Human brain treats prosthetic devices as part of the body

Contact: Jyoti Madhusoodanan jmadhusoodanan@plos.org 415-568-4545 Public Library of Science

People with spinal cordPeople with spinal cord injuries show strong association of wheelchairs as part of their body, not extension of immobile limbs injuries show strong association of wheelchairs as part of their body, not extension of immobile limbs.

The human brain can learn to treat relevant prosthetics as a substitute for a non-working body part, according to research published March 6 in the open access journal PLOS ONE by Mariella Pazzaglia and colleagues from Sapienza University and IRCCS Fondazione Santa Lucia of Rome in Italy, supported by the International Foundation for Research in Paraplegie.

The researchers found that wheelchair-bound study participants with spinal cord injuries perceived their body’s edges as being plastic and flexible to include the wheelchair, independent of time since their injury or experience with using a wheelchair. Patients with lower spinal cord injuries who retained upper body movement showed a stronger association of the wheelchair with their body than those who had spinal cord impairments in the entire body.

According to the authors, this suggests that rather than being thought of only as an extension of the immobile limbs, the wheelchairs had become tangible, functional substitutes for the affected body part. As Pazzaglia explains, “The corporeal awareness of the tool emerges not merely as an extension of the body but as a substitute for, and part of, the functional self.”

Previous studies have shown that people with prosthetic devices that extend or restore movement may make such tools part of their physical identity, but whether this integration was due to prolonged use or a result of altered sensory input was unclear. Based on the results of this study, the authors suggest that it may be the latter, as the brain appears to continuously update bodily signals to incorporate these tools into a sense of the body. The study concludes that this ability may have applications in rehabilitation of physically impaired people.

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Citation: Pazzaglia M, Galli G, Scivoletto G, Molinari M (2013) A Functionally Relevant Tool for the Body following Spinal Cord Injury. PLOS ONE 8(3): e58312.doi:10.1371/journal.pone.0058312

Financial Disclosure: Funded by the International Foundation for Research in Paraplegie (IRP, P133) and EU Information and Communication Technologies Grant (VERE project, FP7-ICT-2009-5, Prot. Num. 257695. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interest Statement: The authors have declared that no competing interests exist.

PLEASE LINK TO THE SCIENTIFIC ARTICLE IN ONLINE VERSIONS OF YOUR REPORT (URL goes live after the embargo ends).

First evidence that chitosan could repair spinal damage

2010 study posted for filing

Contact: Kathryn Knight kathryn@biologists.com 44-078-763-44333 The Company of Biologists

Chitosan offers hope for spinal injury patients

This release is available in Chinese.

Richard Borgens and his colleagues from the Center for Paralysis Research at the Purdue School of Veterinary Medicine have a strong record of inventing therapies for treating nerve damage. From Ampyra, which improves walking in multiple sclerosis patients to a spinal cord simulator for spinal injury victims, Borgens has had a hand in developing therapies that directly impact patients and their quality of life. Another therapy that is currently undergoing testing is the use of polyethylene glycol (PEG) to seal and repair damaged spinal cord nerve cells. By repairing the damaged membranes of nerve cells, Borgens and his team can restore the spinal cord’s ability to transmit signals to the brain. However, there is one possible clinical drawback: PEG’s breakdown products are potentially toxic. Is there a biodegradable non-toxic compound that is equally effective at targeting and repairing damaged nerve membranes? Borgens teamed up with physiologist Riyi Shi and chemist Youngnam Cho, who pointed out that some sugars are capable of targeting damaged membranes. Could they find a sugar that restored spinal cord activity as effectively as PEG? Borgens and his team publish their discovery that chitosan can repair damaged nerve cell membranes in The Journal of Experimental Biology on 16 April 2010 at http://jeb.biologists.org.

