Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Saturday, April 30, 2011

Stroke rehabilitation conducted by PNF method

PNF - (Proprioceptive Neuromuscular Facilitation) I did not have this but this article explains a lot.
http://www.rehmed.pl/images/upload/pdf_en/2005/1_2005/Pasiut.pdf

short excerpt here:
The PNF (Proprioceptive Neuromuscular
Facilitation) is a method
used in post-stroke treatment, where
the functional therapy is a process of
gradual restitution of patient’s motor
abilities5,6,7. It is a method of neuromuscular
dysfunction treatment,
primarily by means of facilitating the
flow of information, mainly by the
stimulation of proprioceptors8. Restoration
of normal movement based on
movement patterns, basic principles
and techniques is directed towards
normalisation of muscle tone.

Possible exercises here: most of these require a second person,
http://www.rehmed.pl/images/upload/pdf_en/2005/1_2005/Pasiut.pdf
http://www.exrx.net/ExInfo/Stretching.html

http://www.thestretchinghandbook.com/archives/pnf-stretching.php

http://www.bodytrainer.tv/page/1/19-28-PNF+Stretching+%7C+Guideline

http://www.youtube.com/watch?v=4GWlJMSAlu4

Adult human neurogenesis

I am hoping that this takes over from neuroplasticity as the future of stroke rehab.
This is pretty heavy reading but you should at least know enough about it to ask your medical staff.
https://admin.frontiersin.org/neurogenesis/10.3389/fnins.2011.00047/full
Quite a ways down the most interesting line in here is bolded red
Only a few paragraphs are selected here so go to the complete article at the URL.
Neural stem cells reside in well-defined areas of the adult human brain and are capable of generating new neurons throughout the life span. In rodents, it is well established that the new born neurons are involved in olfaction as well as in certain forms of memory and learning. In humans, the functional relevance of adult human neurogenesis is being investigated, in particular its implication in the etiopathology of a variety of brain disorders. Adult neurogenesis in the human brain was discovered by utilizing methodologies directly imported from the rodent research, such as immunohistological detection of proliferation and cell-type specific biomarkers in postmortem or biopsy tissue. However, in the vast majority of cases, these methods do not support longitudinal studies; thus, the capacity of the putative stem cells to form new neurons under different disease conditions cannot be tested. More recently, new technologies have been specifically developed for the detection and quantification of neural stem cells in the living human brain. These technologies rely on the use of magnetic resonance imaging, available in hospitals worldwide. Although they require further validation in rodents and primates, these new methods hold the potential to test the contribution of adult human neurogenesis to brain function in both health and disease. This review reports on the current knowledge on adult human neurogenesis. We first review the different methods available to assess human neurogenesis, both ex vivo and in vivo and then appraise the changes of adult neurogenesis in human diseases.
Introduction: A Brief History of the Adult Mammalian Neurogenesis Discovery
The discovery of adult neurogenesis crushed the century-old dogma that no new neurons are formed in the mammalian brain after birth. However, this finding and its acceptance by the scientific community did not happen without hurdles. At the beginning of the last century, based on detailed observations of the brain anatomy reported by Santiago Ramon y Cajal and others, it was established that the human nervous system develops in utero (Colucci-D’Amato et al., 2006). In adult brains, it was thought, no more neurons could be generated, as the brain is grossly incapable of regenerating after damage (for a more detailed historical report see Watts et al., 2005; Whitman and Greer, 2009). This dogma was deeply entrenched in the Neuroscience community, and Altman’s (1962) discovery of newborn cells in well-defined areas of the adult rodent brain was largely ignored. The phenomenon was reexamined in the 1970–1980s, when Michael Kaplan (Kaplan and Hinds, 1977) and Fernando Nottebohm (Goldman and Nottebohm, 1983) demonstrated the presence of newborn cells in the adult brain of mice and canaries, respectively, and showed that these cells had ultrastructural characteristics of neurons. However, such findings could not be repeated in adult rhesus monkeys, where proliferating cells appeared to be glial and endothelial cells and not neurons (Rakic, 1985; Eckenhoff and Rakic, 1988). Thus, neurogenesis seemed to be absent in adult primates (Eckenhoff and Rakic, 1988).

The field of adult neurogenesis finally took off in the 1990s with the development of new technologies. First, the use of 3H-thymidine, a radioactive nucleotide used to study proliferation when incorporated into the cells during the S phase of the cell cycle, was replaced by its analog, bromodeoxyuridine (BrdU), which could be detected by a specific antibody. Utilization of the BrdU for labeling of newborn cells via immunohistochemistry allowed their further studies by co-labeling with specific neuronal markers (Miller and Nowakowski, 1988). Further, it was shown that neuroprogenitor cells (NPCs), isolated from adult mouse brains, proliferated and differentiated into neurons and astrocytes in vitro (Reynolds and Weiss, 1992). In addition, NPCs labeled with viral vectors were able to migrate and differentiate into neurons in the adult mouse brain (Lois and Alvarez-Buylla, 1993), demonstrating that the adult neurogenesis was functional in rodents. Finally, the existence of adult neurogenesis in humans was firmly established when, in 1998, Gage and colleagues demonstrated for the first time that new neurons were produced in the adult hippocampus (Eriksson et al., 1998).

Currently, adult neurogenesis is one of the hot topics in Neuroscience especially because of the new opportunities it may bring for treatments of neurodegenerative diseases, either by harnessing resident progenitors to regenerate the lost tissue (Sohur et al., 2006) or by cell transplantation therapies (Goldman and Windrem, 2006). The field is currently on the rise, as shown by the exponential growth of publications with the key words “adult” AND “neurogenesis OR neural stem cells” (PubMed search up to December 31, 2010): a total of 6,437 papers have been published, of which 57% (3,695 papers) was published in the last 5 years (Figure 1). However, only 8% of published papers (530 papers) deal with human data (search including the term “human” in the title), suggesting that the research on adult neurogenesis in humans is still in its infancy. Thus, the actual knowledge on adult human neurogenesis is limited and in many cases, data is directly extrapolated from the rodent literature. Herein, we review the methodologies used to assess adult human neurogenesis and its status in several neuropsychiatric disorders.


Methods to Assess Neurogenesis in vivo
More recently, methods have been specifically designed to detect neurogenesis in live human brain by means of magnetic resonance imaging (MRI; Figure 3). In the MRI scanner, the subjects are exposed to a harmless magnetic field that aligns the magnetic spin of all the protons in the tissue in a low energy configuration; next, the subjects receive radiofrequency electrical stimulation, which excites the spins out of equilibrium. The spins then naturally relax back to their original conformation with time constants T1 (spin–lattice relaxation time, for longitudinal magnetization) and T2 (spin–spin relaxation time, for transversal magnetization; Maletic-Savatic et al., 2008). The difference in relaxation times of different molecules, such as water and fat, is used to generate detailed MRI images of the brain. In addition, further information can be extracted from these constants, and different MR modalities have been adapted to study neurogenesis (Modo and Bulte, 2011).

FIGURE 3

Figure 3. Live methods to assess adult human neurogenesis. These methods are based on magnetic resonance, using MRI scanners available in hospitals worldwide. Because there are no side effects, both healthy and diseased people can be re-scanned throughout aging, before and after exercise, to follow-up the effect of pharmacological interventions, etc. Two main methods have been developed to indirectly quantify adult human neurogenesis using different MR modalities: (A) CBV measurement. The dentate gyrus CBV is a proxy for neurogenesis in physical exercise paradigms. This method is based on the consecutive correlation of neurogenesis–angiogenesis, and angiogenesis–CBV. (A1) High resolution MRI slice of the adult human hippocampus (right panel), showing the different hippocampal subregions (entorhinal cortex, EC, green; dentate gyrus, DG, red; cornu ammonis 1, CA1, light blue; and subiculum, SUB, yellow; central panel) and a typical hippocampal CBV map (warmer colors indicate higher CBV). (A2) Quantification of the mean relative hippocampal CBV (rCBV), before (white bars) and after (black bars) exercise in healthy humans. As in mice, physical exercise resulted in a significant increase in CVB only in the DG (asterisk). (B) Spectroscopy. A lipidic metabolite resonating at 1.28 ppm was identified as a marker of rodent NPCs. (B1) Positioning of the voxel of interest in the cortex and the hippocampus of a healthy person. (B2) Spectroscopic analysis of the metabolite content in the hippocampal voxel using SVD and FFT (small upper insert). Identified metabolites are myoInositol (mI, light blue), choline (Cho, purple), creatine (green), N-acetylaspartate (NAA, dark blue), and the 1.28 ppm metabolite (red). (B3) Quantification of the abundance of the 1.28 ppm metabolite in the cortical (CTX) and hippocampal voxels (LH and RH for left and right hippocampus, respectively), normalized over the amplitude of the creatine peak. The hippocampi had much higher content of the 1.28 ppm metabolite than the cortex. The MRI cutaway is printed from permission from the National High Magnetic Field Lab website (http://www.magnet.fsu.edu/education /tutorials/magnetacademy/mri/). Figures (A1–A2) are reprinted by permission from Pereira et al. (2007), copyright 2007, National Academy of Sciences, U.S.A. Figures (B1–B3) are from Manganas et al. (2007) and are reprinted with permission from AAAS.
The major advantage of MR-based methods is that they are performed in live individuals with no side effects, supporting repeated measures and longitudinal studies. Thus, these methods allow a more controlled experimental design, and variables such as the cause or age of death no longer have to be taken into account. Nonetheless, these methods rely on correlations to indirectly quantify neurogenesis, and extensive validation in both rodents and humans is required to demonstrate that they are specific for neurogenesis. More importantly, it is essential to determine whether the data correlate with the number of NPCs, proliferating NPCs (versus other cell types that proliferate), or newborn neurons. Another major advantage of MRI-based methods is that MRI scanners are widely available in hospitals and research centers worldwide. Thus, these methods could be easily implemented in many labs and offer a unique research opportunity to increase our understanding of the role of adult neurogenesis in humans.
Cerebral blood volume measurements
Cerebral blood volume (CBV) can be measured by several methods, one of which is MRI. In MR-based CBV measurements, the contrast agent gadolinium is injected systemically. The chelated gadolinium used is a non-toxic highly lipophobic agent, thus restricted to the intravascular space when the BBB is not challenged (Zaharchuk, 2007). Due to its paramagnetic properties, it creates variations in the local magnetic field which lead to decreased T1 signal intensity. These changes can be used to generate maps of the CBV and cerebral blood flow (CBF) by an array of computational methods (reviewed in Zaharchuk, 2007). Among these, the steady-state T1 method is based on the assumption that the MRI signal derives from two separate compartments – intravascular (vessels) and extravascular (brain parenchyma; Lin et al., 1999). When gadolinium is administered, only the T1 signal from the intravascular compartment will decrease, assuming the BBB is intact. Then, the difference between pre-contrast and post-contrast images normalized over a voxel that contains only blood, such as the sagittal sinus, is used to generate the CBV map (Lin et al., 1999). The main advantage of the steady-state T1 method, compared to other methods such as bolus tracking (also called dynamic imaging), is that it renders absolute estimations of the CBV, supporting longitudinal studies of brain perfusion, and has high spatial resolution. This method has been validated through correlation with estimations of gray matter CBV using other imaging modalities. However, it requires longer acquisition time and has lower signal-to-noise ratio than bolus tracking (Lin et al., 1999). Nevertheless, the steady-state T1 method is well-established for determining CBV (Zaharchuk, 2007) and has been recently used by the group of Scott Small to indirectly assess changes in adult human neurogenesis (Pereira et al., 2007).

