Posts tagged spinal cord
Articles and news from the latest research reports.
Irreversible tissue loss seen within 40 days of spinal cord injury
The rate and extent of damage to the spinal cord and brain following spinal cord injury have long been a mystery. Now, a joint research effort between the University of Zurich, University Hospital Balgrist and colleagues from University College London have found evidence that patients already have irreversible tissue loss in the spinal cord within 40 days of injury. Using a new imaging measurement technique the impact of therapeutic treatments and rehabilitative interventions can be now determined more quickly and directly than before.
A spinal cord injury changes the functional state and structure of the spinal cord and the brain. For example, the patients’ ability to walk or move their hands can become restricted. How quickly such degenerative changes develop, however, has remained a mystery until now. The assumption was that it took years for patients with a spinal cord injury to also display anatomical changes in the spinal cord and brain above the injury site. For the first time, researchers from the University of Zurich and the Uniklinik Balgrist, along with English colleagues from University College London (UCL), now demonstrate that these changes already occur within 40 days of acute spinal cord injury.
Spinal cord depletes rapidly
The scientists studied 13 patients with acute spinal cord injuries every three months for a year using novel MRI (magnetic resonance imaging) protocols. They discovered that the diameter of the spinal cord had rapidly decreased and was already seven percent smaller after twelve months. A lesser volume decline was also evident in the corticospinal tract, a tract indispensable for motor control, and nerve cells in the sensorimotor cortex. The extent of the degenerative changes coincided with the clinical outcome. “Patients with a greater tissue loss above the injury site recovered less effectively than those with less changes,” explains Patrick Freund, the investigator responsible for the study at the Paraplegic Center Balgrist.
Gaining insights into effect of therapies
Treatments targeting the injured spinal cord have entered clinical trials. Gaining insights into mechanisms of repair and recovery within the first year are crucial. Thanks to the use of the new neuroimaging protocols, Freund says, we now have the possibility of displaying the effect of therapeutic treatments on the central nervous system and of rehabilitative measures more quickly. Consequently, the effect of new therapies can also be recorded more rapidly.
“This study is an excellent example of the value of combining the complementary expertise of the two universities,” says UCL’s Dean of Brain Sciences, Professor Alan Thompson, who is one of the senior authors of the study. “It provides exciting new insights into the complications of spinal cord trauma and gives us the possibility of identifying both imaging biomarkers and therapeutic targets.”
The findings are the result of a new three-year neuroscience partnership between the Neuroscience Centre Zurich (ZNZ) and UCL.
Literature:
Patrick Freund, Nikolaus Weiskopf, John Ashburner, Katharina Wolf, Reto Sutter, Daniel R Altmann, Karl Friston, Alan Thompson, Armin Curt. MRI investigation of the sensorimotor cortex and corticospinal tract after acute spinal cord injury: a prospective longitudinal study. The Lancet Neurology. July 2, 2013.
Different neuronal groups govern right-left alternation when walking
Scientists at Karolinska Institutet have identified the neuronal circuits in the spinal cord of mice that control the ability to produce the alternating movements of the legs during walking. The study, published in the journal Nature, demonstrates that two genetically-defined groups of nerve cells are in control of limb alternation at different speeds of locomotion, and thus that the animals’ gait is disturbed when these cell populations are missing.
Most land animals can walk or run by alternating their left and right legs in different coordinated patterns. Some animals, such as rabbits, move both leg pairs simultaneously to obtain a hopping motion. In the present study, the researchers Adolfo Talpalar and Julien Bouvier together with professor Ole Kiehn and colleagues, have studied the spinal networks that control these movement patterns in mice. By using advanced genetic methods that allow the elimination of discrete groups of neurons from the spinal cord, they were able to remove a type of neurons characterized by the expression of the gene Dbx1.
"It was classically thought that only one group of nerve cells controls left right alternation", says Ole Kiehn who leads the laboratory behind the study at the Department of Neuroscience. "It was then very interesting to find that there are actually two specific neuronal populations involved, and on top of that that they each control different aspect of the limb coordination."
Indeed, the researchers found that the gene Dbx1 is expressed in two different groups of nerve cells, one of which is inhibitory and one that is excitatory. The new study shows that the two cellular populations control different forms of the behaviour. Just like when we change gear to accelerate in a car, one part of the neuronal circuit controls the mouse’s alternating gait at low speeds, while the other population is engaged when the animal moves faster. Accordingly, the study also show that when the two populations are removed altogether in the same animal, the mice were unable to alternate at all, and hopped like rabbits instead.
