dreinke

Stroke Survivor - male
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  1. dreinke
    21 days of canoeing therapy. A 21 day canoe trip on the Eagle, Bell and Porcupine rivers in the Yukon and Alaska with Wilderness Inquiry. I wouldn't call it a vacation because we paddled every day and I was quite fatigued every day. I ended up being the only disabled person on the trip. Some learnings taken from the trip:
    1. The 3-legged folding camp stool was an absolute necessity, Crazy creek chairs are not feasible yet because of the problem of getting up off the ground. This way I could have a lap to set the food bowls and actually eat since my left hand is not usable yet for holding a bowl or plate without spilling.
    2. I left my AFO(Ankle Foot Orthotic) packed away for the whole trip. After 10 days I could tell that I was getting a heel strike with my left foot, which the AFO prevents me from doing. Walking over extremely rough ground strengthened my ankle muscles but I could tell I was close to the edge of getting an ankle sprain which really slowed down my walking.
    3.By the time the end of the trip came I was able to lift my left foot over the gunwale of the canoe without having someone else lift it out for me.
    4. kneeling while in tent. This was pretty much a no-no for any of the rockier sites because I still only have a three-point stance, The left arm and hand still collapse too easily.
    5. Moving around in the tent. It was a good thing we had 4-person tents, as I was getting ready for bed I would take up 2/3rds to 3/4ths of the tent as I flailed around getting the sleeping pad and bag ready.
    6.Sleeping bag. Good thing it only got cold on two of the nights. I was able this year to get the sleeping bag zipped all the way up but not able to cinch the drawstring. So I draped my pile jacket over my shoulders. The second night I knew it was going to be cold so I just wore the jacket to bed.
    7.Kneeling to paddle in boat. Because these were Pak-Boats they had aluminum tube frames that made it difficult to get my feet into the correct position. In two hours my knees and ankles would be dying. A lot of this was because I couldn't adjust my position after I got in because I couldn't get my left arm/hand down on the gunwale to push myself into a slightly different position.
    8. Paddling on the left side. The first day I used the velcro hand wrap to attach my left hand to the paddle shaft. This only worked somewhat well. This was because the lower hand on the paddle shaft slides along it until the paddle is planted in the water. The rest of the trip I didn't use the velcro thing. I could manage about 5-6 paddle strokes before I had to put the paddle shaft on the gunwale and pull the shaft out so the hand was lower down on the shaft. I probably only paddled on the left side maybe 10% of the time due to this problem. Paddling on this side required a lot of concentration and looking at the hand to make sure it was still positioned correcly. Which didn't allow me to look at the scenery.
    9. Paddling on the right side. I never tried velcroing my left hand to the t-grip because I observed how my right hand worked by clasping and upclasping the grip on every stroke. I ended up prying my hand open enough to force the T-grip in and curled the thumb around the end. I could paddle anywhere from 3-70 strokes before having to reposition the hand again. The paddle stroke still left a lot to be desired, I was never able to get the full extension on the left arm to get a vertical shaft but it was better than last year where the left hand didn't get off the chest. This year it was at least 10-12 inches out from the chest. Paddling on this side was much better, mainly because I could do it without full concentration, allowing me to see the scenery and talk to other paddlers.
    10. Some of our participants calculated that we would need to do around 500,000 canoe strokes. We did around 600 miles, averaging about 30 miles per day in 7-8 hours.
    11.finger intrinsics
    First some definitions. Intrinsic muscles are those completely contained within the hand/wrist unit. The extrinsic muscles are contained in the forearm and connected to the hand by tendons and provide
    most of the power and range of motion of the joints of the hand.
    Intrinsics stabilize the hand in fine motor tasks.
    I have been working a lot on passively flexing and unflexing my fingers which are the extrinsic muscles, flexors and extensors but have not been working on the intrinsics mainly because I think I need to get the extrinsics working first and I don't know how to start engaging them.
    On my canoe trip on the day I ripped the skin off my left palm we were paddling downstream with an upstream wind of 20-30 mph and I was paddling as best as I could on the right side with my left hand gripping the t-grip. My extension of my left arm was pretty poor, only able to get it out maybe 10-12 inches from my chest. We beat against the wind for a couple of hours until we were all forced ashore. After some consultations it was decided to set up camp, sleep and start paddling again in the evening when the wind usually dies down. So we slept from 5-10 pm and started again at midnight paddling until 3 am(24 hour daylight is wonderful at this latitude) I didn't sleep too well because the left hand was aching a lot. I think what occurred is that I totally overworked my finger flexors and the intrinsic muscles in the hand started firing to try to help hold the paddle. This was a wonderful occurence to find out about since it may lead me to a way to get the intrinsics firing again.
    12. Tiredness or being knackered as our English friends say. During the rest stops/lunch breaks I could easily fall asleep. This is somewhat of a conundrum since according to my latest physical I have a resting heart rate of 53, which at my age of 53 puts me in the athlete category. If I am an athelete, why am I so tired all the time?
    13. Setting up tents was a problem because the tents had sleeves for the poles, not conduciveto one-handed help.
    On the river we saw black bears, fox, moose, bald eagles, sandhill cranes.
    We paddled past the 25,000 acre Porcupine River forest fire, saw some complete trees go up in flames.
  2. dreinke
    In order for me to recover I will have to neuroplastically modify my brain and in order to do that I will probably have to fail millions of times for each muscle control. As long as I can get up again and fail all over again. Albert Einstein has a quote 'Insanity: doing the same thing over and over again and expecting different results.' Does this imply that all stroke survivors that believe in using neuroplasticity are insane for that belief? Or should we just ignore Einstein because we are smarter than him?
    I will succeed at failing.
    Dean
     