Having initially tested mannose and found that it did not repair spinal cord nerve membranes, Cho decided to test a modified form of chitin, one of the most common sugars that is found in crustacean shells. Converting chitin into chitosan, Cho isolated a segment of guinea pig spinal cord, compressed a section, applied the modified chitin and then added a fluorescent dye that could only enter the cells through damaged membranes. If the chitosan repaired the crushed membranes then the spinal cord tissue would be unstained, but if the chitosan had failed, the spinal cord neurons would be flooded with the fluorescent dye. Viewing a section of the spinal cord under the microscope, Cho was amazed to see that the spinal cord was completely dark. None of the dye had entered the nerve cells. Chitosan had repaired the damaged cell membranes.

Next Cho tested whether a dose of chitosan could prevent large molecules from leaking from damaged spinal cord cells. Testing for the presence of the colossal enzyme lactate dehydrogenase (LDH), Borgens admits he was amazed to see that levels of LDH leakage from chitosan treated spinal cord were lower than from undamaged spinal cords. Not only had the sugar repaired membranes at the compression site but also at other sites where the cell membranes were broken due to handling. And when the duo tested for the presence of harmful reactive oxygen species (ROS), released when ATP generating mitochondria are damaged, they found that ROS levels also fell after applying chitosan to the damaged tissue: chitosan probably repairs mitochondrial membranes as well as the nerve cell membranes.

But could chitosan restore the spinal cord’s ability to transmit electrical signals to the brain through a damaged region? Measuring the brain’s response to nerve signals generated in a guinea pig’s hind leg, the duo saw that the signals were unable to reach the brain through a damaged spinal cord. However, 30·min after injecting chitosan into the rodents, the signals miraculously returned to the animals’ brains. Chitosan was able to repair the damaged spinal cord so that it could carry signals from the animal’s body to its brain.

Borgens is extremely excited by this discovery that chitosan is able to locate and repair damaged spinal cord tissue and is even more enthusiastic by the prospect that nanoparticles of chitosan could also target delivery of neuroprotective drugs directly to the site of injury ‘giving us a dual bang for our buck,’ says Borgens.

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IF REPORTING ON THIS STORY, PLEASE MENTION THE JOURNAL OF EXPERIMENTAL BIOLOGY AS THE SOURCE AND, IF REPORTING ONLINE, PLEASE CARRY A LINK TO: http://jeb.biologists.org

REFERENCE: Cho, Y., Shi, R. and Borgens, R. B. (2010). Chitosan produces potent neuroprotection and physiological recovery following traumatic spinal cord injury. J. Exp. Biol. 213, 1513-1520.

This article is posted on this site to give advance access to other authorised media who may wish to report on this story. Full attribution is required, and if reporting online a link to jeb.biologists.com is also required. The story posted here is COPYRIGHTED. Therefore advance permission is required before any and every reproduction of each article in full. PLEASE CONTACT permissions@biologists.com

THIS ARTICLE APPEARS IN THE JOURNAL OF EXPERIMENTAL BIOLOGY ON: 16 April 2010. EMBARGOED UNTIL FRIDAY, 16 April 2010, 00.15 HRS EDT (05:15 HRS BST)

Medical Examiner keeps thousands of brains for ‘tests’ families call needless

  • By SUSAN EDELMAN
  • Last Updated:  12:56 PM, October 28, 2012
  • Posted: 10:30 PM, October 27, 2012

EXCLUSIVE

It’s the great brain robbery.

The city Medical Examiner’s Office has kept the brains of more than 9,200 deceased New Yorkers — from the elderly to newborns — in the past eight years, records obtained by The Post show.

The stunning revelation comes as three families publicly question whether the city is yanking brains so rookie pathologists can “practice,” for scientists’ experiments, or for no good reason at all.

“Vasean’s organs were removed for ‘testing’ without any investigative or medical necessity,” charges a suit by the family of Vasean Alleyne, an 11-year-old Queens boy killed by a drunken driver. Months after his burial, his mom was shocked to read in the autopsy report that her son’s brain and spinal cord had been taken.

Brooklyn mom Cindy Bradshaw was stunned to learn she had buried her stillborn son, Gianni, without his brain. The ME kept it — though an autopsy found his death was caused by an abnormality in her umbilical cord and placenta.