The basis for the CBV studies of neurogenesis is the correlation between angiogenesis and neurogenesis. Increased cortical CBV correlates with angiogenesis in ischemia (Lin et al., 2002; Seevinck et al., 2010) and gliomas (Aronen et al., 2000; Cha et al., 2003). In turn, angiogenesis occurs in the hippocampal neurogenic niche (Palmer et al., 2000), and both angiogenesis and neurogenesis are elevated in the hippocampus following physical exercise (van Praag et al., 2005; Van der Borght et al., 2009). Thus, because of the correlation of CBV–angiogenesis and angiogenesis–neurogenesis, the CBV might provide an indirect measure of neurogenesis in the adult human hippocampus (Pereira et al., 2007). In fact, the CBV increased selectively in the human dentate gyrus (DG, where NPCs reside) after a 12-week exercise paradigm, and this increase correlated with cognitive performance, such as declarative memory but not delayed recognition (Pereira et al., 2007). As a validation experiment, the authors showed that in running mice, the CBV increased in the DG and not in other hippocampal areas, and this increase correlated with the number of 1- to 3-week-old BrdU+ cells (Pereira et al., 2007). More recently, others have demonstrated increased number of micro-vessels occurring in parallel to increased proliferation (Ki67+ cells) and the number of newborn cells committed to the neuronal lineage (DCX+ cells) after 10 days of running (Van der Borght et al., 2009). However, it remains to be elucidated if the angiogenesis–neurogenesis coupling occurs in conditions other than exercise, which would render the CBV measurements for assessments of human neurogenesis more widely applicable.

Neurogenesis in the Adult Human Hippocampus
In rodents, the hippocampal neurogenic cascade starts with the quiescent neuroprogenitors (QNPs; type-1 cells; radial glia), which reside in the SGZ. QNPs proliferate, giving rise to a transient population, the amplifying neuroprogenitors (ANPs; type-2a cells) which in turn proliferate and differentiate into neuronal-committed NBs (type-2b and type-3 cells). Finally, at the end of a 4-week period, the surviving NBs become mature neurons integrated into the circuitry (reviewed by Kempermann et al., 2004; Encinas and Enikolopov, 2008).

In humans, adult hippocampal neurogenesis was demonstrated by analysis of postmortem tissue of cancer patients (Eriksson et al., 1998), and changes in it under different conditions such as physical exercise and aging have been observed indirectly using CBV (Pereira et al., 2007) and 1H-MRS (Manganas et al., 2007) in healthy adults in vivo. The presence of functional NPCs in the adult human hippocampus was further demonstrated by culture, expansion, and differentiation of human NPCs in vitro (Kukekov et al., 1999; Roy et al., 2000; Moe et al., 2005). A recent study has shown that the adult human SGZ contains DCX-expressing cells that co-localize both with markers of proliferation (MCM2, Ki67, PCNA) and mature neurons (NeuN, β-III-tubulin), supporting the existence of NBs throughout the human lifespan (Knoth et al., 2010).

Other studies, however, failed to detect NPCs or proliferating cells in the adult hippocampus of epileptic patients using immunohistochemical methods, such as expression of nestin, vimentin, or Ki67 (Arnold and Trojanowski, 1996; Del Bigio, 1999; Blumcke et al., 2001; Seress et al., 2001; Fahrner et al., 2007). This conflicting literature can be explained by different sensitivities of the particular method used in each study. Overall, future work is needed to determine all components of the hippocampal neurogenic niche and the cellular types that comprise human neurogenic cascade.

Relevance of Adult Neurogenesis to Human Disease
The majority of studies on human neurogenesis compare findings in healthy people to those in patients with a variety of neurological diseases. A summary comparing the alteration in neurogenesis in rodent models of disease and human patients is shown in Table 2. These studies use immunohistochemistry to detect biomarkers of proliferation or specific cell-types, and thus are only able to report differences in proliferation and putative NPCs and NBs (pNPCs, pNBs), but not actual neurogenesis (i.e., formation of new neurons). Thus, we label these detected cells “putative” because none of the studies demonstrated that proliferating cells differentiated into mature, functional neurons. To directly reach the conclusion that neurogenesis is occurring lineage tracing using BrdU or analogs is required.

TABLE 2

Table 2. Adult neurogenesis during disease.
Alzheimer’s Disease
Alzheimer’s disease (AD) is characterized by accumulation of β-amyloid and neurofibrillary tangles containing hyperphosphorylated tau protein throughout the cortex and the hippocampus, resulting in progressive dementia (Curtis et al., 2007a). Some pathological features of AD can be modeled in transgenic mice overexpressing amyloid precursor protein and presenilin 1 (APP/PS1). In these mice, memory impairment and increased hippocampal proliferation and neurogenesis were observed at 9, but not 3 months of age (Yu et al., 2009). However, earlier works showed that 6-month-old APP/PSE1 mice have unaltered proliferation and short-term survival (1–13 days), whereas they have a significant reduction of long-term survival (30–42 days) and differentiation (Verret et al., 2007). In addition, other transgenic mouse models of AD have shown otherwise. For instance, in triple transgenic mice (APP/PSE1/Tau) there is a gradual decrease in SGZ proliferation starting at 6 months of age (Rodriguez et al., 2008). On the other hand, 3-month-old mice expressing mutated APP have increased proliferation (Jin et al., 2004a) although this increase was reverted to control levels in older animals (Lopez-Toledano and Shelanski, 2007). Finally, in 6-week-old transgenic mouse expressing human APP showed decreased proliferation in control housing conditions as well as a decreased 4-week survival in enriched environment conditions (Naumann et al., 2010). In postmortem hippocampal samples from patients with advanced AD, an increased expression of NB proteins (DCX, PSA-NCAM, and NeuroD) compared to age-matched controls was reported, suggesting increased neurogenesis perhaps as a compensatory mechanism to cope with the AD-related cognitive impairment (Jin et al., 2004b). However, a more recent study of presenile AD patients failed to demonstrate increased proliferation in the DG, whereas it showed an increased proliferation (Ki67+ cells) associated with gliogenesis and angiogenesis in other hippocampal regions. Further, the same study attributed changes in DCX immunolabeling to postmortem breakdown (Boekhoorn et al., 2006). Thus, it is clear that more comprehensive studies are needed to clarify the changes in SGZ neurogenesis in AD. Furthermore, the relation between potentially altered neurogenesis and the cognitive impairments observed in AD remains to be elucidated (Lazarov et al., 2010).

Subventricular zone neurogenesis is also altered in mouse AD-models. For instance, transgenic APP or PSE1 mice as well as wild-type mice infused in the lateral ventricles with βA peptide had reduced SVZ proliferation compared to control mice (Haughey et al., 2002; Rodriguez et al., 2009; Veeraraghavalu et al., 2010). Decreased proliferation and neuronal differentiation were also observed in cultured NPCs isolated from PSE1 mutant SVZ (Veeraraghavalu et al., 2010) and from APP/PS1 mutant SVZ (Demars et al., 2010). In human AD patients, decreased proliferation (Ki67+ cells) accompanied by a puzzling increase in nestin expression was observed in postmortem sections (Ziabreva et al., 2006). In agreement, cultured embryonic human NPC had decreased proliferation and increased apoptosis when treated with Aβ peptide compared to control NPCs treated with vehicle (Haughey et al., 2002). Thus, there are consistently lower levels in SVZ neurogenesis in AD patients as well as in and rodent AD models, prompting the suggestion that impaired SVZ neurogenesis may have functional consequences in AD (Curtis et al., 2007a). For instance, olfactory deficits significantly predict development of AD in patients with mild cognitive impairment (Devanand et al., 2000), although whether these olfactory deficits are related to decreased SVZ neurogenesis remains unknown.