  3. dreinke
    Therapists ask me what therapies have worked in my rehab. I can understand why because they want to add that therapy to their roster of abilities.
     
    Survivors ask me what exercises worked in my rehab. They are hoping that if they can just find the right exercise to do they will recover.
     
    Both of these questions are invalid because the first thing to understand is how recovery occurs and where you are in the process. Until you know that can you select a therapy or exercise to work on. If you are working on penumbra recovery in the first 6-12 months then you take the little pieces of movement you do have and keep extending them longer and farther. If you are trying to get back functions that were in the dead brain area then you need to work on neuroplastic therapies that move those functions; try passive movement, mental imagery, thermal stimulation.
     
     
     
     
    Until we get the whole concept of what needs to be done to recover changed from this specific therapy or exercise will we finally come up with a therapy model for stroke rehab. So don't enable the doctors and therapists by accepting a therapy or exercise without them specifying how it meets the protocol of recovery. See my blog on restructure stroke rehab model at
    http://oc1dean.blogspot.com/2010/11/restructure-stroke-rehab-model.html and theoretical basis of stroke rehab for my ideas at
    http://oc1dean.blogspot.com/2010/11/theoretical-basis-of-stroke-rehab.html. I actually think they are pretty good.
  4. dreinke

    3 reasons I survived

    By dreinke,

    I think there were 3 reasons I survived my event.
     
    1. I was in fantastic physical shape. I had just completed a 6 day whitewater canoeing trip in Canada, 23 miles falling 1100 feet, only 5 portages. One of those being 1.5 miles long. On the Dog River Ontario by Wawa. Here are some pictures, I am in the red canoe, red helmet. Dog River album; http://www.rapidsriders.net/gallery2/v/dog2007/
     