“Do they really want to know what happened to the person, or are they just experimenting?” Bradshaw asked.

“The death had nothing to do with the brain,” said her lawyer, Daniel Flanzig. “It’s unconscionable — and unlawful — for the Medical Examiner not to return it to the family for a complete burial.”

Others suspect organs are used as a training tool.

“I think they collect brains to allow a new neuropathologist to practice on various body parts,” said Anthony Galante, a lawyer for the family of Jesse Shipley, 17, who was killed in a car crash in 2005. Friends gawked at his brain in a labeled jar on a class trip to the Staten Island morgue — two months after his funeral.

“When it comes to investigating deaths, the law gives the Medical Examiner’s Office broad authority, including the retention of tissue at autopsy for further testing,” said a city Law Department spokeswoman, declining further comment. The ME also declined to comment.

In November 2010, a judge ruled the city must notify families of seized organs. The ME began giving kin a form with three options: wait to claim the body pending “further testing” of organs; collect the organs later; or just let the city dispose of the organs.

The disposal method is not mentioned. But an internal ME document spells it out: “Medical waste is incinerated. Please do not tell NOK (next-of-kin) that unclaimed organs are ‘cremated. . .’ ”

Under The Post’s Freedom of Information Law request, the ME gave a list of 9,200 brains and 45 spinal cords removed between Nov. 1, 2004, and July 1, 2012. Some 7,700 brains were taken before the notifications began.

The ages of the decedents range from 99 to fetuses.

Brains harden in formaldehyde several weeks before they can be “cut” by scientists.

In Staten Island, ME staff delayed tests for “months” until a half-dozen brains were ready — to make a pathologist’s trip from Manhattan “worth his while,” according to testimony in the Shipley case.

But Jesse’s death was no mystery: “He was killed in an auto accident. His skull had multiple fractures,” lawyer Galante said.

Two days after Bradshaw’s son was stillborn, April 28, an ME pathologist told her, “The autopsy was complete and I could pick him up any time,” she said. The cause of death was a pregnancy complication, the autopsy confirmed. “He was a healthy baby.”

But the ME called back hours after the May 4 funeral.

“I forgot to tell you, the brain is still here,” the pathologist said.

The only explanation given Bradshaw, she said: “It’s routine.”

susan.edelman@nypost.com

http://www.nypost.com/p/news/local/city_sitting_on_brains_cTMsOuGmPkRRDxBQm0IvNJ

Active ingredients in marijuana found to spread and prolong pain : Transforms transient normal pain into persistent chronic pain

2009 study posted for filing

Contact: Jim Kelly
jpkelly@utmb.edu
409-772-8791
University of Texas Medical Branch at Galveston

Research has implications for medical use of drug and concepts of chronic pain

GALVESTON, Texas — Imagine that you’re working on your back porch, hammering in a nail. Suddenly you slip and hit your thumb instead — hard. The pain is incredibly intense, but it only lasts a moment. After a few seconds (and a few unprintable words) you’re ready to start hammering again.

How can such severe pain vanish so quickly? And why is it that other kinds of equally terrible pain refuse to go away, and instead torment their victims for years?

University of Texas Medical Branch at Galveston researchers think they’ve found at least part of the answer—and believe it or not, it’s in a group of compounds that includes the active ingredients in marijuana, the cannabinoids. Interestingly enough, given recent interest in the medical use of marijuana for pain relief, experiments with rodents and humans described in a paper published in the current issue of Science suggest these “endocannabinoids,” which are made within the human body, can actually amplify and prolong pain rather than damping it down.

“In the spinal cord there’s a balance of systems that control what information, including information about pain, is transmitted to the brain,” said UTMB professor Volker Neugebauer, one of the authors of the Science article, along with UTMB senior research scientist Guangchen Ji and collaborators from Switzerland, Hungary, Japan, Germany, France and Venezuela. “Excitatory systems act like a car’s accelerator, and inhibitory ones act like the brakes. What we found is that in the spinal cord endocannabinoids can disable the brakes.”