Stroke/Ischemia
A stroke, or cerebrovascular accident, results from occlusion of cerebral arteries leading to decreased local blood flow (ischemia) or from a hemorrhage. In the stroked tissue, two areas of injury can be discriminated: the core infarcted area, where neurons die of necrosis and very little, if any, regeneration is possible; and the penumbra area, which surrounds the infarcted area, is perfused by collateral arteries, and is not irreversibly damaged. Given that the ischemic stroke is the third most frequent cause of mortality in industrialized countries, major scientific efforts have been directed toward discoveries of therapies to facilitate recovery from the insult.

In rodent and non-human primate models of stroke, such as occlusion of the medial cerebral artery occlusion (MCAO), adult neurogenesis is up-regulated both in the SVZ–RMS–OB and the hippocampus (Jin et al., 2001; Zhang et al., 2001; Koketsu et al., 2006; Lledo et al., 2006). In addition, stroke also induces ectopic neurogenesis in penumbra areas, such as the striatum, due to atypical migration of SVZ newborn cells (Arvidsson et al., 2002). Cortical neurogenesis in the penumbra area in rodent models of stroke has been found by some (Gu et al., 2000; Jin et al., 2003) but not by others (Arvidsson et al., 2002). Interestingly, the newborn cells differentiated into striatal neurons and acquired the same phenotype of the neurons which had died as a consequence of the stroke, suggesting that neuronal replacement can occur in the stroked striatum (Arvidsson et al., 2002). Although the vast majority of the striatal newborn cells died, possibly due to an unfavorable environment (Arvidsson et al., 2002), stroke-induced striatal neurogenesis seems to have functional consequences in rodents, since it has been shown that the transgenic ablation of the NB protein DCX prevented stroke-induced neurogenesis and worsened the sensorimotor and behavioral deficits after MCAO (Jin et al., 2010).

This research indicated that harnessing aberrant striatal neurogenesis in stroke may be useful to reduce the neurological deficits in patients (reviewed in Zhang and Chopp, 2009). The patients who suffered the ischemic, middle cerebral artery stroke showed increased proliferation of putative B cells (Ki67, GFAP+ cells) and putative C cells (PSA-NCAM+ cells), in the ipsilateral SVZ compared to the contralateral side of the stroke (Marti-Fabregas et al., 2010). In addition, there were traces of ectopic neurogenesis not in the striatum, but in the cortex. A significant increase in proliferating Ki67+ cells and pNBs (PSA-NCAM+ cells) was found in the cortical penumbra region of ischemic stroke patients compared to age-matched controls (Jin et al., 2006; Macas et al., 2006) as well as in perihematomal regions in patients with intracerebral hemorrhage (Shen et al., 2008). The relevance of this increase in cortical neurogenesis in stroke patients remains to be investigated, but the phenomena certainly raise the hope that neurogenesis might be harnessed as a possible treatment for stroke patients.

Conclusion
Overall, studies of adult human neurogenesis, even though hampered by limitations of the available methodologies for both ex vivo and in vivo assessments, are promising. Development of new antibodies targeted to human antigens will certainly improve immunohistochemical data, but even then, such labeling will provide only putative information. It is in combination with BrdU labeling that the production of new neurons can be assessed and quantified. As more BrdU labeled tissue is generated, the changes in the neurogenic cascade that accompany brain disorders will be elucidated. However, several considerations need to be taken into account when studying postmortem human tissue, in particular the postmortem delay, the cause of death, and the age at the time of death. Thus, the future of adult human neurogenesis research and the prospects of harnessing its potential for treatments of brain disorders will heavily depend on the development and thorough validation of methods for in vivo assessments, as those offer unique opportunity for both cross-sectional and longitudinal studies of the neurogenic niches while they are intact within the living brain tissue.

Received: 20 January 2011; Accepted: 23 March 2011;
Published online: 04 April 2011.

Acute stroke treatment options - Cleveland Clinic

From the web chats put on by the Cleveland clinic
http://www.clevelandclinic.org/health/chatreg/ChatPage.aspx?ChatId=1229

Acute Stroke Treatment Options
A stroke, or "brain attack," occurs when the blood supply is cut off from part of the brain. When this happens, the blood-deprived brain loses its supply of oxygen and nutrients. When the brain is deprived of blood for even a few minutes, it begins to die. Immediate treatment of a stroke may limit or prevent brain damage. Take advantage of this chat to speak to a Cleveland Clinic interventional neurologist, Gabor Toth, MD about techniques, medications and treatment options when acute stroke occurs.
Date: Thursday, May 5, 2011
Time: 12:00 PM (EST)

I have tried to get into these several times but have been unsuccessful. For this one I will have lots of questions on the future of acute stroke rehab. If you want you can grab some of my ideas posted here and ask them also.

Friday, April 29, 2011

Motor recovery plateau

http://www.mendeley.com/research/reconsidering-the-motor-recovery-plateau-in-stroke-rehabilitation-1/

Abstract
Termination of motor rehabilitation is often recommended as patients with cerebrovascular accident (CVA) become more chronic and/or when they fail to respond positively to motor rehabilitation (commonly termed a "plateau"). Managed-care programs frequently reinforce this practice by restricting care to patients responding to therapy and/or to the most acute patients. When neuromuscular adaptation occurs in exercise, rather than terminating the current regimen, a variety of techniques (eg, modifying intensity, attempting different modalities) are used to facilitate neuromuscular adaptations. After presenting the concepts of the motor recovery plateau and adaptation, we similarly posit that patients with CVA adapt to therapeutic exercise but that this is not indicative of a diminished capacity for motor improvement. Instead, like traditional exercise circumstances, adaptive states can be overcome by modifying regimen aspects (eg, intensity, introducing new exercises). Findings suggesting that patients with chronic CVA can benefit from motor rehabilitation programs that apply novel or different parameters and modalities. The objectives of this commentary are to (1) to encourage practitioners to reconsider the notion of the motor recovery plateau, (2) to reconsider chronic CVA patients' ability to recover motor function, and (3) to use different modalities when accommodation is exhibited. References: 65

Eating Again After Stroke

I was only on the soft food diet for two weeks luckily so I didn't need any therapy for eating. To pass the swallowing test they gave me a Red Delicious apple to eat. I dislike them because they are only red , not delicious, mainly mealy.

http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=20477

You can see a picture of the device at the link.
WARWICK, R.I. (Ivanhoe Newswire) -- Food is one of the great pleasures in life, but some are robbed of that enjoyment after suffering a stroke. Swallowing is one of the many basic functions that can be taken away, but now there's a device that could ease the pain and frustration. It's helping people get off feeding tubes and take a seat at the dinner table.

After his stroke sitting down for a meal turned into a chore for 84-year-old Joseph Grant.

"It was just hard for him and he couldn't drink liquids, plain liquids at all," Joseph's wife Marilyn recalled to Ivanhoe.

His throat muscles were weak and the former monk, magician and dentist was miserable.

Joseph turned to therapists who introduced him to a new device that would do the swallowing work for him. It sends electrical currents to the throat muscles. Combined with an exercise routine, it returns them to their former strength.

Lisa Mathers, a speech pathologist at Kent Regency Genesis Healthcare in Warwick, R.I., works with Joseph for about an hour five days a week. After a month, the results are usually much better than traditional therapy.

"It was a real long road of traditional therapies, oral motor exercises," Mathers told Ivanhoe. "It was very time consuming, sometimes discouraging, because it took such a long time and it didn't always rehabilitate the muscle."

Joseph says he's now able to eat and drink just about anything on the menu.

"Oh yeah, it's a lot better -- a tremendous amount better," Joseph said. Now, mealtime is a much more enjoyable experience.

The VitalStim device works best on patients with neurological problems from a stroke, Parkinson's disease, or multiple sclerosis.

Yoga and stroke rehabilitation

I started a yoga class three weeks ago. It requires watching the demonstration and trying to figure out what parts I can do and what I have to modify. I have never taken a yoga class before so the names and positions are new to me. The first week was up and down positions including downward dog, Since I can't flatten my left hand at all and the left elbow collaspes I would do a 3-point version. Rather unstable. The instructor finally told me to change it to a low dog. Some of the lying down positions I concentrate on relaxing the left arm so it will lay on the floor. If I do any other movement like lifting my legs my bicep goes spastic and pulls my forearm perpendicular to the floor. Multitasking just is not possible. She is a former dancer so she makes movements flow into each other, I really slow it down, specially going up and down. It looks as ungraceful as hell.

Search for some of my other yoga posts warning about some extreme poses.

Mental Practice With Motor Imagery Does Not Help In Stroke Recovery

This was depressing, I am basing a lot of my therapy on mental imagery since I have a huge dead spot to relocate.
But this series from 2010 says it is effective.
http://commons.pacificu.edu/cgi/viewcontent.cgi?article=1021&context=otpf&sei-redir=1#search="The+Effectiveness+of+Mental+Imagery+on+the"
http://www.sciguru.com/newsitem/8319/Mental-Practice-With-Motor-Imagery-Does-Not-Help-In-Stroke-Recovery/
Until researchers actually give us a damage diagnosis broken down by penumbra vs. dead area, none of these studies are reproducible or valid.

April 28th, 2011

A new clinical study shows that mental practice with motor imagery is not beneficial in stroke recovery. Motor imagery has been believed to be an effective neuro-rehabilitation technique.
Motor imagery is a mental process by which a subject simulates a given action. Several studies have demonstrated that mental simulation of movement activates the same brain areas that are activated when these movements are actually executed. The current study is based upon these findings and the argument that if mental simulation of the physical activity can activate specific brain areas, then "we can 'jog' the brain" in the absence of actual bodily movement. In addition, it is also known that brain plasticity plays an important role in recovery following brain injury. The researchers, in this study, evaluated the therapeutic benefit of mental practice with motor imagery for upper limb motor weakness in stroke patients.



Image Credit: NINDS, NIH
These MRI images show ischemic stroke and recovery


Stroke is caused by the interruption of the blood supply to parts of the brain and the symptoms depend on what part of the brain is damaged. This can be due to blockage of blood vessels causing reduced or no blood flow, or hemorrhage (blood loss). A stroke can cause permanent neurological damage; a very severe stroke can cause death.