     
    2. My brain reserve was pretty substantial.
     
    http://www.physorg.com/news154620279.html
     
    3. I received the clot busting drug tPA within 1 hour. Even so the dead area was substantial. I was listed in critical condition the first day. 3 years later my parents finally told me that when they left the hospital that first night they were positive that I wouldn't survive the night. Of course I had no idea I was that bad. And my doctors never told me anything
  6. dreinke

    split-belt treadmill

    By dreinke,

    Physical Therapists Use A Split-belt Treadmill To Help Stroke Patients Walk More Easily
    http://www.sciencedaily.com/videos/2008/1207-retrain_your_brain_after_stroke.htm
    The other problem is that it looks like it will be very expensive so that few clinics will be able to afford them, similar to Lokomat training. Luckily I moved to a clinic with the Lokomat and thought that using it was probably the most helpful in getting somewhat of a normal gait.
    When the legs move at speeds different from one another, the brain receives an error signal and the brain and nervous system use the feedback to adjust. The cerebellum recalls this message even after the treadmill stops and for a few minutes, stroke patients can walk easier.
    http://www.ncbi.nlm.nih.gov/pubmed/21084921
    BACKGROUND AND PURPOSE: Even after rehabilitation, many individuals with strokes have residual gait deviations and limitations in functional walking. Applying the principles of motor adaptation through a split-belt treadmill walking paradigm can lead to short-term improvements in step length asymmetry after stroke. The focus of this case study was to determine whether it is possible to capitalize on these improvements for long-term gain.
     
    CASE DESCRIPTION: The participant was a 36-year-old woman who was 1.6 years poststroke. She had a slow walking speed and multiple specific gait deviations, including step length asymmetry.
     
    INTERVENTION: The participant walked on a split-belt treadmill 3 d/wk for 4 weeks, with the paretic leg on the slower of the two treadmill belts. The goal was 30 minutes of split-belt treadmill walking each day, followed by overground walking practice to reinforce improvements in step length symmetry.
     
    OUTCOMES: With training, step length asymmetry decreased from 21% to 9% and decreased further to 7% asymmetry 1 month after training. Self-selected walking speed increased from 0.71 m/s to 0.81 m/s after training and 0.86 m/s 1 month later. Percent recovery, measured by the Stroke Impact Scale (SIS), increased from 40% to 50% posttraining and to 60% 1 month later.
     
    DISCUSSION: Improvements in step length symmetry were observed following training and these improvements were maintained 1 month later. Concomitant changes in clinical measures were also observed, although these improvements were modest. The outcomes for this participant are encouraging given the relatively small dose of training. They suggest that after stroke, short-term adaptation can be capitalized on through repetitive practice and can lead to longer-term improvements stroke.
     
     
     
    There should be a way to duplicate this without having the split-belt treadmill but no one will research this since nothing could be sold as part of it.
  7. dreinke
    I was having an Q&A at a stroke forum on Alzheimers and the worry was getting it and what possibly could prevent that from happenning. I responded with this research.
     
     
    Caffeine Treats Alzheimer's?
    Something from one of the newfeeds I subscribe to. Ivanhoe is only free for 7 days so I'll have to copy them from now on.
    http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=21856
    try this instead
    http://www.everydayhealth.com/alzheimers/specialists/coffee-for-alzheimers-prevention.aspx
     
    This just came in.
    Upping your coffee intake 'doubles the risk of a stroke'
     
