%3DX%26scisig%3DAAGBfm1RQ0ouYlphaM6wdOJoLQ0PS8lwGA%26oi%3Dscholaralrt#search=%22http%3A%2F%2Firis.lib.neu.edu%2Fcgi%2Fviewcontent.cgi%3Farticle%3D1079%26context%3Dmech_eng_theses%22

Abstract

Robotic neurorehabilitation is a rapidly growing field in both research and industry. Robotics offer the ability to create less labor-intensive rehabilitation for therapists, while providing an interactive experience for patients. Robotic therapy also provides the advantage of object data

collection for therapists to track patient progress; however, there is still both a clinical and market need for a low-cost, assistive hand rehabilitation

system. Therefore, the comprehensive design, control, and initial testing of an actuated, assistive 2 degree of freedom hand rehabilitation system

with a virtual environment is presented.

The 2 degree of freedom hand rehabilitation system, named the Navigator hand rehabilitation system, can provide assistive or resistive mode exercise for flexion and extension of the fingers, as well as pronation and supination of the wrist. The system incorporates a rack and pinion into a series elastic actuator to provide assistive exercise for flexion and extension of the fingers. A belt drive is used to provide actuation to pronation and

supination of the wrist.

 

The design, implementation of an impedance control system utilizing position and load feedback is also presented. Both automated control results and preliminary pilot data of resistive mode exercises are presented. A virtual environment to interact with the Navigator system was designed and implemented. The virtual environment incorporates both degrees of freedom, allowing the user to combine the motions and associate the movements with virtual tasks. The impedance controller and virtual environment interact via serial communication.

The Navigator device was designed to provide a low cost solution to providing assistive exercisein 2 DOF with an accompanying virtual environment for a home and clinical setting.

Retrograde BMP Signaling at the Synapse: A Permissive Signal for Synapse Maturation and Activity-Dependent Plasticity

For your doctor to decipher and create a stroke protocol. The bolded is very cool. 

Retrograde BMP Signaling at the Synapse: A Permissive Signal for Synapse Maturation and Activity-Dependent Plasticity

1. Brett Berke¹,
2. Jessica Wittnam¹,
3. Elizabeth McNeill²,
4. David L. Van Vactor², and
5. Haig Keshishian¹

Abstract

At the Drosophila neuromuscular junction (NMJ), the loss of retrograde, trans-synaptic BMP signaling causes motoneuron terminals to have fewer synaptic boutons, whereas increased neuronal activity results in a larger synapse with more boutons. Here, we show that an early and transient BMP signal is necessary and sufficient for NMJ growth as well as for activity-dependent synaptic plasticity. This early critical period was revealed by the temporally controlled suppression of Mad, the SMAD1 transcriptional regulator. Similar results were found by genetic rescue tests involving the BMP4/5/6 ligand Glass bottom boat (Gbb) in muscle, and alternatively the type II BMP receptor Wishful Thinking (Wit) in the motoneuron. These observations support a model where the muscle signals back to the innervating motoneuron's nucleus to activate presynaptic programs necessary for synaptic growth and activity-dependent plasticity. Molecular genetic gain- and loss-of-function studies show that genes involved in NMJ growth and plasticity, including the adenylyl cyclase Rutabaga, the Ig-CAM Fasciclin II, the transcription factor AP-1 (Fos/Jun), and the adhesion protein Neurexin, all depend critically on the canonical BMP pathway for their effects. By contrast, elevated expression of Lar, a receptor protein tyrosine phosphatase found to be necessary for activity-dependent plasticity, rescued the phenotypes associated with the loss of Mad signaling. We also find that synaptic structure and function develop using genetically separable, BMP-dependent mechanisms. Although synaptic growth depended on Lar and the early, transient BMP signal, the maturation of neurotransmitter release was independent of Lar and required later, ongoing BMP signaling.