The article published in the April 22 online edition of the peer-reviewed scholarly journal Brain reports the finding of a single-blind randomized controlled trial in which a large sample of unselected stroke patients within six months following stroke undertook a program of either four weeks of motor imagery training, or a control training program.

Patients underwent 45-minute training sessions three days a week for four weeks. The participants in the test group were directed to imagine a variety of different hand movements such as opening and closing, reaching, grasping, ironing and washing under the arms. The study included two control conditions, an attention-placebo control condition and a routine-care control condition. Among the 121 patients participated, 41 were in the motor imagery training group, 39 in the attention-placebo control group and 41 in the normal care control group.

The authors did not find any significant difference between test and control groups on the primary outcome measure, which was recovery of the upper extremity function following cortical injury. According to the research paper, "this trial demonstrates clear nil-findings with regards to the efficacy of mental practice with motor imagery in stroke rehabilitation, raising some important issues with regards to the clinical benefit of mental practice."

The authors of the study were, Magdalena Ietswaart, Marie Johnston, H. Chris Dijkerman, Sara Joice, Clare L. Scott, Ronald S. MacWalter and Steven J.C. Hamilton from institutions in the UK and the Netherlands.

The same authors had previously reported beneficial effect of mental practice, and they now conclude that the benefit of mental practice previously found was due to combined physical and mental practice. This study shows that mental practice alone does not enhance motor recovery in patients early post-stroke.

Source paper: Ietswaart M, Johnston M, Dijkerman HS, Joice S, Scott CL, MacWalter RS and Hamilton SJC. Mental practice with motor imagery in stroke recovery: randomized controlled trial of efficacy. Brain 2011; April 22; doi: 10.1093/brain/awr077.

Other References:
Dijkerman HC, Ietswaart M, Johnston M, MacWalter RS. Does motor imagery training improve hand function in chronic stroke patients? A pilot study. Clin Rehab 2004;18:538.

Butler AJ, Page SJ. Mental practice with motor imagery: evidence for motor recovery and cortical reorganization after stroke. Arch Phys Med Rehabil. 2006;87:S2.

And they consider this science? Only a four week trial and they have no idea if they are trying to assist damage recovery or dead brain relocation. The emperor is truly naked on this one.

Apoptosis: a target for neuroprotection

Sounds like another research possibilty to stop cell death.
http://www.ncbi.nlm.nih.gov/pubmed/15359610

Abstract
Accumulating evidence strongly suggests that apoptosis contributes to neuronal death in a variety of neurodegenerative contexts. Activation of the cysteine protease caspase 3 appears to be a key event in the execution of apoptosis in the central nervous system. As a result, mice null for caspase 3 display considerable neuronal expansion, usually resulting in death by the second week of life. Consistent with the proposal that apoptosis plays a central role in human neurodegenerative disease, caspase-3 activation has recently been observed in stroke, spinal cord trauma, head injury and Alzheimer's disease. Indeed, peptide-based caspase inhibitors prevent neuronal loss in animal models of head injury and stroke, suggesting that these compounds may be the forerunners of non-peptide small molecules that halt the apoptotic process implicated in these neurodegenerative disorders. The present review will summarise some of the recent data suggesting that apoptosis inhibitors may become a practical therapeutic approach for both acute and chronic neurodegenerative conditions.

Therapie. 2004 Mar-Apr;59(2):185-90.

So in 7 years I wonder what has been found out. Everytime I find something new it just brings up even more questions. Don't the current stroke researchers have this same sense of wonder of what is going on? And if they do what are they doing about it?

Using technology to optimize recovery in upper limb stroke rehabilitation

I'm not sure I believe the blanket statement that a skilled therapist is better than technologies. Parts may be true, but finding that skilled therapist is nigh onto impossible. And with millions needing therapy there will never be enough extremely skilled ones. There is a Bell curve you know, not everyone can be above average.
http://eprints.ecs.soton.ac.uk/22228/


Abstract
A skilled therapist working one-to-one with a patient for one or two hours a day may be an ideal environment to optimize recovery of upper limb function following stroke and is likely to be superior to technologies that ‘replace the therapist’. Repeated studies have found that there is no single therapeutic approach that is more effective than any other, but intensity is critical. The recent Randomized Controlled Trial of the MIT Manus, published by Lo et al, found that robot therapy was not superior to intensive conventional therapy. Given that one-to-one intensive therapy is unaffordable can technology be used to improve outcome and if so how? The key factors appear to be: increasing intensity of practice; motivating patients to maximize engagement, effort and compliance; performance of functional and relevant tasks; increasing Central Nervous System (CNS) excitability and early intervention. The evidence that technologies can be used to deliver on these key factors will be discussed and in particular the evidence and potential for combined therapies such as electrical stimulation (both peripheral and transcranial direct current stimulation [tDCS]) with robot therapy will be presented.

Who has the library for stroke information?

The answer, as pathetic as it is - is noone.
This is why you have all these survivors creating their own web pages and searching. I've done this myself with this blog.
To see what the future of stroke information dispensation should look like we only need to visit the Alzheimers Association virtual library.
http://www.alz.org/library/index.asp


As you can see they provide all these services:
answer questions about Alzheimer's disease and related dementias
search for materials on topics
locate statistics
find a certain article or book title
connect you with resources
I asked one of the librarians a question.
What are the details behind this study that says Stroke survivors double their chances of getting Alzheimers?
http://www.physorg.com/news124976505.html

Is it because of the area of the stroke?, frontal lobe,hippocampus motor,pre-motor or sensory cortex? Or do the toxins disperse throughout the brain regardless of the epicenter of the stroke?
The librarians seem to be associated with various libraries and they have to look up the answers themselves. The best way would be to have a single database of information. My librarian from Syracuse was not able to answer the question. I know it was extremely hard and I didn't really expect an answer, but what I hoped would happen is that they would take the question down and pass it to their experts to solve and then get back to me via email. I might try asking this question of the 2 US associations but I know they will not know the answer. Take this question and ask your countries association what the answer is. If only to show how little they actually know.

Bionic Leg makes stroke rehabilitation easier

http://www.ubergizmo.com/2011/04/tibion-bionic-leg-makes-stroke-rehabilitation-easier/


The size of this orthotic is huge
Stroke patients know that early detection is vital, as every single second counts since delayed help will result in the worsening of one’s condition. Having said that, once one has received ample and correct medical treatment for their condition, the long hard road of recovery begins – and this would mean going through rehabilitation programs that are specially designed for stroke patients. Those who need help with walking again might look towards the Tibion Bionic Leg – where it was originally designed for people with muscle problems, arthritis, as well as those who are in post surgery to regain missing strength. This redesigned medical tool is touted to help stroke patients benefit from the therapeutic advantages of the system.
Currently being primed for use in the US by rehabilitation centers as part of their training aid in helping recover a proper walking gait, the software used will control the knee – and this software has been specially rewritten to work for stroke rehab. According to the company, the system is currently going through trials with 24 different patients over at the New York Presbyterian hospital.

Among the key components that are found in the Tibion Bionic Leg would be a pressure-sensing shoe insert that detects and measures the amount of weight a patient is applying to his/her affected leg, a computer into which the therapist programs the amount of support to be provided to the patient’s affected leg during different tasks, a couple of motors within the Bionic Leg to provide adequate support and an angle sensor in the knee, which informs the computer what the patient is doing or likely to do. Let’s hope it won’t be too expensive to the masses when available.


I can't see this being any cheaper than the Bioness or Walk-aide but it might allow severely affected survivors to walk again. One time my PT put a full leg AFO on that went to my thigh. It weighed so much that I didn't have the muscle power to move it. He would walk behind me and kick the foot of the orthotic to get that leg to move. Unless the Tibion leg is also self powered I don't see how someone needing all that support will ever be able to move that leg.

3D rehabilitation system to improve arm function following stroke

If you follow this thru the the full PDF you can see pictures of what they are doing, electrical stimulation with a supported arm.
http://onlinelibrary.wiley.com/doi/10.1002/pnp.191/abstract
Abstract
In the September/October 2009 issue of Progress in Neurology and Psychiatry, we featured an article describing a promising new 2D robotic and electronic stimulation system developed at the University of Southampton for rehabilitation of arm movement following stroke. Here, the scientists who developed the system describe a further extension of the technique to a new 3D system known as SAIL (Stimulation Assistance through Iterative Learning). Copyright © 2011 Wiley Interface Ltd.

I really question the results being from the 3d part, Looking at the setup you can see that the arm is totally supported. That de-weighting of the arm is what I believe allows the patient to focus totally on the muscles necessary for the specified movement rather than needing to focus on shoulder muscles to hold up the arm. And I've already posted on the issues with even this kind of limited multitasking for survivors.

iron deposition and acute stroke rehab

While I was browsing thru Dr. Steenblocks site and his religious belief in HBOT I saw iron deposition. This article discusses it as a possible factor in cell death following a stroke. I couldn't see where it actually proposes a way to prevent that unless the purchased article says something. I really wish researchers would say what they mean in 8th grade terms, they should be smart enough to be able to convey their meaning to those less smart than them.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6X1H-4CJVR53-1&_user=10&_coverDate=07%2F31%2F2004&_rdoc=1&_fmt=high&_orig=gateway&_origin=gateway&_sort=d&_docanchor=&view=c&_searchStrId=1734337935&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=004bdd0b5bd897661e0afdd5418e2ee3&searchtype=a
The role of iron neurotoxicity in ischemic stroke
Purchase
$ 31.50


References and further reading may be available for this article. To view references and further reading you must purchase this article.