To get to this conclusion, the researchers began by studying what happened when they applied a biochemical mimic of an endocannabinoid to inhibitory neurons (the brakes, in Neugebauer’s analogy) on slices of mouse spinal cord. Electrical signals that would ordinarily have elicited an inhibitory response were ignored. They then repeated the procedure using slices of spinal cord from mice genetically engineered to lack receptors where the endocannabinoid molecules could dock, and found that in that case, the “brakes” worked. Finally, using electron microscopy, they confirmed that the receptors were in fact on inhibitory, not excitatory neurons. Endocannabinoids docking with them would suppress the inhibitor neurons, and leave pain signals with a straight shot to the brain.

“The next step was to make the leap from spinal slices to test whether this really had anything to do with pain,” Neugebauer said. Using anesthetized rats, he recorded the spinal cord electrical activity produced by an injection in the hindpaw of capsaicin– a chemical found in hot peppers that produces a level of pain he compared to a severe toothache. Although the rats were unconscious, pain impulses could be detected racing up their spinal cords. What’s more, formerly benign stimuli now generated a significant pain response — a response that stopped when the rats were treated with an endocannabinoid receptor blocker.

“Why was this non-painful information now gaining access to the spinal “pain” neurons?” Neugebauer said. “The capsaicin produced an overstimulation that led to the peripheral nerves releasing endocannabinoids, which activated receptors that shut down the inhibitor neurons, leaving the gates wide open.”

Finally, the researchers recruited human volunteers to determine whether a compound that blocked endocannabinoid receptors would have an effect on the increased sensitivity to pain (hyperalgesia) and tendency for normally non-painful stimuli to induce pain (allodynia) often reported in areas of the body near where acute pain had been inflicted. In this case, the researchers induced pain by passing electricity through the volunteers’ left forearms, with the intensity of the current set by each volunteer to a 6 on a scale of 1 to 10. At a second session a month later, the volunteers who had received the receptor blocker showed no reduction in perceived acute pain, but had significantly less hyperalgesia and allodynia — a result that matched up well with the endocannabinoid hypothesis.

“To sum up, we’ve discovered a novel mechanism that can transform transient normal pain into persistent chronic pain,” Neugebauer said. “Persistent pain is notoriously difficult to treat, and this study offers insight into new mechanisms and possibly a new target in the spinal cord.”

It also raises questions about the efficacy of marijuana in relieving acute pain, given that endocannabinoids and the cannabinoids found in marijuana are so biochemically similar. “If you had a toothache, you probably wouldn’t want to treat it with marijuana, because you could actually make it worse,” Neugebauer said. “Now, for more pathological conditions like neuropathic pain, where the problem is a dysfunction within the nerves themselves and a subsequent disturbance throughout the nervous system that’s not confined to the pain system, marijuana may be beneficial. There are studies that seem to show that. But our model shows cannabinoids over-activating the pain system, and it just doesn’t seem like a good idea to further increase this effect.”

Social contact can ease pain related to nerve damage, animal study suggests

Contact: Adam Hinzey
Adam.Hinzey@osumc.edu
Ohio State University

COLUMBUS, Ohio – Companionship has the potential to reduce pain linked to nerve damage, according to a new study.

Mice that were paired with a cage-mate showed lower pain responses and fewer signs of inflammation in their nervous system after undergoing surgery that affected their nerves than did isolated mice, suggesting that the social contact had both behavioral and physiological influences.

The social contact lowered the pain response and signs of inflammation even in animals that had experienced stress prior to the nerve injury.

These mice experienced a specific kind of nerve-related pain called allodynia, which is a withdrawal response to a stimulus that normally would not elicit a response – in this case, a light touch to the paw.

“If they were alone and had stress, the animals had increased inflammation and allodynia behavior,” said Adam Hinzey, a graduate student in neuroscience at Ohio State University and lead author of the study. “If the mice had a social partner, both allodynia and inflammation were reduced.”