Predictors of Gains During Inpatient Rehabilitation in Patients with Stroke � A Review

And if you idiots would think for just a little bit you would realize that stopping  the neuronal cascade of death resulting in less dead and damaged neurons would be the most helpful thing to do rather that figure out which ineffective stroke therapy is the worst.
http://www.dl.begellhouse.com/journals/757fcb0219d89390,forthcoming,8120.html

Enoch Chang
University of California, Irvine

Eric Chang
University of California, Irvine

Samantha Cragg
University of California, Irvine

Steven Cramer
University of California, Irvine

ABSTRACT

Stroke remains a major cause of disability. The cost of stroke rehabilitation is substantial. Understanding the factors that predict response to inpatient stroke rehabilitation may be useful, for example, to best individualize the content of therapy, or to maximize the efficiency with which resources are directed. This review reviewed the literature and found that numerous variables were associated with outcome after inpatient stroke rehabilitation. The strongest evidence exists for factors such as age, stroke subtype, nutritional status, psychosocial factors such as living with family prior to stroke or presence of a caregiver. Functional status on admission, urinary incontinence, post-stroke infection, and aphasia each can also impact prognosis. Strengths and weaknesses of cited studies are considered in an attempt to inform design of future studies examining the factors that predict response to inpatient rehabilitation after stroke.

Approaching a new stroke rehabilitation therapy with a SonicPainter

What does your doctor think of this idea?

Approaching a new stroke rehabilitation therapy with a SonicPainter

Daniel S. Scholz^1*, Liming Wu¹, Johann Schneider¹, Jens Rollnik² and Eckart Altenmüller¹

• ¹Institute of Music Physiology and Musicians' Medicine, Hanover University of Music, Drama and Media, Germany
• ² BDH Klinik Hessisch Oldendorf, Germany

Despite cerebral stroke being one of the main causes of acquired disability worldwide there is still no well-established and effective therapy to improve motor functions. Recently, attempts have been made to improve gross-motor rehabilitation after stroke by mapping patient movements to sound, which provides an additional sensory input supporting impaired proprioception, and which we refer to as sonification. However, to date there exists no established sonification-supported therapy.
In order to examine and validate how a movement-to-sound mapping in sonification could be most effective, we designed a two-dimensional paradigm called “SonicPainter”. Participants' computer mouse movements were sonified in real-time with a modified sine-tone. In randomized blocks, the sound's parameters pitch and brightness were either mapped onto the vertical and horizontal movement axes, respectively, or vice versa. Twenty-six elderly healthy participants were tested and showed an advantage in learning pitch as compared to brightness as a means to learn spatial locations of sound parameter combinations.
In a future clinical study, 3D music-supported movement-sonification will be used as a therapeutic training method to enhance stroke patients' arm movement rehabilitation through supported proprioception.

Upper Extremity Rehabilitation Equipment for Stroke Patients in Taiwan: Usage Problems and Improvement Needs

At least they are trying to figure out problems in rehab, compared to our pathetic stroke associations.
http://onlinelibrary.wiley.com/doi/10.1002/oti.1360/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false

1. Lan-Ling Huang¹,
2. Chang-Franw Lee²,
3. Ching-Lin Hsieh³,
4. Mei-Hsiang Chen^4,*

Article first published online: 5 NOV 2013

DOI: 10.1002/oti.1360

Abstract

The purpose of this study was to survey occupational therapists for the usage problems and for their improvement needs for upper extremity rehabilitation equipment (UERE). A questionnaire was given to experienced occupational therapists from 113 hospitals that provide occupational therapy services with three or more professional full-time therapists. A total of 48 hospitals sent back questionnaires, and 184 valid questionnaires were received. Most of the UERE had two major problems: The base of the equipment was unstable, and the equipment was uninteresting to use. The therapists reported that three major needs for design improvement in the UERE were adjustability of functions, exchangeability of components and recording of movement data. Some therapists had suggestions for designing new types of UERE, such as manual dexterity training equipment, activities of daily living oriented equipment, sensory re-education equipment, arm supination and pronation training equipment, and wrist extension training equipment. These findings reveal the genuine user needs of upper extremity devices and provide useful applications to the development and re-design of these devices. However, obtaining opinions primarily from experienced occupational therapists may pose a methodological limitation of this study. In future research, it is advised to include patients' opinions and also investigate whether a clinician's years of experience would affect his or her viewpoint of usage problems and improvement needs of the UERE

Neuroplasticity in the Intact Brain – Experience-dependent Learning and Neurobiological Substrates

A good discussion of what, when and how neuroplasticity occurs. Your doctor better know about this before you do.
http://www.rainbowrehab.com/neuroplasticity-intact-brain/