Magdy H. Selim, , a and Rajiv R. Ratan, b, 1

a Department of Neurology, Division of Cerebrovascular Diseases, Harvard Medical School, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Palmer 127, Boston, MA 02215, USA

b Burke/Cornell Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY, USA

Received 6 April 2004; accepted 6 April 2004. Available online 7 June 2004.

Abstract
Stroke is the second leading cause of death worldwide, and its incidence is expected to rise with the projected increase in the number of aging population. Disturbances of brain iron homeostasis have been linked to acute neuronal injury following cerebral ischemia. Free iron catalyzes the conversion of superoxide and hydrogen peroxide into hydroxyl radicals, which promote oxidative stress leading to subsequent cell death/apoptosis. In recent years, considerable evidence has emerged regarding the role of iron neurotoxicity following experimental cerebral ischemia. Few clinical studies have also attempted to investigate the role of iron in stroke patients. The present review will examine the currently available evidence for iron-mediated neurotoxicity and the potential mechanisms underlying deregulation of iron homeostasis in the brain following cerebral ischemia. Understanding the changes in brain iron metabolism and its relationship to neuronal injury in ischemic stroke could provide new therapeutic targets to improve the outcome of stroke patients.

Author Keywords: Ferric; Ferrous; Stroke; Ischemia; Hypoxia; Neuronal

Article Outline
1. Iron homeostasis is important for normal brain function
2. The link between iron and ischemic stroke
3. Evidence for iron involvement in ischemic neuronal injury
3.1. Animal data
3.2. Clinical data
4. Source(s) of released iron in the brain after ischemic stroke
5. The relationship between brain iron load and severity of neuronal damage after stroke
6. Temporal profile of iron-mediated neuronal injury after ischemic stroke
7. Summary

Periodic whole body acceleration

I have no clue if this is just an alternative therapy looking for a home. I certainly won't be using it.
http://www.ncbi.nlm.nih.gov/pubmed/18357918
Vasa. 2007 Nov;36(4):261-6.
Periodic whole body acceleration: a novel therapy for cardiovascular disease.
Kohler M, Amann-Vesti BR, Clarenbach CF, Brack T, Noll G, Russi EW, Bloch KE.
SourcePulmonary Divison, Dept. of Internal Medicine, University Hospital of Zurich, Switzerland.

Abstract
BACKGROUND: Periodic whole body acceleration in the spinal axis (pGz) applied by a motion platform is a novel treatment modality that induced endothelial nitric oxide release into the circulation of animals, healthy subjects and patients with inflammatory diseases during single treatment sessions in previous studies. We hypothesized that patients with advanced arteriosclerotic diseases who are not candidates for a surgical intervention would clinically benefit from repeated pGz treatments over several weeks through improvement of endothelial function.

PATIENTS AND METHODS: 11 patients, 5 men (37 to 71 y) with stable ischemic heart disease, LVEF < 35%, NYHA stage > II, and 6 patients (51 to 83 y, 1 woman) with intermittent leg claudication, Fontaine stage II, were enrolled after optimization of pharmacological therapy. PGz was applied for 40 min, 5 days/week during 5 weeks. Quality of life (SF-36 questionnaire), exercise performance, and endothelial function were assessed at baseline, during the treatment period, and 4 weeks after discontinuation of pGz.

RESULTS: PGz was well tolerated. In heart failure paitents, pGz therapy improved quality of life, increased 6 min walking distance by a mean +/- SE of 105 +/- 24 m, and improved postischemic skin hyperemia (p < .05 in all instances). In 4 of 6 patients with intermittent claudication, quality of life, treadmill walking distance and post-ischemic skin hyperemia improved with pGz therapy (p < .05). Four weeks after discontinuation of pGz, most therapeutic effects had vanished in both patient groups.

CONCLUSIONS: In patients with severe heart failure and with leg claudication who remain symptomatic despite maximal medical therapy and who were not candidates for surgery, periodic acceleration applied over several weeks improved quality of life and exercise capacity. The clinical benefits appear to be mediated through improved endothelial function.

PMID: 18357918 [PubMed - indexed for MEDLINE]

shoe wear and stroke rehabilitation

I bought new shoes about a month ago. They're from Payless with the velcro straps, I pulled out the insole to accomodate my AFO. just yesterday I noticed I had scuffed a hole by the left toes on the sole. My previous shoes had lasted 5 years. Because I switched back to wearing my AFO again - I had gone a year without it - My gait has gotten sloppier. I can walk faster but I am not paying as much attention to lifting my foot. I have also started evening walks around our block without the cane. Because the AFO really constrains dorsiflexion it actually is making parts of my gait worse. I end up having to hip hike a lot more and will eventually have to go to therapy to correct that flaw. Oh well, live and learn and file that away in your library of stroke info.

Stemgevity and stroke rehab

I guess the whole stroke rehab world is totally missing the boat. Dr. Steenblock sells it for $89.95 for 90 capsules.
Stemgevity™ Stem Cell Mobilizing Formula™

STEMGEVITY™ assists your body to do its job NATURALLY, IMMEDIATELY, and SAFELY. This can join Neuroaid in the pantheon of stroke nostroms.

Stemgevity™ was formulated under the direction of Dr. David Steenblock, a world-renowned physician and STEM CELL expert. Dr. Steenblock and his research facility have been exploring formulations that assist your body in awakening, releasing, and promoting STEM CELL activity for many Years.
http://www.strokedoctor.com/


I do notice that there are no scientific research studies mentioned that state that this does any good.

I am not endorsing this, this probably belongs to the stroke nostroms I blogged about earlier from the 1800s except this probably does not contain any illegal or dangerous substances. My God, from reading his blog he is a miracle worker, he should get the Nobel prize for medicine.

Wednesday, April 27, 2011

Stemedica treats stroke patient with StemCells

This one looks like it is just on the safety testing part, but you could see if you want to volunteer.
http://blogs.terrapinn.com/stem-cells/2011/03/24/stemedica-treats-stroke-patient-stemcells/


Stemedica Cell Technologies, Inc. announced today that it has successfully used adult allogeneic mesenchymal stem cells to treat a stroke patient in a study conducted at the University of California, San Diego (UCSD). A total of 35 patients will be enrolled in the clinical trial.

The goal of this study, led by principle investigator Michael Levy, MD, PhD, FACS, chief of pediatric neurosurgery at Children’s Hospital San Diego (CHSD) and professor of neurological surgery at UCSD, is to determine tolerance and therapeutic outcomes for intravenously-delivered adult allogeneic mesenchymal stem cells and to hopefully pave the way for a new therapeutic category of treatment for ischemic stroke.

“This clinical trial marks a significant achievement in the treatment of debilitating ischemia-related pathologies including ischemic stroke,” said Nikolai Tankovich, MD, PhD, president and chief medical officer of Stemedica. “We believe these specially designed mesenchymal stem cells are able to tolerate, survive and repair ischemic tissues caused by an infarction of the brain, heart, kidney, retina and other organs. In addition, these mesenchymal stem cells are capable of up regulating an array of important genes that are essential for the synthesis of critical proteins involved in recovery.”

More than 800,000 Americans suffer a stroke annually and according to the American Heart Association, stroke is the fourth leading cause of death – costing an estimated $73.7 billion in 2010 for stroke-related medical costs and disability.

Watch this space for more updates on stem cells and stroke treatments!

Learn more about stem cells and their applications at Stem Cells USA & Regenerative Medicine Congress.

Read the full press release from Stemedica here.
http://www.stemedica.com/info/allogeneic-adult-stem-cells/stem-cell-clinical-trials/2011-0324-Stemedica-Treats-First-Patient-with-Ischemic-Allogeneic-Mesenchymal-Stem-Cells.asp

Tuesday, April 26, 2011

alpha tocotrienols and stroke

I hadn't really seen anything about this until I was contacted by a PR firm wondering if I wanted to blog on this. I tried asking, Why me? but she didn't respond.
So here goes:
What are they? A natural component of Vitamin E that is found in barley, rice bran and palm oil products. Your standard vitamin E supplements only contain the tocopherols.
This report suggests that a level of this vitamin E can protect the brain after a stroke. But it takes about eight to 10 weeks of supplementation to build up to an adequate level in your system. For most Asians having a rice diet they would naturally have this.
http://www.sciencedaily.com/releases/2010/01/100111122645.htmhttp://www.ncbi.nlm.nih.gov/pubmed/20823491
marketing websites here:
www.carotech.netwww.tocotrienol.orghttp://www.tocotrienol.org/images/stories/pdf_upload/Magazines/tocomin%20natural%20neuroprotective%20vitamin.pdf
I'm afaid that this is attempting to be the next statin blockbuster, so beware. Although for survivors it might be one more prevention. I'll wait until more trials are done.
It does talk about stopping glutamate damage which I discussed here;
http://oc1dean.blogspot.com/2011/02/protecting-brain-from-glutamate-storm.htmlI'm more interested in acute phase intervention with this. Dr. Sen has proven that tocotrienols, taken orally, cross the blood-brain barrier.
None of this is going to help me, I need either hard neuroplasticity, neurogenesis or stem cells.

neurological testing

There was a good discussion on testing of Wernicke’s area and how to go about validating the damage.

http://theness.com/neurologicablog/?p=3164
But it is impossible to completely isolate one subsystem within the brain, and so other functions can interfere with our testing, and we have to tease this out by using multiple tasks and then triangulating to the common element that seems to be causing trouble. This is most true for cognitive function.