More than 20 million Americans experience the nerve pain known as peripheral neuropathy as a consequence of diabetes or other disorders as well as trauma, including spinal cord injury. Few reliable treatments are available for this persistent pain.

“A better understanding of social interaction’s beneficial effects could lead to new therapies for this type of pain,” Hinzey said.

Hinzey described the research during a press conference Monday (10/15) in New Orleans at Neuroscience 2012, the annual meeting of the Society for Neuroscience.

In the study, researchers paired one group of mice with a single cage-mate for one week while other mice were kept socially isolated. For three days during this week, some mice from each group were exposed to brief stress while others remain nonstressed.

Researchers then performed a nerve surgery producing sensations that mimic neuropathic pain on one group of mice and a sham procedure that didn’t involve the nerves on a control group.

After determining a baseline response to a light touch to their paws, researchers tested all groups of mice behaviorally for a week after the surgery. Mice that had lived with a social partner, regardless of stress level, required a higher level of force before they showed a withdrawal response compared to isolated mice that were increasingly responsive to a lighter touch.

“Animals that were both stressed and isolated maintained a lower threshold – less force was needed to elicit a paw withdrawal response. Animals that were pair housed and not stressed withstood a significantly greater amount of force applied before they showed a paw withdrawal response,” Hinzey said. “Within animals that were stressed, pairing was able to increase the threshold required to see a withdrawal response.”

He and colleagues examined the animals’ brain and spinal cord tissue for gene activation affecting production of two proteins that serve as markers for inflammation. These cytokines, called interleukin-1 beta (IL-1B) and interleukin-6 (IL-6), are typically elevated in response to both injury and stress.

Compared to animals that received a sham procedure, isolated mice with nerve damage had much higher levels of IL-1B gene expression in their brain and spinal cord tissue. The researchers also observed a significant decrease in gene activity related to IL-6 production in the spinal cords of nonstressed animals compared to the mice that were stressed.

“We believe that socially isolated individuals are physiologically different from socially paired individuals, and that this difference seems to be related to inflammation,” said Courtney DeVries, professor of neuroscience at Ohio State and principal investigator on this work. “These data showed very nicely that the social environment is influencing not just behavior but really the physiological response to the nerve injury.”

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This work was supported by funds from the National Institute of Nursing Research. Additional co-authors include Brant Jarrett and Kathleen Stuller of Ohio State’s Department of Neuroscience.

Contact: Adam Hinzey, Adam.Hinzey@osumc.edu

Written by Emily Caldwell, (614) 292-8310; Caldwell.151@osu.edu

(Hinzey will be at Neuroscience 2012 from Oct. 13-17; during this time, contact Hinzey via email or by calling Emily Caldwell at (614) 893-4261.)

Editor’s note: Hinzey will present his poster (No. 786.04) between 11 a.m. and noon (CT) Wednesday (10/17) in Hall F-J at the Ernest N. Morial Convention Center in New Orleans.

New study proves that pain is not a symptom of arthritis, pain causes arthritis

2008 study posted for filing

Contact: Greg Williams
Greg_Williams@urmc.rochester.edu
585-273-1757
University of Rochester Medical Center

New treatments will seek to interrupt ‘crosstalk’ between joints and the spinal cord

Pain is more than a symptom of osteoarthritis, it is an inherent and damaging part of the disease itself, according to a study published today in journal Arthritis and Rheumatism. More specifically, the study revealed that pain signals originating in arthritic joints, and the biochemical processing of those signals as they reach the spinal cord, worsen and expand arthritis. In addition, researchers found that nerve pathways carrying pain signals transfer inflammation from arthritic joints to the spine and back again, causing disease at both ends.

Technically, pain is a patient’s conscious realization of discomfort. Before that can happen, however, information must be carried along nerve cell pathways from say an injured knee to the pain processing centers in dorsal horns of the spinal cord, a process called nociception. The current study provides strong evidence that two-way, nociceptive “crosstalk” may first enable joint arthritis to transmit inflammation into the spinal cord and brain, and then to spread through the central nervous system (CNS) from one joint to another.