There are some animals, such as desert mice and kangaroos, which only hop. The researchers behind the study speculate that the locomotive pattern of these animals could be attributable to the lack of the Dbx1 controlled alternating system.
(Source: ki.se)
Dream of regenerating human body parts gets a little closer
Damage to vital organs, the spinal cord, or limbs can have an enormous impact on our ability to move, function – and even live. But imagine if you could restore these tissues back to their original condition and go on with life as normal.
Well, this is the dream for regenerative medicine. And while humans missed out on these abilities in the evolutionary lottery, a recent study in mice shows we’re making small progress to achieving this dream.
Learning from animals
Nature has provided the animal kingdom with many different ways to achieve perfect regeneration. Some amphibians – such as salamanders – are famous for their superhero-like ability to regenerate heart, brain, spinal cord, tail and can even whole limb tissue throughout their life.
Although organ and spinal cord regeneration are clinically important and worthy of intense research investment, regrowing whole limbs provides a flagship example of perfect regeneration in the salamander.
It has been known for more than a hundred years that if a salamander loses a limb, it grows right back. This process is extremely precise and removal of the limb at the shoulder regrows a full limb, but removal at the wrist only regrows the missing hand portion.
Interestingly, there does not seem to be a limit on how many times they can perform this clever trick and each time the limb comes back perfect.
But mammals (including humans and mice) seem to have missed out on this important skill. The question of how to enhance the regenerative capabilities in humans, either by adding the missing ingredients, or activating these latent abilities currently lies wide open.
Extending regeneration to mammals
Mammals currently only have the capacity to regenerate the very tip of their finger. But the result is far from perfect. A range of studies in mice have shown the digit-tip regrowth is severely restricted. Removal of the very tip of the mouse digit will be replaced, but removal of the tissue a small distance further up the digit and closer to nail bed (the equivalent to a human cuticle), will fail to regrow.
Last week, a group of researchers from the United States and Japan published work extending our understanding of the mechanism by which a resident stem cell population within the mouse digit tip nail bed can be activated to induce digit tip regeneration. In other words, we can now grow more of the digit back in mice and possibly more of the human finger.
Resident stem cells are specialised cells found at various locations within the body. When activated, these cells multiply and then transform into other cell types required to replace worn out cells under conditions of normal tissue maintenance.
This work builds on previous studies identifying the stem cell population in the nail bed by unveiling a signalling mechanism that could be exploited to enhance the amount of tissue that could be regrown. The potential for repair after injury appears very limited in many tissues and organs. Understanding how to enhance stem cell activation in these tissues may stimulate repair not previously thought possible.
The ability to switch on and mobilise resident stem cells in regeneration will be important in a wide range of new therapies, particularity for organs affected by injury or disease. On a world stage, momentum is currently growing for these types of strategies. It is clear that once refined, these approaches are sure to have a profound influence on many different aspects of clinical medicine, opening up the possibility of replacing diseased or injured tissues.
We may be some way off from the dream of replacing whole limbs in humans but recent progress confirms that by deepening our understanding of stem cell activation, we can directly unlock more regeneration in mammals than normally possible.
Neurostimulation Lowers Need for Opioids in Chronic Pain
Expert Panel of Physicians and Neuroscientists Announce International Guidance on Using Neurostimulation to Significantly Reduce the Need for Opioids in Chronic Pain
Recognizing that treatment of chronic pain can be confounding, the Neuromodulation Appropriateness Consensus Committee (NACC), an international group of more than 60 leading pain specialists, has created the first consensus guidelines for the use of neurostimulation in chronic pain.
Neurostimulation is an established and growing area of pain therapy that treats nerves with electrical stimulation rather than drugs. The NACC findings, announced at the International Neuromodulation Society (INS) 11th World Congress, address provider training, patient screening, and treatment recommendations.
While the extent and suffering of chronic pain is becoming better recognized, the danger of opioids for addiction, diversion or misuse is well known. Long-term opioid use can lead to the need for escalating doses to bring relief, and raises the risk of physical dependence, overdose, weight gain, depression, and immune and hormone system dysfunction.
“Many studies contain insufficient evidence to prove the safety or effectiveness of any long-term opioid regimen for chronic pain,” said study lead author Dr. Timothy Deer, INS president-elect and director of the Center for Pain Relief in Charleston, W. Va. “Indeed, many patients discontinue long-term opioid therapy due to insufficient pain relief or adverse events.”
Neurostimulation has been shown in clinical studies to be safe and effective for properly selected patients, and is approved by the FDA to treat chronic pain of the trunk and limbs. It belongs to a family of therapies known as neuromodulation because they modulate, or alter, the function of nerves, such as nerves that may have become hypersensitized or damaged, or are otherwise sending pain signals long past the initial injury. Since the components of neurostimulators bear some resemblance to heart pacemakers, they are sometimes called pain pacemakers.