For example, if I want to test Wernicke’s area (in the superior posterior temporal lobe) I will give the patient several verbal commands (without non-verbal cues) and see if they can interpret them. Wernicke’s area translates ideas into words and words into ideas, and so we test its function by testing verbal comprehension. However, in order to test this one piece of the brain, the patient also needs to be able to attend to the exam (they need to be alert and attentive), then need to be able to hear and get that information to Wernicke’s area, they need to have the general cognitive ability to understand what is happening and that they are expected to do something, and they need to be able to move to execute whatever command I gave them. And they may decide just to be uncooperative with the exam, for whatever reason. So many parts of the brain and nervous system need to work together to perform even a simple task.
We isolate Wernicke’s function, and other functions, by controlling for variables. So I will give the patient many commands, some easier for Wernicke’s area to interpret, and others more challenging – but with all other variables being equal. If commands that are difficult from a language comprehension point of view are what give the patient the most difficulty, then that is probably the part of the brain that is not working.

Wernicke’s area is mapped on lots of brain maps so the neurologist should be able to tell from the beginning on the 3d MRI if that area was directly affected. And use that same MRI to see how much of the white area underlying it was damaged or dead. By starting from this point the trial and error method could become a lot more scientific. Please any neurologists reading this, educate us survivors on why this wouldn't work.

Plateau - a bad word @#()& in stroke recovery

There is probably not a single stroke patient who has not been told they have plateaued. It is not a true medical term. I would argue that is a term used by the medical insurance world to deny therapy and save themselves money.
This is one of the research results in NIH;
http://www.ncbi.nlm.nih.gov/pubmed/16777768
Recovery plateau following stroke: fact or fiction?
Abstract
PURPOSE: 'Plateau' is an expression frequently used in relation to decisions to discharge patients from physiotherapy following stroke. This paper critically considers the concept of recovery plateau in stroke, exploring (i) the evidence for plateau, (ii) potential contributing factors, and (iii) the consequences for patients, therapists and services.

SEARCH STRATEGY: The concept of recovery plateau in stroke was reviewed drawing on standard critical appraisal methodology for the search strategy and critique. Electronic searches using Web of Knowledge, MEDLINE, CINAHL, Department of Health Website and the Cochrane Library from the earliest dates of coverage until February 2005 identified quantitative and qualitative literature related to stroke, plateau, recovery, outcome, rehabilitation and physiotherapy.

DISCUSSION: The concept of plateau is ambiguous. Recovery has been considered to plateau within the first 6 months, yet recent studies indicate later recovery is possible. We suggest that 'plateau' relates not only to the patient's physical potential, but is influenced by how recovery is measured, the intensity and type of therapy, patients' actions and motivations, therapist values, and service limitations.

CONCLUSION: 'Plateau' is conceptually more complex than previously considered. Current conceptualizations may limit potential recovery and hinder service development. Research into plateau which takes account of contextual issues of therapy provision is required.

Published in July, 2006
So since then no medical person should have used that term.

Stroke bloggers deny it exists;
http://www.strokeadvice.com/strokerecoveryplateau.html
The next ones from Peter Levine are required reading, especially the part where therapist=recovery is not true.
http://recoverfromstroke.blogspot.com/2010/09/upward-spiral-of-recovery-ii.html
http://recoverfromstroke.blogspot.com/2010/05/pizza-and-therapy-so-much-in-common.html
This one from the Phoenix written as a letter to another survivor is very very good. If you can't get in, please sign up, its an excellent stroke forum.
http://www.strokeboard.net/index.php?app=blog&blogid=618&showentry=9885

So if a therapist says you can't get any more therapy because you have plateaued, DEMAND a scientific backed research study to prove their point. Or point them here and let me correspond with them. It may be the only way they will ever crack open research papers on stroke rehab. They do work for you, you know.

Monday, April 25, 2011

when bad things happen to good people

I've been reading this Harold Kushner book and this famous set of lines was an interesting explanation.

To try to understand the book and its answer, let us take note of three statements which everyone in the book, and most of the readers, would like to be able to believe:

A. God is all-powerful and causes everything that happens in the world. Nothing happens without His willing it.
B. God is just and fair, and stands for people getting what they deserve, so that the good prosper and the wicked are punished.
C. Job is a good person

As long as Job is healthy and wealthy, we can believe all three of those statements at the same time with no difficulty. When Job suffers, when he loses his possessions, his family and his health, we have a problem. We can no longer make sense of all three propositions together. We can now affirm any two only by denying the third.

How many neurons did you lose during your stroke?

I have to look again at my medical records.
Within an hour of getting to the hospital I got tPA. It looks like I had 90 minutes from onset to tPA.
So lost neurons = 171 million
lost synapses = 1260 billion
lost mylinated fibers = 675 miles
Lost 5.4 years in brain age.

In each minute, 1.9 million neurons, 14 billion synapses, and 12 km (7.5 miles) of myelinated fibers are destroyed. Compared with the normal rate of neuron loss in brain aging, the ischemic brain ages 3.6 years each hour without treatment.
It has been estimated that the adult brain has around one hundred billion neurons and an even larger number of glial cells.
And with the one neuron handling functions I should be able to handle that minute loss: http://oc1dean.blogspot.com/2011/04/single-neuron-power.html

This is something our doctors should be keeping track of, it would be a much better way of describing damage rather than mild, severe, catastrophic.
Someday this will be correlated with a 3d MRI and cubic volume of the stroke.
Considering my damage, my penumbra(partially damaged area) was also 171 million neurons. With that small a percentage dead and damaged I wonder why I was so close to dying.

Nutraceuticals Promote Human Stem Cells

I wish this was written in readable terms, I'm not spending $49 to read details that probably don't translate to any therapy protocol.
http://www.liebertonline.com/doi/abs/10.1089/scd.2006.15.118

A viable alternative to stem cell transplantation is to design approaches that stimulate endogenous stem cells to promote healing and regenerative medicine. Many natural compounds have been shown to promote healing; however, the effects of these compounds on stem cells have not been investigated. We report here the effects of several natural compounds on the proliferation of human bone marrow and human CD34+ and CD133+ cells. A dose-related effect of blueberry, green tea, catechin, carnosine, and vitamin D3 was observed on proliferation with human bone marrow as compared with human granulocyte-macrophage colony-stimulating factor (hGM-CSF). We further show that combinations of nutrients produce a synergistic effect to promote proliferation of human hematopoietic progenitors. This demonstrates that nutrients can act to promote healing via an interaction with stem cell populations.

multitasking and stroke rehab

I know lots of us want to get back to multitasking but if you believe the research we never were able to do it.

http://www.ccbi.cmu.edu/news/sandiegouniontribune-dualtask.html
Scientists have bad news for people who think they can deftly drive a car while gabbing on a cell phone.
The first study using magnetic resonance images of brain activity to compare what happens in people's heads when they do one complex task, as opposed to two tasks at a time, reveals a disquieting fact: The brain appears to have a finite amount of space for tasks requiring attention.

The neurologica blog gives us this statement; Most people cannot effectively multitask, even if they think they can. Only about 2.5% of people can genuinely multitask – perform two demanding cognitive tasks simultaneously without both suffering.
http://theness.com/neurologicablog/?p=3123

And this famous test pretty much proves you can't, I failed it. from Prof. Simons's YouTube channel;
http://www.youtube.com/profsimons select the selective attention test.

Rebecca Dutton blogs about it here:
http://homeafterstroke.blogspot.com/2011/03/only-magic-bullet-ive-found.html
basically as a stroke survivor you have to stop multitasking.

My most obvious occurrence of this was being told vocally by my wife to pick up 3 items from the grocery store. I ended up having to go to the store 3 times to get all the items.

aFGF delivered intranasally induces neurogenesis

This is the second study after TGF alpha that requires nasal delivery in order to bypass the blood-brain barrier. Maybe they should start thinking about delivery via nanoparticles or exosomes.
http://oc1dean.blogspot.com/2010/12/nanoparticles-and-stroke-rehab.html
http://oc1dean.blogspot.com/2011/03/exosomes-delivering-drugs-to-brain.html

http://www.ingentaconnect.com/content/maney/nres/pre-prints/1743132810Y.0000000004Acidic fibroblast growth factor delivered intranasally induces neurogenesis and angiogenesis in rats after ischemic stroke
Abstract:
Background: Enhancing angiogenesis and neurogenesis is a novel therapeutic strategy for stroke treatment. Acidic fibroblast growth factor (aFGF) has been shown to have both angiogenesis and neurogenesis effects in animals with cerebral ischemia. But aFGF can not enter the brain freely after system administration due to the filtration of the blood-brain barrier (BBB). Intranasal administration of aFGF as a noninvasive method can bypass the BBB and enter the central nervous system directly without systemic adverse effects. Methods: To investigate the therapeutic effects of intranasally delivered aFGF, adult male Sprague Dawley rats were subjected to middle cerebral artery occlusion (MCAO) and intranasally administrated with aFGF or saline starting at 24 hours and once daily for the subsequent 6 days. BrdU (50mg/kg) was intraperitoneally injected daily for 13 days. A modified neurological severity scores test was performed before and at 1, 7, 14 days after MCAO. Infarct volumes were evaluated after hematoxylin and eosin staining. Immunohistochemistry was performed to detect BrdU immunoreactive cells and BrdU / DCX double labeled cells. Microvessels were labeled by FITC-dextran and the numbers, length and diameters of vessels were also measured. Results: Intranasal aFGF did not significantly reduce the lesion size, but did improve neurological functional recovery. In the subventricular zone and the striatum, numbers of BrdU immunoreactive cells were significantly increased in aFGF group at day 14, and the majority of BrdU positive cells were co-labeled with DCX. At 14 days after ischemia, the percentage of BrdU positive endothelial cells around the ischemic lesions were significantly increased in aFGF group, compared with control. Quantitative analysis of FITCdextran perfusing vessels revealed a significant increase of vessels in the boundary regions of ischemia in the rats treated with aFGF. But there were no significant differences concerning the length and the diameter of the vessels between groups. Conclusion: In summary, aFGF may enhance neurogenesis and angiogenesis after focal cerebral ischemia. Intranasal administration of aFGF may be a feasible approach for ischemic stroke treatment.