Furthermore, if joint arthritis can cause neuro-inflammation, it could have a role in conditions like Alzheimer’s disease, dementia and multiple sclerosis. Armed with the results, researchers have identified likely drug targets that could interfere with key inflammatory receptors on sensory nerve cells as a new way to treat osteoarthritis (OA), which destroys joint cartilage in 21 million Americans. The most common form of arthritis, OA eventually brings deformity and severe pain as patients loose the protective cushion between bones in weight-bearing joints like knees and hips.

“Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and inevitable part of aging,” said Stephanos Kyrkanides, D.D.S., Ph.D., associate professor of Dentistry at the University of Rochester Medical Center. “Recent studies have revealed, however, that specific biochemical changes contribute to the disease, changes that might be reversed by precision-designed drugs. Our study provides the first solid proof that some of those changes are related to pain processing, and suggests the mechanisms behind the effect,” said Kyrkanides, whose work on genetics in dentistry led to broader applications. The common ground between arthritis and dentistry: the jaw joint is a common site of arthritic pain.

Study Details

Past studies have shown that specific nerve pathways along which pain signals travel repeatedly become more sensitive to pain signals with each use. This may be a part of ancient survival skill (if that hurt once, don’t do it again). Secondly, pain has long been associated with inflammation (swelling and fever).

In fact, past research has shown that the same chemicals that cause inflammation also cause the sensation of pain and hyper-sensitivity to pain if injected. Kyrkanides’ work centers around one such pro-inflammatory, signaling chemical called Interleukin 1-beta (IL-1β), which helps to ramp up the bodies attack on an infection.

Specifically, Kyrkanides’ team genetically engineered a mouse where they could turn up on command the production of IL-1β in the jaw joint, a common site of arthritis. Experiments showed for the first time that turning up IL-1β in a peripheral joint caused higher levels of IL-1β to be produced in the dorsal horns of the spinal cord as well.

Using a second, even more elaborately engineered mouse model, the team also demonstrated for the first time that creating higher levels of IL-1β in cells called astrocytes in the spinal cord caused more osteoarthritic symptoms in joints. Past studies had shown astrocytes, non-nerve cells (glia) in the central nervous system that provide support for the spinal cord and brain, also serve as the immune cells of CNS organs. Among other things, they release cytokines like IL-1β to fight disease when triggered. The same cytokines released from CNS glia may also be released from neurons in joints, possibly explaining how crosstalk carries pain, inflammation and hyper-sensitivity back and forth.

In both mouse models, experimental techniques that shut down IL-1β signaling reversed the crosstalk effects. Specifically, researchers used a molecule, IL-1RA, known to inhibit the ability of IL-1β to link up with its receptors on nerve cells. Existing drugs (e.g. Kineret® (anakinra), made by Amgen and indicated for rheumatoid arthritis) act like IL-1RA to block the ability IL-1β to send a pain signal through its specific nerve cell receptor, and Kyrkanides’ group is exploring a new use for them as osteoarthritis treatment.

The implications of this process go further, however, because the cells surrounding sensory nerve cell pathways too can be affected by crosstalk. If 10 astrocytes secrete IL-1β in response to a pain impulse, Kyrkanides said, perhaps 1,000 adjacent cells will be affected, greatly expanding the field of inflammation. Spinal cord astrocytes are surrounded by sensory nerve cells that connect to other areas of the periphery, further expanding the effect. According to Kyrkanides’ model, increased inflammation by in the central nervous system can then send signals back down the nerve pathways to the joints, causing the release of inflammatory factors there.

Among the proposed, inflammatory factors is calcitonin gene related peptide (CGRP). The team observed higher levels calcitonin-gene related peptide (CGRP) production in primary sensory fibers in the same regions where IL-1β levels rose, and the release of IL-1β by sensory neurons may cause the release of CGRP in joints. Past studies in Kyrkanides reveal that CGRP can also cause cartilage-producing cells (chondrocytes) to mature too quickly and die, a hallmark of osteoarthritis.

