Stroke - Science topic
A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)
Questions related to Stroke
I was struggling with this situation. Common studies investigating the sEMG of post-stroke patients are focused on the muscles of the hand rather than the leg or the arm. Why?
I mean, I know that the hand muscles are more accessible, but how could we generalize that the processes happening in hand can be generalized to the rest of the body?
I, Darshan Prakashbhai Parmar, MPT student, from Government Physiotherapy College Jamnagar, am conducting a survey on 'EFFICACY OF PELVIC PNF TO IMPROVE TRUNK CONTROL, BALANCE AND GAIT PATTERN IN NEUROLOGICAL CONDITIONS' as a part of my Evidence Based Study(EBS) under the supervision of my Guide, Dr. Karishma Jagad (MPT-NEURO), Sr. Lecturer at Government Physiotherapy College Jamnagar.
We therefore request physiotherapists practicing in India to kindly fill this questionnaire, which will hardly take around 10-15 minutes. The link for the survey is provided below. The responses will be kept anonymous.
I further request you to forward the link to your friends or colleagues.
*(In case the link does not open, please copy and paste the link in your web browser or you can whatsapp me on +917984377793, I will share the form link there.)*
Thank you for your time and participation.
Take care and stay safe
I have a stainless steel 2 mm thick raw material. A 3 diameter hole is to be punched into it. My punch is made of ASP2023 or HSS material. It is giving a life of only 3000 - 4000 strokes before chipping off.
Which is the best coating to be used to increase the life of my punch. The target punch life that I need is 70000.
I am working on cortical stroke model. Prior to any experimentation, I need to group rats into right-handed and left-handed. I decided to apply the skilled reaching task (food reaching task) and I am following guidlines approved by previous published papers, yet I have not succeeded in training the rats and familiarization with the apparatus.
Has anyone worked with this test. Comments would be appreciated.
According to your clinical experience, which approach you prefer in clinic and do you think that it is better than other one approach? (For Stroke patients only)
A top-down approach such as using task-specific interventions.
A bottom-up approach, using weight bearing, PNF, and NDT techniques
We have one patient who presented pulmonary embolism and haemmorhagic stroke in same time.
So, anyone can help us for the management of anticoagulation ?
I would like to measure the TTC stained mouse/Rat stroke brain infarct in a square millimeter area using ImageJ.
Where can I download the datasets used by ISLES challenges regarding stroke Lesion segmentation? It has not been possible for me to get it from its website. Or any other public dataset about this subject.
I know that an infant's brain can repair itself when damaged but why doesn't the same happen in adults after stroke or brain injuries?
I search researcher that evaluate the physical activity with wearable tracker ( possibly armband of bodymedia) during the first year post stroke. I have 40 patients actually and I wanted to make comparison with different environnement
I am studying MSc Public health . Related to my academic work I have to conduct a research.
There are a large number of articles using EEG and fMRI to study the evaluation and prediction of upper limb function of subjects after stroke, and there is a lack of research on lower limb function. Is it because EEG and fMRI are not suitable for studying lower limb function or are there any technical difficulties?（For example, it may be difficult for EEG to collect signals from brain regions that are in charge of lower limb functions？）
I would like to carry out this research in Mulago hospital-Uganda, however, I have not been able to find a standardised tool.
My friend is looking for coauthors in Psychology & Cognitive Neuroscience field. Basically you will be responsible for paraphrazing, creating figures, and collecting references for a variety of publications. Please leave your email address if you are interested. 10 hours a week is required as there is a lot of projects to be done!
When I tried to run the ‘MR segment-normalize’ module of the Clinical Toolbox for SPM12, I got the following error:
12-May-2021 16:29:03 - Running ‘MR segment-normalize’
12-May-2021 16:29:03 - Failed ‘MR segment-normalize’
Undefined function ‘clinical_mrnormseg_job’ for input arguments of type ‘struct’.
In file “C:\Users\Neuroimager\Desktop\spm12\toolbox\Clinical-master\tbx_cfg_clinical.m” (???), function “clinical_local_mrnormseg” at line 319.
The following modules did not run: Failed: MR segment-normalize
For more details of the information entered:
I would appreciate it very much if anyone could help me on this issue.
Thanks so much,
I am planning to treat in vitro cultured glial cells with the stroked brain lysate. Do anyone has such experience of treating culture cells with fresh tissue lysates? If yes, could you please let me know the procedure.