Regulation of neurogenesis by extracellular matrix and integrins

This is another of those research results that I wish would be written in laymans' terms.

http://www.ncbi.nlm.nih.gov/pubmed/21499331

Abstract
Deciphering the factors that regulate human neural stem cells will greatly aid in their use as models of development and as therapeutic agents. The complex interactions of cells with extracellular matrix (ECM) proteins probably contribute to proper central nervous system development mediating processes which regulate proliferation and differentiation of neural stem/rogenitor cells. Many of these interactions involve transmembrane integrin receptors. Integrins cluster in specific cell-matrix adhesions to provide dynamic links between extracellular and intracellular environments by activation of numerous signal transduction pathways which may influence cell behaviour profoundly by influence on both gene expression and post-transcriptional signalling cascade. In this review we introduced and discussed a number of extracellular and intracellular factors engaged in the transduction of signals induced by cell adhesion to its environment, including matrix components, extracellular proteolytic enzymes, integrins and non-receptor tyrosine kinases.

Sunday, April 24, 2011

Desperate Stroke Patient Goes to China

I guess they missed the scientific results showing that acupuncture doesn't do anything for stroke patients;
http://oc1dean.blogspot.com/2011/02/acupuncture-and-stroke-rehab.html
But then she uses option 2 to deny what might ruin her livelihood;
http://oc1dean.blogspot.com/2011/04/evidence-to-change-your-beliefs.html

http://www.huffingtonpost.com/nalini-chilkov/another-failure-of-medici_b_850234.htmlAt the age of 40 Devin Dearth's life changed forever. Devin, a vital and active loving husband, father, champion body builder and successful businessman suffered a massive hemmorhagic stroke at 5 a.m. while working out at his gym in a small midwestern town. The stroke damaged his brainstem so extensively that he was not expected to live. While medicine in America excels at high tech emergency medicine, it fails miserably at supporting recovery and the restoration of normal function and does almost nothing to sustain and nourish health over the long term. Devin had to go to China to get proper care. The care he needed was denied to him at home.

Devin has insurance. Great. Emergency services covered. Hospital care covered. Not so great, the rehabilitative care that Devin needed then and continues to need now is not covered by his insurance plan. His insurance company refused to pay for the helicopter that airlifted Devin from his very small town to a hospital in Lexington, Kentucky equipped to save his life. His family received a bill for $20,000 for the air ambulance. Without air transport, Devin would have died before ever getting to the hospital. You can't get approval at 5 a.m. in the morning for special services, but that is what is required. Welcome to health care in America.

After three weeks in intensive care, uncertain if he would survive, he could finally breathe on his own. This one time champion body builder then started rehabilitative care, for a limited amount of time only. He was approved for only 20 days of therapy after suffering a massive brain stem stroke He was making good progress and then the insurance coverage ran out. Devin, still debilitated, unable to walk, sit up, speak, feed or bathe himself was sent home. His family was now in charge. His wife and kids had to lift him from bed to wheelchair. His doctors and therapists knew he was progressing well and that he needed continued therapy. The insurance company said no. Coverage is no longer available. Go home.

9000 Needles: A Story of Hope, Courage and One Family's Unconventional Journey Towards Stroke Recovery is an award winning documentary film made by Devin's brother, David Dearth who refused to accept that his brother was going to go without the care he needed.

David searched worldwide and discovered a renowned Acupuncture Treatment Program for Stroke Rehabilitation at First Teaching Hospital of Tianjin University in China under the direction of Dr. Shi Xuemin. Devin's family has now been to China twice for several months at a time, where Devin has received exceptional care, daily acupuncture and physical therapy that allowed him to make dramatic progress.(And this dual therapy is why the conclusion is not supported) Stroke patients with the financial means to do so come here from all over the world. We watch as after only one acupuncture treatment Devin began to move his previously immobile leg on his own for the first time. After only weeks, he no longer drooled out of the side of his mouth. After several months he could sit up and was beginning to walk and to talk again.

According to the 2010 China Connection Global Health Report stroke patients receiving care at the Tianjin Hospital Program have better outcomes than patients treated with standard post stroke treatment in the U.S.

85 percent are able to walk without assistance (Only 51 percent of U.S. patients completing rehabilitatioin in the U.S. walk without assistance.)

95 percent regain almost complete knee flexion compared with 50 percent in the U.S.

98 percent return to live in their homes instead of long term care facilities while only 68 percent of U.S. stroke patients are able to live in their own homes.

According to Dr. Lee Schwamm, Vice Chairman of Neurology at Massachusetts General Hospital and Chairman of the American Stroke Association Program

None of these conclusions are valid since there is no scientific starting base for comparison.

Millions of dollars are spent in hospital and acute care settings where patients are moved out of rehab too quickly, often before they are ready. The insurance focus is on regaining minimum levels of independent living and the costs of rehab services are often in excess of $100,000 after insurance expires. This is staggering for most families. Millions of dollars are spent on acute care, but far too little is available for rehabilitation.

Tianjin Hospital patients also see decreases in blood pressure and cholesterol which are causes of stroke, reaping secondary benefits of this approach. Forty-six percent of Tianjin patients have reduced need for blood pressure and cholesterol lowering medications upon completing the program. This is significant because lowering high blood pressure and elevated cholesterol will decrease the risk of a second stroke.

9000 Needles is a story of an extraordinary family who went halfway around the world in search of healing.

9000 Needles is the story of a family's journey to an Acupuncture Stroke Treatment Program in China.

9000 Needles is the story of the power of Acupuncture to heal.

9000 Needles is the story of the failure of health care in America, demonstrating that insurance companies, not the patient's doctors, nor the patients themselves now decide who gets care and how much. It is the story of rationing by insurance companies. It is the story of an inhumane American healthcare system devoid of compassion and common sense. It is a story of how health care in America is a business devoid of heart, devoid of caring.

Devin suffered his stroke over three years ago. Each year he is offered a very limited amount of care by his insurance company. This means he will never have the opportunity to recover as much function as might be possible for him. When the allotment for care has been used up, it's over until next year. He is on his own. Patients who suffer severe strokes need ongoing and aggressive post stroke rehabilitative care. This care is not available to him. He lives in a small town in the Midwest. The closest acupuncturist is a 90 minute drive away. There is no facility where he can receive all the services he needs under one roof. And even if such a facility existed, his insurance would not cover his treatments. He cannot even get ongoing physical therapy and speech therapy throughout the year. His insurance company has decided he is a disposable person, no longer worthy of services. He can stay in his wheelchair as far as they are concerned.

One of the treatments that helps him the most, acupuncture, is not covered at all.

The film 9000 needles, which chronicles Devin's journey and treatment is emotionally moving. See it. As we watch, we share in the in the love and anguish of this family, the courage of this patient and the dedication and skill of his Chinese doctors. The film shows Devin's remarkable progress day by day, week by week, needle by needle, over 9000 needles in all.

This film makes us aware of the failures of our health care system, the power of Acupuncture and the importance of support, love and devotion from loved ones. Not only is it necessary to reform health care and reign in the abuses of the insurance industry in America, but this film compels us to bring acupuncture care into the American health care system as a standard of care for stroke patients. We will have to convince the insurance companies first.

I have practiced Acupuncture for three decades. In all these years I have never lost my sense of awe for the power of this elegant system of healing. This film reminded me once again of the profound results that are possible with Chinese Medicine. This is an exceptionally safe and cost effective ancient system that is now well integrated into modern medicine in China today. There is no reason it cannot be integrated with medicine in America. It is my hope that acupuncturists in America will be included in the health care teams of both in-patient and out-patient stroke treatment centers as part of our own American health care system.

In order for this to be so, we must all write to our legislators and to insurance companies and lobby for the inclusion of acupuncture in the American health care system and all insurance policies, including Medicare. We must also lobby for humane care in which the doctor decides how much and what type of care a patient needs. Insurance companies pay their own on staff doctors to deny care. These are not the doctors who should be making clinical decisions. We must put decision making back in the hands of the patient's doctors. We must allow patients to be part of the decision making process.

 Watch this film. Write to your legislators. Demand a humane health care system. Don't let insurance companies run our health care system and make heartless and mercenary decisions that rob us of our humanity and our dignity and the quality of our lives. Take action. Write a letter today.

For more information on 9000 Needles, visit the film's official website www.9000Needles.com. Set up a screening. Watch it with your friends, family and health care professionals.

NEWS FLASH 9000 Needles is showing in Los Angeles at the Regent Theater Hollywood on Thursday May 5th at 8:30 p.m. as part of the AWARENESS FESTIVAL

For more information on the Devin Dearth Foundation, visit www.devindearth.org.

For more information about visiting First Teaching Hospital of Tianjin University visit the website of China Connection Global Healthcare

Dr. Nalini Chilkov has been practicing Chinese Medicine and Acupuncture and Integrative Cancer Care for over thirty years.

And in those thirty years she hasn't looked scientifically at her work. In her blog reply to my criticism she didn't understand spontaneous recovery.

Clinical Trial of Cell Therapy for Stroke Disability

I'm not sure I like harvesting my bone marrow and injections directly into my brain give me the queasies.
But it does seem to be for chronic patients which I like.

http://www.disabled-world.com/medical/clinical-trials/stroke-disability.php#ixzz1KTCtDvvR

The Stanford University School of Medicine and SanBio Inc. today announced the initiation of a Phase 1/2a clinical trial testing the safety and efficacy of a novel allogeneic cell therapy product, SB623, on patients suffering from stable deficits resulting from previous stroke injuries. For details regarding this clinical trial, please refer to the Clinicaltials.gov website http://www.clinicaltrials.gov/ct2/show/NCT01287936.
It is still recruiting patients so if you are interested, contact them.