    http://www.dailymail.co.uk/health/article-1337684/Upping-coffee-intake-doubles-risk-stroke.html?ito=feeds-newsxml
    So do you want to prevent Alzheimers but have the greater possibility of a stroke? In my opinion/case my stroke was not a bleed so I will take the extra risk, anyway I need the caffeine in order to function during the day. This is the perfect question to ask your doctor and see if they are following the latest news. :Dr_Evil: :juggle:
  8. dreinke
    Since I think too much about all things stroke related I came across nanoparticles and tried to envision what use they could be for stroke rehab.
    They have several interesting abilities;
    1. They can cross the blood-brain barrier
    http://www.ncbi.nlm.nih.gov/pubmed/16154222
    2. They are already used to treat thrombi in parts of the body.
    http://www.springerlink.com/content/vj1528n166147410/
    3. They can be magnetically directed.
    http://www.redorbit.com/news/video/health/4/magnetic_nanoparticles_remotely_control_neurons_and_animal_behavior/32320/
    For our purposes they could be used to deliver a clot-busting drug directly to the clot using the magnetic properties to guide it. And since the amount could be sized to the clot size the risk of bleeding could be lowered significantly and the 3-4.5 hour window for tPA ignored.
    The more interesting delivery mechanism would be to deliver neuronal growth factors, c3a peptides http://www.news-medical.net/news/20091123/C3a-peptide-regulates-the-generation-of-new-nerve-cells-in-the-brain-Study.aspx and NOGO receptors http://www.nature.com/nature/links/010118/010118-1.html to the penumbra and dead brain areas. Or deliver stem cells to the most likely place for them to survive and start working.
    And after we deliver these growth factors or stem cells we can use connectomics to find out if they are working as we expected.
    http://oc1dean.blogspot.com/2010/11/wiring-diagram-of-brain.html
     
    This could be incredibly useful for those who need some magical properties in order to recover, not all of us are willing to spend the rest of our lives working on recovery. :yadayada: :2cents:
  9. dreinke
    This was great because if we can get neurogenesis to work in the highest brain centers we might be able to correct most brain problems. And I could increase my brain reserve again.
    http://oc1dean.blogspot.com/2010/09/brain-reserve.html
    The news from 1999, what the hell takes so long to get this important information disseminated? Every PMR doctor and neurologist should have known about this within one week of publication. Where is the social network for doctors?
     
    http://www.princeton.edu/pr/news/99/q4/1014-brain.htm
    News from
    PRINCETON UNIVERSITY
    Office of Communications
    Stanhope Hall, Princeton, New Jersey 08544-5264
    Telephone 609-258-3601; Fax 609-258-1301
     
    Contact: Steven Schultz sschultz@princeton.edu (609) 258-5729
    Date: October 14, 1999
     
     
    Scientists Discover Addition of New Brain Cells in Highest Brain Area
    <b>Finding reverses long-held beliefs and has implications for designing therapies
    </b>PRINCETON, N.J. -- In a finding that eventually could lead to new methods for treating brain diseases and injuries, Princeton scientists have shown that new neurons are continually added to the cerebral cortex of adult monkeys. The discovery reverses a dogma nearly a century old and suggests entirely new ways of explaining how the mind accomplishes its basic functions, from problem solving to learning and memory.
     
    Elizabeth Gould and Charles Gross report in the Oct. 15 issue of Science that the formation of new neurons or nerve cells -- neurogenesis -- takes place in several regions of the cerebral cortex that are crucial for cognitive and perceptual functions. The cerebral cortex is the most complex region of the brain and is responsible for highest-level decision making and for recognizing and learning about the world. The results strongly imply that the same process occurs in humans, because monkeys and humans have fundamentally similar brain structures.
     
    "This is an absolutely novel result," says William T. Greenough, director of the neuroscience program at the University of Illinois' Beckman Institute. "These data scream for a reanalysis of human brain development." :You-Rock:
     
    The traditional view among neuroscientists has been that the primate brain is different from other organs in that it is not capable of repairing itself or growing new cells, that no new neurons are added to the brain in maturity. This dogma has gradually eroded in the last decade as evidence accumulated for neurogenesis in several evolutionarily older parts of the brain such as the olfactory system and the hippocampus, which is believed to play role in memory formation. In the last year, Gould and her colleagues helped this erosion by proving neurogenesis in the hippocampus of several types of monkeys.
    :goodjob: :juggle:
    The new finding in the cerebral cortex is much more dramatic, the Princeton team believes, because the cortex is the largest and most advanced part of the brain. After the discoveries in the hippocampus, says Gould, most scientists remained convinced that adult neurogenesis was an anomaly and could not be found in the newer, higher parts of the brain. They believed, for example, that the brain relies on a stable structure for storing memories.
     