Thanks in advance!
I am looking at sex differences in acute stroke symptoms through meta analysis.
One of the symptoms I am looking at is "vision symptoms" but some studies report multiple vision symptoms in their population.
One study has reported that 28/268 women experienced vision loss, and 5/268 women experienced hemianopia. There is no way to know whether any of these women experienced both vision loss AND hemianopia.
Is there a way I can combine these two symptoms into one value to represent "vision symptoms" in this study to include in my meta analysis? Or will I need to meta-analyse each sub-symptom on their own, so a separate analysis for "vision loss" and "hemianopia"?
Patient with neurological problems have different problems. This will impaired their physical, cognitive and even social interaction and so forth.
So, which approach and why that approach is used?
Look into more discussion and information.
A large majority of intracerebral hemorrhages, especially in younger patients, are due to hypertensive emergency. Often, these patients will get started on a titratable continuous IV drip medication like Nicardipine in the emergency room. However, there was a recent paper in Neurocritical Care journal that suggests that starting oral antihypertensives in conjunction during this very acute stage can lower morbidity, costs, and hospital/ICU stays. The rebuttal is of course that blood pressures on oral antihypertensives are subject to peaks and troughs with medication administration until steady state is reached. During this time, overshooting the target and causing hypotension can cause significant ischemia to surrounding cellular tissue that may be amenable to rehab, and hence worsening long-term outcomes [though this has not yet been systematically analyzed]. What is your opinion on this?
I have some brain slides that I CV stained, and I need to learn how to assess infarct volume and quantify it comparing it to the other hemisphere or my controls. I looked online for a protocol or a description of the steps but couldn't find any.
I have both ImageJ and Sigma Scan Pro software, I still can't use them both well so I can learn on either of them.
I need to produce data similar to this:
If we have a biochemical parameter we wish to compare between ischemic vs haemorrhagic stroke, (idea being this parameter is responsible for ischemic stroke), what is the adequate number we should study?
with the same background, is it necessary that we compare this with healthy individuals?
I am having some difficulties trying to discern whether the following studies are cross-sectional or cohort (they do not state in their methodology)
I believe they might be cross-sectional, with the last one perhaps being cross-sectional cohort, but if anyone could help I would greatly appreciate it!
Physical fitness is essential to allow people to carry out everyday activities. It is often particularly low in stroke survivors. It may limit their ability to perform everyday activities and also worsen any stroke-related disability. So, it is recommended that seniors do exercises in order to improve cognitive function, quality of life, and the ability to maintain physical activity. On the other hand, other researchers say that training programs increase the risk of having another stroke.
A lot of variations in spatiotemporal parameters during gait performance among stroke survivors have been recorded. Studies have slso shown that such variations in gait paramets during gait performance have strong (confounding) influence on the outcome/results of gait analysis conducted among these individuals. A number of factors have been pointed out as contributing factors to the observed variations in gait performance. Such include fear of falling, fatigability/post stroke fatigue and environmental factors. It is therefore of serious concern to me to find out how these variables could be assessed objectively as this would help me immensely in my current study.
I am planing an experiment to figure out the effect of an compound for recovery after stroke.
I am wondering whether sham mice group is necessary for this study.
Some reference didn't use sham or others did it.
In my opinion, only two groups (compound-treated mice and compound-non treated mice after stroke) are enough to demonstrate the effect of the compound.
Will reviewer ask the sham result during paper submission process?
I am looking for actuators with an area of 1x1 mm² or smaller. The actuators should have a stroke of 0.5 mm or similar/bigger. The actuators have to be capable of being mounted as an array.
Thank you for your input.
I've been writing review articles on the following topics:
1. Stroke and MMP-9 research
2. CRISPER cas-9 and MMP-9
3. Heterogeneity of Monocytes among stroke patient
3. COVID-19 Pathophysiology
4. Brain on a chip
Is anyone interested in collaborative writing and publication? Please let me know. We can share our ideas on extending the content of the paper and get it published mutually.
Professionals with an interest in stroke and neurology research are most welcome.
I am working on school reform. The work is not having the full desired effect. I am trying to do my analysis of this subject under the concept of “organizational stroke.”
In your opinion, why we have not obtained the results we want, in the general and specific terms of reform and studies for the school. ?