SB623 is derived from adult bone marrow and has shown safety and efficacy in rodent models of stroke disability. "SB623 represents a significant step forward in the development of regenerative therapies for the treatment of brain injury," said Keita Mori, SanBio CEO. "We are pleased to initiate a first-in-man study of SB623."

SB623 will be administered by intracranial injection into the damaged region of the brains of patients who have suffered an ischemic stroke. Product safety is the primary focus of the study but various measurements of efficacy will also be tested.

"This is a completely new approach to therapy for stroke victims," said Dr. Gary Steinberg, the Lacroute-Hearst Professor, Chairman of the Department of Neurosurgery, and Director of the Stanford Institute for Neuro-Innovation and Translational Neurosciences at the Stanford University School of Medicine, and Principal Investigator of the study. Sub-Investigator Dr. Neil Schwartz, Clinical Assistant Professor of Neurology, Stanford Stroke Center, said, "If successful, this cell therapy offers hope to otherwise permanently disabled patients."

About SB623: SB623 is a proprietary regenerative cell therapy consisting of cells derived from genetically engineered bone marrow stromal cells obtained from healthy adult donors. SB623 is implanted directly adjacent to the area damaged by stroke and functions by producing proteins that aid the healing process.

About SanBio: SanBio is a privately held San Francisco Bay Area biotechnology company focused on the discovery and development of new regenerative cell therapy products.

About Stanford: Stanford University Medical Center integrates research, medical education and patient care at its three institutions - Stanford University School of Medicine, Stanford Hospital & Clinics, and Lucile Packard Children's Hospital. For more information, please visit the Office of Communication & Public Affairs site at http://mednews.stanford.edu/.

For more information: www.san-bio.com

I do have some serious questions about injecting them next to the lesioned area. That area might have compromised blood supply and if it gets to the lesion itself it won't have a blood supply at all. How did they get around this problem? Have they tested if the injected cells even survive? Testing for non-impact could be a sucess if the cells die but don't cause problems as they die.

glove for rehabbing stroke victims

I'm glad others are working on this but this one assumes you have full extension and flexion control. with spasticity you would never be able to get a glove on. They mention other gloves costing $30,000 but I've never seen any others. Which goes to show you how pathetic stroke rehabilitation knowledge is distributed.
This here is the only glove I've found and I couldn't tell if it ever made it to production.
http://oc1dean.blogspot.com/2011/03/rehabilitation-glove-uses-artificial.html

http://www.gizmowatch.com/entry/students-develop-glove-for-rehabbing-stroke-victims/At present, the aging population has resulted in a new, very large market in developed countries. As a result more hi-tech medical assistance is in demand to effectively treat patients at home, and with as little pain and discomfort as possible. To extend help to stroke patients suffering physical impairments in the comfort of their homes, Southeast Asian Justin Tan has come forward with a biomedical sensor glove. The glove is designed to recover mobility in such patients through playing of video games.


Such patients who find it difficult to travel up and down to doctors and therapists might find relief to the fact that the sensor glove enables patients to train in the comfort of their own homes with bare minimum supervision, while still under the monitoring eye of the doctor. With the help of 3D models the patients themselves can keep an eye on their progress and on the other hand these reports are also getting transferred to the supervising doctor saving on the extra costs and inconvenience on travelling to and from the hospital.

The Sensor Glove was developed by four final-year McGill Mechanical Engineering undergraduates under the supervision of Professor Rosaire Mongrain on a design request from the Tan’s company Jintronix Inc. The device which effectively used up a great deal of intense research both by Jintronix and the student group can track the movements of the wrist, the palm and the index finger using several Inertial Measurement Units.

Similar gloves nonetheless exist in the current market and costs about $30,000, but the students used more accurate and less expensive sensors, dropping the manufacturing price to $1000. However, the company plans to introduce the product in the market at about $500, making it fairly accessible to stroke patients. To receive a better funding for further development, Tan has submitted the proposal to an independent not-for-profit organization dedicated to improving the health and well-being of people in developing countries.

Molecular Therapy for Improved Post-Stroke Motor Recovery

I wish I could tell from this if this was just promoting spontaneous recovery or for chronic recovery.
I wonder if sensory recovery and pre-motor recovery would fall into the same process?

http://www.medindia.net/news/Molecular-Therapy-for-Improved-Post-Stroke-Motor-Recovery-83986-1.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+allhealthnews+%28Medindia+Health+News%29


After the acute treatment window closes, the only effective treatment for stroke is physical/occupational therapy. Now scientists from Children's Hospital Boston report a two-pronged molecular therapy that leads to significant recovery of skilled motor function in a rat model of stroke. Their findings are reported April 20 in the Journal of Neuroscience.


By combining two molecular therapies—each known to promote some recovery on its own—the researchers achieved more nerve growth and a greater recovery of motor function than with either treatment alone. One therapy, inosine, is a naturally-present molecule that promotes nerve growth; the other is NEP1-40, an agent that counteracts natural inhibitors of nerve growth.

"When you put these two together, you get much stronger growth of new circuits than either one alone, and very striking functional improvements," says senior author Larry Benowitz, PhD, of the Children's Department of Neurosurgery.

Strokes in humans often damage the motor cortex on one side of the brain, interfering with skilled motor functions on the opposite side of the body. Led by Laila Zai, PhD, a postdoctoral fellow in Benowitz's lab and the study's first author, the researchers modeled this scenario by inducing strokes on one side of the rats' brains—specifically in a part of the motor cortex that controls forelimb movement. They then examined the rats' ability to perform a skilled reaching task—retrieving food—with the forelimb on the opposite side.

After 3 to 4 weeks, rats treated with both inosine and NEP1-40 could perform the task—which required coordinated movements of the paw and digits—with success rates equivalent to those before the stroke. Benowitz likens the complexity of this task to a person eating with utensils or operating a joystick.

Ablation in Ischemic Stroke

From wikipedia; Ablation is removal of material from the surface of an object by vaporization, chipping, or other erosive processes. The procedure here is lasers.
http://mediligence.com/blog/2011/04/20/ablation-in-ischemic-stroke/?utm_source=rss&utm_medium=rss&utm_campaign=ablation-in-ischemic-stroke


I like the idea, but I can see a problem with this, in the process of removing the clot it might just break it into smaller pieces meaning moving the stroke further down the artery. This is similar to trying to destroy an asteroid heading for the earth, if you don't vaporize it into very small pieces, the large pieces will still destroy the earth.
But even so it could be useful for those past the tPA time limit.

Ischemic stroke is a common condition: recent epidemiologic studies estimate that there are 750,000 strokes in the US each year, with an overall mortality rate of 27%. The annual cost of stroke in the US in 1993 was $30 billion, with the total lifetime cost per patient ranging from $90,000 to $228,000, depending on the type of stroke type.

Strokes may be one of two types. About 80% of strokes are ischemic, meaning that central nervous system (CNS) tissue dies when the blood supply leading to the brain is blocked by a blood clot. Brain cells that are not able to get enough blood and oxygen die, which may result in a disabling injury or death. About 20% of strokes are hemorrhagic, in which the rupture of abnormal blood vessel(s) produce locally disrupted tissue structure and produce the toxic effects of blood products, leading to cell death. Stroke is the leading cause of disability and the third leading cause of death among adults in the US.

There are various ways of classifying strokes. One of these, the Oxford Community Stroke Project classification, relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four classifications predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.

Current and Emerging Treatment Trends. For patients with ischemic stroke or transient ischemic attack caused by atherothromboembolism, immediate and long-term aspirin usually reduces the relative risk of recurrent stroke, MI, and death attributable to vascular causes. The choice of intervention for acute ischemic stroke depends upon a number of variables. The patient must be seen and evaluated within a limited temporal window (about 6 hours), and treatment decisions must be made rapidly. There are several parameters that may influence outcome, including blood pressure, serum glucose, supplementary oxygenation, and temperature. Three potential treatments are thrombolysis, anticoagulation, and revascularization; the pros and cons of each must be weighed by the treating physician.

In increasing numbers of primary stroke centers, pharmacologic thrombolysis (‘clot bustng’) with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery. However, the use of tPA in acute stroke is controversial. Some feel that the drug causes additional bleeding in up to 6% of patients who receive it.

Ablation in ischemic stroke. There are characteristics of thrombi (clots) which favor absorption of laser emissions and make the use of lasers quite attractive alternatives for breaking up a clot. These include the oxyhemoglobin of red blood cells, platelets, fibrin and water. Ultraviolet (excimer) lasers, visible lasers, Nd:YAG and Erbium:YAG lasers at peak absorption frequencies can achieve ablation and vaporization of thrombus.

The San Diego, CA, company PhotoThera is developing a non-invasive near-infrared laser device for treatment of ischemic stroke. The NeuroThera® Laser System is an investigational device that seeks to improve neurological outcomes via noninvasive delivery of near-infrared (NIR) laser energy called Transcranial Laser Therapy (TLT) into the brain. The system consists of a moveable console, a fiber optic cable, and a handpiece. A trained clinician uses the handpiece to direct the TLT to twenty predetermined treatment sites on the patient’s scalp. The total procedure time is approximately 2-3 hours. The company believes that the NeuroThera® Laser System may offer a compelling option for the treatment of acute ischemic stroke up to twenty-four hours following onset of stroke symptoms.

According to the PhotoThera, clinical evidence suggests that the TLT works by affecting the mitochondrial photoreceptor molecule in the red to near-infrared region, the enzyme, Cytochrome c Oxidase (CcO). This enzyme plays a key role in the mitochondrial electron transport chain. Energy absorption by CcO promotes electrons into an excited state. The resulting photo-excitation can result in a cascade of events that can promote and/or inhibit certain cellular pathways, leading to beneficial cellular effects. It is these cellular effects that may ultimately lead to clinical benefits such as improved recovery from a stroke, wound healing, tissue regeneration, decreased inflammation, or pain relief.