Joining Kyrkanides in the publication from the University of Rochester School of Medicine and Dentistry were co-authors M. Kerry O’Banion, M.D., Ph.D., Ross Tallents, D.D.S., J. Edward Puzas, Ph.D. and Sabine M. Brouxhon, M.D. Paolo Fiorentino was a student contributor and Jennie Miller was involved as Kyrkanides’ technical associate. Maria Piancino, led a collaborative effort at the University of Torino, Italy. This work was supported in part by grants from the National Institutes of Health.

“Our study results confirm that joints can export inflammation in the form of higher IL-1β along sensory nerve pathways to the spinal cord, and that higher IL-1β inflammation in the spinal cord is sufficient in itself to create osteoarthritis in peripheral joints,” Kyrkanides said. “We believe this to be a vitally important process contributing to orthopaedic and neurological diseases in which inflammation is a factor.”

Paralyzed patients regain some sensory function after neural stem cell treatment

By Michelle Castillo
 
 

StemCells’ human neural stem cell

(Credit: StemCells Inc.)

(CBS News) For most people who are paralyzed, there is no treatment available to help them regain full function of their limbs. 

 

But, promising new research from a phase 1 study conducted at the University of Zurich sponsored by StemCells, Inc. shows that six months after the implantation of neural stem cells, two out of three complete injury patients – meaning they had no neurological function below the point of injury – were able to gain some sensory function.

 

“We haven’t made progress in how to address injury after they occur, but using neural stem cells in a transplant lets us, for the first time, think we can repair this,” Dr. Stephen Huhn, a neurosurgeon and the vice president and head of the CNS program at StemCells, Inc. said to HealthPop.

 

The phase 1 study was intended to see if the implantation treatment had any unwanted side effects. For the procedure, 20 million neural stem cells were implanted directly into the spinal cord, something that has never been done before. Then, any reactions were monitored including complex examinations of sensory function – for example light touch, sensitivity to temperature and sensitivity to subtle electronic stimulation – as well as electrostimulation of the spinal cord itself.

 

What researchers were surprised to find was that the neural stem cell implantation was able to return some sensation to these paralyzed patients, who were all injured at the thoracic or chest level.

 

Hugh explained that if you think of the spinal cord and its 31 segments as a building with a series of floors, these patients could not access the floor below the point of the initial trauma. However, after the implantation, one patient was able to access three to four floors (or spinal cord segments below the paralysis point) and the other was able to reach five or six floors.

 

“These patients have had such an injury to their spinal cord that to see this kind of effect is amazing. They contain the worst of the worst injuries,” he explained.

 

While the other patient did not regain sensation, none of the patients had any negative side effects. Huhn believes this means that the treatment may be able to work even better for people who have limited function after a traumatic injury. Since the treatment has been deemed to be safe, the next phase is to test the implantation on nine other people who have incomplete injuries or some limited sensation or function after an injury.

 

Huhn recognizes that the field of stem cell research is controversial. The world’s only other trial using stem cells to treat spinal injury – which used embryonic stem cells – was ended in 2011 for financial reasons, according to the New Scientist. But, Huhn feels that the unique properties of neural stem cells and potential benefits warrant their use in medical treatment. Neural stem cells have the unique ability to divide and replicate themselves though cell culture. This means that for this trial, the team was able to use only one donated brain source to supply all the material needed for the study.

 

“This is a very delicate area, and we appreciate that neural stem cells are one of the first discoveries that we’ve had in which we can think about biologically repairing the nervous system,” “Now we have a tool, a technology – something we can think about repairing the central nervous system with.”

 

The information was presented at the International Spinal Cord Society’s (ISCoS) annual meeting in London on Sept. 3

http://www.cbsnews.com/8301-504763_162-57505238-10391704/paralyzed-patients-regain-some-sensory-function-after-neural-stem-cell-treatment/?tag=contentMain;contentBody