My question is about a study with tennis players. I have two categorical independent variables: skill level (3 levels) and type of stroke (three different strokes). I have one continuous dependent variable (ball speed). I want to compare if there exist differences between strokes and between levels in this variable (ball speed). I have think about Two-Way Mixed ANOVA or simply perform two One-Way's ANOVA, one including the skill level as the independent variable and another including the type of stroke... You think in this case it is interesting studying the interaction between level and type of stroke. I think so but I would like to listen the opinion of an expert... Two-Way Mixed ANOVA is adequate? I have forgotten to say that each player has performed the three different type of strokes.
Thanks very much,
I'm doing a retrospective case-control study on the outcome of stroke patients were either A) Community Onset or B) In-hospital onset
We have an n of ~1400 patients over several years. We wanted to do a multivariate analysis comparing patient outcome of whether their outcome by discharge from hospital was either A) Functionally Independent or B)Death/Dependency (no longer able to care for themselves)
We wanted to look a the following variables which we've tracked to see if there is a difference between community and hospital-onset stroke
1) Pre-hospital independence (YES/NO) *Defined as an OHS of <3
2) Patient Age
3) If they had atrial fibrillation (YES/NO)
4) If they received Thrombolytic Therapy (YES/NO)
5) If they received endovascular thrombectomy (YES/NO)
6) Sex (MALE/FEMALE)
For the inpatients, we're curious to know if there is a difference between those who had a procedure and those who did not but I think that has to go in a within-group analysis later on.
Most of my stats background comes from behavioural sciences where I worked with continuous data, not discrete data. I don't know/think a multiple-ANOVA would be the right approach here.
I thought about doing a Logistic-regression or a binomial - regression but I'm not if that fits especially with the patient age being a factor.
I thought of taking OUT patient age and doing a 2x7 Chi-square but then the sample size may contribute to a type 1 error.
Could anyone offer advice on the best to analyse this data or is the question setup flawed?
- With an improvised document, a plagiarism issue was reversely raised. And several plagiarism issues were raised intentionally afterward.
- Slander with ungrounded information has been made to you in front of people despite your commitment to the lab’s work and projects even though they were out of your task and interest for more than 2 years.
- Incorrect information has been continuously produced to avoid academic discussion, concealing the fact. Even last week, wrong information was given out to people again.
Are you willing to publicize this matter, although the advisor is being investigated by school?
Memory is an exciting and still mysterious function, and if we can easily find places of memory, do we know where in the brain our memory is stored?
We have seen it, it is plural. We cannot therefore associate it with a single place. There is, however, a place of "passage": the seahorse, involved through the circuit known as Papez. And cerebral imaging techniques make it possible to identify some structures particularly involved in memory processes, including the hippocampus, but also the amygdala and the prefrontal cortex. They operate in systems that are constantly interacting, and are linked to our emotions: there is no memory that is not linked to the emotional context in which it was recorded.
The fleeting memory of the sensory organs:
Our brain is the strategic center of memory circuits. Our five senses are constantly called upon to send their information to the hippocampus. These pass through the filter of the emotional brain, or limbic system, to be projected to the areas of the cerebral cortex that are dedicated to them. However, in the very short term, various sensory memories (visual, olfactory, tactile, taste, auditory) are managed by the sensory organs.
Thus, the back of the retina is involved in the phenomenon of retinal persistence, retaining information for a few hundred milliseconds, when the auditory nerve and the cells at the back of the ear retain over this same period of time the memory of a sound. . The same goes for the other three senses, always with this principle: withhold information for the time necessary to select the important elements. Knowing that this filtering takes place upstream of the short-term memory, to capture and encode a “good” message, it is therefore important to correct any sensory deficit. As for short and long term memories, they are fully taken care of by the brain.
There are several arguments in favor of an important role of a region located at the front of the brain - the prefrontal cortex - in short-term memory. In particular, when it comes to keeping the data necessary for reasoning available. As for the encoding of information in long-term memory, it involves the hippocampus, the temporal lobes and the structures of the limbic system which are connected to them.
The seahorse: an obligatory crossroads:
Made up of different structures buried deep in the center of the brain, the limbic system plays an important role in fear, pleasure, pain, aggression, and other emotional behaviors. But several of its components also participate in the memorization of certain memories. This is particularly the case with two structures: the hippocampus, and the amygdala.