    "People thought: If the cerebral cortex is important in memory, how could it change?" says Gross. "In fact the opposite view is at least as plausible: if memories are formed from experiences, these experience must produce changes in the brain."
     
    Although practical applications of the discovery could be years, even decades away, the results suggest that scientists may one day exploit natural repair mechanisms to treat brain injuries or diseases, such as Alzheimer’s and Parkinson’s. The Princeton scientists found that the new neurons were formed in the lining of the cerebral ventricles, large fluid-filled structures deep in the center of the brain, and then migrated considerable distances to various parts of the cerebral cortex. This type of migration, which had never been seen before, may prove useful in guiding therapeutic cells to desired sites in the brain that have lost their functioning neurons through disease or injury.
     
    "It shows there are natural mechanisms in the brain that, someday, might be harnessed for therapeutic purposes to replenish damaged areas of the brain," says Gould. For now, that possibility remains speculative. Such work would fall to other scientists who have expertise in human diseases.
     
    Greenough, of the Beckman Institute, says the study also has major implications for theories about how the brain develops. In particular, it casts doubt on the notion that the all-important time for brain development is from zero to three years of age, and raises the likelihood that experiences through adolescence and adulthood can affect the physical structure of the brain. "If what they have shown holds true for all primates, including humans, it means we really need to rewrite the book on brain development and the way that experience can affect the brain," says Greenough.
     
    The Gould and Gross discovery also may require neuroscientists to draw a less bold distinction between the brains of humans and other animals, says Fernando Nottebohm of Rockefeller University. Scientists have observed neurogenesis in birds and rats for many years, but assumed that as evolution advanced and mental capacities increased, the brain supported less and less neurogenesis. "What you can say now is that the primate brain is more like that of songbirds," says Nottebohm, who believes that theories of the brain have been too "human-centric."
     
    "It is a very interesting paper," Nottebohm says. "And I think it will do the field a great deal of good."
     
    For their experiments, Gould and Gross took advantage of the unique properties of a chemical known as BrdU. When cells are exposed to BrdU during cell division, the chemical becomes incorporated into the DNA of newly formed cells. The researchers injected BrdU into rhesus monkeys, whose brain structure is fundamentally similar to that of humans. Then, at intervals ranging from two hours to seven weeks, they looked for evidence of the chemical in neurons in the cerebral cortex. In all cases, there were neurons with BrdU in their DNA, which showed that those cells had to have been formed after the BrdU injection.
     
    The earliest cells, found in the walls of the ventricles and then migrating toward the cortex, were not yet mature. By the time they reached the neocortex -- a matter of days -- they had developed into mature neurons. In a final test, the researchers showed that the cells extended axons, the long, thin extensions of neurons that send messages to other neurons. They injected a chemical tracer into the brains of several of the animals a few weeks after the BrdU injections. The tracer has the property of traveling from the end of an axon back to the body of the neuron. An examination of the animals’ brains showed neurons that had both labels, the BrdU and the tracer, suggesting that the new cells had formed working axons and were participating in the functional circuitry of the brain.
     
    Within the cerebral cortex, the researchers found neurogenesis in three areas: 1) the prefrontal region, which controls executive decision making and short-term memory; 2) the inferior temporal region, which plays a crucial role in the visual recognition of objects and faces, and 3) the posterior parietal region, which is important for the representation of objects in space.
     
    Interestingly, there was no sign of neurogenesis in a fourth area, the striate cortex, which handles the initial, and more rudimentary, steps of visual processing. That contrast suggests that neurogenesis may play a role in performing higher brain functions. Virtually all theories of learning and memory hold that memories are formed by modifications at the synapse, which is the transmission junction between neurons. On the basis of the new findings, it is now conceivable that the introduction of new neurons into the circuitry of the brain may play a role in memory.
     
    Gould and Gross emphasize that any ideas about the functions of the new neurons are highly speculative. But the fact that there is neurogenesis in the cognitive and executive portions of the brain opens vast new areas that can be explored.