The hippocampus is made up of several layers of neurons. It is greatly involved in the consolidation of long-term memory, in particular in a type of memory that can be brought out through language (it is said to be declarative), and more precisely that of facts and places (called episodic, because keeping traces of episodes of life). Its role is such that it is carefully examined on MRI scans in Alzheimer's disease. Because a radiological sign of atrophy of the hippocampi, linked to Alzheimer's disease, is visible on MRI and thus allows us to grade the course of the disease.
Memories of various and varied events are however not stored in the hippocampus: the information only passes through this structure, as in a crossroads where they are associated before reaching other areas of the cerebral cortex (occipital region for visual memories, temporal for auditory memories, etc.) where they will be kept. Conversely, our spatial memory is partly archived in the hippocampus.
At the heart of the emotional brain:
Another structure of the limbic system involved in memorization, the amygdala is shaped like a blackberry and is located in front of the hippocampus. Neuroimaging studies have shown that its activity increases when the individual visualizes an emotionally charged scene, and even more so in cases of post-traumatic stress, or fears. But like the hippocampus, it is not affected by any other type of long-term memory, called implicit or procedural.
Unconscious, that is to say automatic, this emotional memory is mobilized the longest. Moreover, this implicit memory is that of know-how - tying a shoe, tying a tie, driving a car, etc. And it is rather associated with changes in the cerebellum (cerebral structure closely related to motor control) or in the basal ganglia (also called basal ganglia) and the motor cortex.
The two hemispheres of the brain:
The cortex, also known as gray matter, is the outermost layer of the brain and includes all other structures. It is made up of two cerebral hemispheres. Separated by a groove, however, they are not isolated and communicate with each other through nerve fibers called the corpus callosum. We know that they are always helping each other and exchanging information. But since the work of the American Roger Sperry (Nobel Prize for physiology or medicine in 1981), it is classic to consider that they each have their specialties - each hemisphere also receives sensory information and controls the motor responses of half opposite of the body.
So when there is a stroke of the left hemisphere, the right side of the body is paralyzed (hemiplegia) and there may be aphasia, which is difficulty speaking or understanding language. The left hemisphere would in fact mainly take care of what is analytical: numbers, calculations and all the processes related to numbering. But he would also be responsible for most of the language processing, both oral and written. Knowledge allows us to stimulate and re-educate speech and memory through speech therapy, for example when a patient suffers from particular forms of Alzheimer's, or when he presents vascular signs in addition to neurodegeneration.
The right hemisphere, on the other hand, would be more involved in the management of novelty, learning, visuospatial skills, the perception of faces or the understanding of common expressions, metaphors or innuendo. This can make it difficult to organize your bedroom, write essays or analyze an abstract art painting in the event of an injury in the right hemisphere. Ultimately, if locating memory remains a matter of research, knowing the circuits involved helps us better understand and deal with its failures.
I've heard garlic and high nitrate foods like arugula or beets typically occupy high ranking here. What others do you know of or recommend? What's your top 10 list, based on what research? Thanks.
I am doing a systematic review looking at factors that could predict the level of burden in stroke carers. I have narrowed down to the final studies I want to use and I have their data. Unfortunatley the only data I have are the Means and SDs of the factors and burden levels. I am trying to work out how I can look at if there is a correlation or not, but I can't work out how to do it. Everything I try (except for SPSS summary independent samples t-test) doesn't seem to work, I think because it takes each result from a study as one participant and I cant find anyway of me saying for this study there were x participants and this as the mean result. Can anyone help?
Dear Clinical Rehabilitation colleagues, I have just finished Malcolm Gladwell's excellent book 'Outliers' (2011) for probably the 4th time and would like to recommend such a tremendous and inspiring book to any clinical therapist or anyone working in the neuroplasticity field. I have read all Malcolm's books and in fact his most recent'Talking To Strangers' was also excellent because of the important issues it raises (I can assure everyone I am not related to Malcolm or have no vested interest in promoting his work but it introduces some really interesting psychological concepts, although as far as I'm aware Malcolm never mentions how these could possibly be applied in the clinical setting). I am interesting in getting a discussion started because I believe that there needs to be a fundamental shift in our approach to rehabilitating patients (especially neurology) towards achieving greater successful outcomes. I believe that the same psychological principles mentioned in outliers can apply to clinical rehabilitation and I would be very interested to develop this over the coming years. I have already started writing focus and editorials for journals based on his work.
As a Physical Therapist (Physiotherapist in Ireland) and now researcher who is very interested in developing and improving clinical rehabilitation post stroke etc, I would like to consider outliers in this context and would be interested if you agree. I firmly believe that a new approach to rehabilitation is required and the current 'passiveness' that takes place needs to be replaced with 'psychological education' to equip patients with the confidence for success. For me all physiotherapy is 70% psychology (partly placebo effect) and 30% physical interventions.
I believe that a lot of the psychological approaches mentioned in Malcolm's book could be applied to clinical rehabilitation and would indeed improve current outcomes. Regarding 'Outliers' can I make some observations please;
Introduction: I believe that patients rehabilitating from home rather than in a rehabilitation setting can benefit from a similar 'Rosetto Effect'.
Chapter 1 & 2: We can apply the principle of the 10,000 hour rule to rehabilitation. Success in rehabilitation is also the result of 'Cumulative Advantage' (availability of home-based rehab equipment, access to professional supervision, means of receiving real-time feedback) but in order to achieve this we need to find a way to motivate patients to do the '10,000 hours of meaningful rehabilitation'. After 30 years of experience I truly believe that almost all patients can get a successful recovery if they are willing to work really really really hard.
Chapters 3 & 4: In a similar fashion to practical intelligence that is gained from rich parents, stroke patients need to take control of their therapy and if they start to steer their therapy then they will create a neuroplasticity in their brains that will result in improved success. I believe there is an element of stereotyping that exists in elderly patients who accept 'their lot' and don't have the confidence to fight hard enough to make a full recovery.
Chapters 5 & 6: Again, emphasises the concept that hard work or 'grit' will make us successful. Same principle can be applied to rehabilitation. The ability of a patient to question their therapist/consultant and to guide treatment is probably a result of their cultural background and again this type of disadvantage can lead to poor results.
Chapters 7 & 8: The concept of Power Distance Index again fits with patient potential in rehabilitation. Medicine is general is a passive process, where the patient waits to be told what to take/do. I believe that patients need to be educated to improve confidence and realise that rehab techniques will be more successful if initiated by the patient themselves. Lets give them a menu of therapies and let the patient decide which is best suited to them. We need more of a personal approach. Again, hard work and effort important for good results.
Chapters 9 & 10: Could a new form of KIPP School be created for rehabilitation excellence where the emphasis is 70% education/psychological approach and 30% physical interventions. I believe the reverse is happening unsuccessfully at present.
Its recommended to stand on the shoulders of giants and none are greater than Malcolm Gladwells. I would be very interested in your opinion to these comments (whether you agree or disagree) and this book has inspired me so much, brought great enjoyment to my life and has been inspirational to hundreds of people like me. I think a change is needed!!
I was wondering if there was an optimal time for performing the follow up assessment when evaluating the long term effect of a rehabilitation technology (such as VR, robot assisted therapy,...) in a stroke population. Especially for upper limb function, activity and participation. Is there any paper supporting the fact that stroke patients’ long term retention should be assessed a certain time after the intervention ?
If i intend to carry out a cross sectional comparative study (analytical study design) to assess the association of cardiac diseases among young stroke patients, where do I begin? Do I enroll stroke patients in a medical ward and then select old and younger stroke patients based on an age demarcation and then proceed with the analysis? In that case, how do I calculate my sample size? Do I use the formula:
n = P(1-P)Z2/(error)2 for descriptive, hospital-based cross-sectional study or,
do i need two proportions for two different groups (P1, P2) and use this one instead:
n=(Z1-a+Z1-b)2 (P1Q1+P2Q2)/ (P1-P2)2
[a=alpha=probability for type I error, b=beta=probability for type II error]
If the latter equation is to be used, then how do I find out P1 and P2 from previous studies to construct a sample for this study? What would P1 and P2 stand for this study? P1=young stroke patients? P2=old stroke patients??
hi, if we are doing a single centered study, can we estimate/calculate sample size based on patients in that hospital?
e.g i want to conduct a research on stroke patients. so my population will be stroke patients in the country or stroke patients in that hospital ?
offcourse if we want to generalize the results, we take whole countrys stroke patients available in literature.
but lets suppose due to lack of time, or economic factors, we want to do single centered study where stroke patients may not be that high ? then how to justify sample size ?
i have seen many papers where sample size in hospitals was 100, 150, 90 etc. but they never mention how did they calculate this. can anyone share some evidence based answer ?
Farm level implementable other than chemical control, trenches formation, fire strokes usage and making sounds.
Hi everyone. How to calculate the AP, AP per 100,000 population and Attributable Cases, for Health Endpoint e.g. Mortality due to IHD in Adults by using Impact Evaluation function in AirQ+ 2.0 software for the whole population (for ages 25+/30+) where the PM2.5 level is below 40ug/m3? The current AirQ+ 2.0 interface already divided the calculation to different age groups. No calculation interface available for the whole population. Thank you - Iqbal
I would like to conduct the systematic review of stroke studies. I found that the GRADE-CERQual tool is useful to evaluate the strength of qualitative evidence. It is possible if I use this approach for my review?
Thanks for your help
I am running in vitro experiments using 'healthy donor blood'. It appears that clots formed from some samples do not respond to treatment with Alteplase. Any ideas, please, friends and colleagues?
Thanks in advance :)
Excitation: 5.3V rms, 2000 hz
Bobbin: SS tube, 3.5 mm ID, 4.65 mm OD
Primary coil is wound over the entire length of bobbin
Two secondary coils are wound over primary -- one in each half section.
Sum of two secondary outputs: 3.72 V rms
Length of bobbin, number of turns of primary and secondary coils
I am doing some experiments regarding stem cell transplantation in an animal stroke model. Now I need to quantify phagocytic microglia in the brain after stroke. I want to quantify them by immunostaining-based method, not by flow cytometry. It will be very helpful if someone suggest me what will be the suitable marker for phagocytic microglia in stroke condition. Thank you in advance.
The association of free radicals in the pathophysiology of chronic diseases like degenerative brain disorders (AD, PD, HD, Stroke) has been evident by a substantial research.
I'm wondering if there is any literature on prognostic pessimism (PP) within areas of aphasia, speech disorders, stroke treatment, or any other similar area. I've found literature on PP and psychological disorders and some physical diseases (COPD / asthma) but looking for presence of PP in speech disorders.
There are relatively many and growing efforts to find pharmacological alternatives to neurodegenerative and mental disorders, in this effort, successful trials have been carried out with the application of erythropoietin (EPO) 1-3 and similar molecules that do not induce erythropoiesis such as NeuroEPO, in which we have been working for several decades 4-7.
Unlike the EPO produced in the kidneys, the one produced by the mammalian brain does not appear in the databases of its sequencing nor does it have results of its molecular characteristics.
If we consider our brain the target of many mental disorders, it seems logical to think that we should know more about the molecular characteristics of its main components such as cerebral erythropoietin.
1. Sosa Testé I, J.C García Rodríguez, García JD. New goal in ischemia stroke therapy:rHu-EPO nasal application. (2006) Rev. Acta Pharmacol. Sin,2 006; 27 (Suppl 1): 97.
2. J. C. García Rodríguez and Iliana Sosa Testé. The nasal Route as a Potential Pathway for Delivery of Erythropoietin in the treatment of Acute Ischemic Stroke in Humans. (2009) TheScientificWorldJOUNAL 9,970-981. Review.
3. Yamila Rodríguez Cruz, Yuneidys Mengana Támos, Adriana Muñoz Cernuda, Nelvis Subirós Martines, Alina González-Quevedo4, Iliana Sosa Testé, and Julio César García Rodríguez. Treatment with Nasal Neuro-EPO Improves the Neurological, Cognitive, and Histological State in a Gerbil Model of Focal Ischemia. (2010) TheScientificWorldJOURNAL 10, 2288–2300.
4. Julio César García-Rodríguez and Yamila Rodríguez-Cruz The Therapeutic Potential of Neuro-EPO Administered Nasally on Acute Cerebrovascular Disease. Current Psychopharmacology, 2012, 1, 3; 228-232. PubMed FI:2.5
5. Yamila Rodríguez Cruz, Manon Strehaiano, Teresita Rodríguez Obaya Julio César García Rodríguez and Tangui Maurice. An Intranasal Formulation of Erythropoietin (Neuro-EPO) Prevents Memory Deficits and Amyloid Toxicity in the APPSwe Transgenic Mouse Model of Alzheimer’s Disease. Journal of Alzheimer’s Disease 55(2017) 231–248 DOI 10.3233/JAD-160500 IOS
6. Garzón Fernando, Rodríguez Yamila, García Julio Cesar and Rama Ramón. Neuroprotective Effects of neuro-EPO Using an In Vitro Model of Stroke. Behav. Sci. 2018, 8, 26; doi:10.3390/bs8020026.
7. Ramón Rama, Fernando Garzón, Yamila Rodríguez, Tanguí Maurice, Julio César García Rodríguez. Neuroprotective effect of Neuro-erythropoietin in neurodegenerative diseases: “Alea jacta est”. Neural Regen Res (2019) 14(9):1519-1521 Doi:10.4103/1673-5374.255968.
I intend to measure a muscle function on stroke patients and I read but with no supportive evidence that patients should stop having paracetamol or antibiotics month before the test because it may affect the outcome results.
Anybody has any idea or suggest evidence to support this notion
I have a question and hope that you will share with me your experience in this field.
We have conducted a study (review of patients medical records) to assess if abnormal hemoglobin (Hb) levels are associated with stroke severity in our settings. We are interested in both; high and low Hb levels. As for me, I though the right thing is to dichotomize Hb levels into normal and abnormal status in the Regression Analysis. Upon submitting the work to a journal, the reviewers mentioned that Hb levels should have been continuous variable. As both extreme can be a determinant of stroke severity, how the results would be interpreted in this way!
Thank you for your time, Majeda
Defects in the brain tissue of a rat model I am working with look like small ischemic (not hemorrhagic) strokes when I do H&E stains. I would like to confirm this suspicion by staining the (paraffin-embedded) tissue with some markers. So far I am thinking of a panel using the following: fibrinogen, fibronectin, GFAP for astrocytes. As I'm not familiar with stroke research I'm not sure if there's any common ones I've missed! I would be grateful for any advice.
i am a graduate student, i want to do a research about slow stroke back massage. I want to know is there any right order of the massage movement (as it is in original) because most of the research that I found used modification of SSBM, and i wonder how much pressure should I apply while doing the massage. I find it difficult to find book about it too... If you have an info about this please share, thank you.
I am doing reserch that prospectively follow pt with atrial fibrillation on warfarin for incidence of stroke hemorrhagic due to SIde effect of warfarin or ischemic due to cardioembolism I WONDER if NONcontrast CT beside history and exam and coagulation profile is sufficient to diffrentiate ischemic from hemorrhagic
The FRAX® tool has been developed to evaluate fracture risk of patients. But it does not include falls which are a well established clinical risk factor for fracture. Also, previous studies have suggested an up to 4-fold increase in the risk of fractures in those with stroke compared to healthy controls.
So, is FRAX tool really useful & necessary for "Stroke survivors" to computes the 10-year probability of fractures ?
Post Tpa for stroke- how soon after the administration of tpa -can the patient get out of bed and resume activity with assistance ?
It seems that we're heading industrial revolution 4.0, what are other steps that we can invent, create and execute?
Stroke or Brain attack is the 2nd killer of human around the world according to WHO.
Any brilliant idea or solution?
I have stress-stroke profile of a deformed rebar from the company. Moreover, the gauge length of the test specimen is known (G.L. = 100 mm). The estimated strain using equation (i.e., strain = stroke/gauge length) seems wrong. I am seeking some useful suggestion. Thanks in advance.
Other than differences caused by stroke, would cognitive function (and other symptoms) differ in a group that includes all types of VCI compared to those that have a very specific type subcortical ischaemic vascular cognitive impairment
Looking for a free self-report or proxy-report assessment to administer to patients with brain injury with good psycometric properties. I am an oppucational therapist, so I need it to capture a person's ability to reintegrate back into their daily life (activities of daily living, work, community reintegration, etc). Something similar to the Stroke Impact Scale, but for brain injury, would be great! Any suggestions or links would be great! Currently digging around through the NeuroPT EDGE documents for inspiration
Once their medical issues have stabilised, physiotherapy, speech and language therapy and occupational therapy are the three main types of rehabilitation sought by stroke victims. Given the scope of the project, it would seem an omission to not consider speech and language therapy.