The NACC recommends neurostimulation be used earlier in the treatment of some kinds of chronic pain, such as failed back surgery syndrome and complex regional pain syndrome. A study being presented at the world congress shows neurostimulation effectiveness correlates with early use in those conditions, with the added benefit of shortening the time patients spend trying other methods and containing long-term costs of managing chronic pain.
The most common form of neurostimulation, spinal cord stimulation (SCS), was introduced in 1967 and is now implanted in some 4,000 patients annually in the United States. With SCS, appropriately selected patients who have had back and/or leg pain longer than six months often find their symptoms relieved by 50 percent or more. The therapy uses slender electrical leads placed beneath the skin along the spinal cord and connected to a compact pulse generator, about the size of a pocket watch, that sends mild current along the leads to elicit a natural biological response and limit pain messages sent to the brain. Patients try the minimally invasive technique to see if it works for them before receiving a permanent implant.
“The lessons learned over the last few decades of clinical practice have influenced neurostimulator design, placement, and programming – and added new insights into spinal anatomy and pain physiology,” said INS President Dr. Simon Thomson, consultant in in pain medicine and neuromodulation at Basildon and Thurrock University NHS Trust in the United Kingdom.
Although neurostimulation devices may seem novel at first, using electrical current to limit pain dates back to antiquity, when standing on an electric fish was one remedy. Use of modern neurostimulation devices is likely to expand as the aging populace lives longer with chronic conditions, while technological refinements and clinical evidence continue to accumulate.
“A reduction in opioid use among patients treated with spinal cord stimulation was shown in a several studies, notably a 2005 randomized controlled clinical trial led by Dr. Richard North under the auspices of the Johns Hopkins University School of Medicine,” commented INS Secretary and study co-author Dr. Marc Russo, director of the Hunter Pain Clinic in New South Wales, Australia. “Broad-based studies show that within two years, using spinal cord stimulation rather than repeat back surgery is not only a more cost-effective use of health resources, it also is correlated with higher rates of return to work.”
Consensus committee authors believe that when appropriately applied, neurostimulation to target treatment directly to nerves can improve productivity and quality of life for chronic pain patients, offering a potentially less costly and risky option than repeat surgery or long-term painkiller use. They recommend:
- Neuromodulation providers receive at least 12 hours of continuing medical education per year directly related to improving outcomes with neuromodulation, with additional mentoring by a credentialed provider at a hospital officially accredited by the Joint Commission on Accreditation of Healthcare Organizations or its equivalent.
- Spinal cord stimulation should be used early in the treatment of failed back surgery syndrome as long as there is no progression of a neurological condition requiring semi-urgent intervention.
- Patient selection decisions should be made with any clinicians who are treating co-existing conditions, who may include the patient’s primary care provider, cardiologist, or neurologist.
- Due to the emotional impact of the experience of pain, an assessment of a psychologist or psychiatrist is recommended within the first year of implant.
- Spinal cord stimulation and peripheral nerve stimulation should be considered earlier, when possible, and are recommended to be trialed in the first two years of chronic pain.
- Peripheral nerve stimulation (beyond the spine) should be reserved for patients in whom the pain distribution is primarily in a named nerve that is known to connect the area of pain. Temporary relief of the patients’ pain by an injection of local anesthetic in the nerve distribution should be seen as an encouraging sign for the use of this therapy.
- To cover an area that is not located in the distribution of a named peripheral nerve, stimulation of a peripheral nerve field with electrodes placed in the subcutaneous area just beneath the skin may give relief if stimulation from SCS does not reach this area. In many cases a hybrid of two or more of these methods may present the best chance of an acceptable outcome.
- SCS should be used as an early intervention in patients with Raynaud’s syndrome and other painful ischemic vascular disorders, which involve insufficient blood supply to part of the body. If ischemic symptoms persist despite initial surgical or reasonable medical treatment, SCS should be trialed.
- In the use of spinal cord stimulation to treat painful diabetic peripheral neuropathy, decision-making should be performed on an individualized basis, considering current diagnoses and other factors. A type of SCS that stimulates a structure at the edge of the spinal column, the dorsal root ganglion, may be most suited for this disorder.
(Source: newswise.com)
Restoring paretic hand function via an artificial neural connection bridging spinal cord injury
Functional loss of limb control in individuals with spinal cord injury or stroke can be caused by interruption of the neural pathways between brain and spinal cord, although the neural circuits located above and below the lesion remain functional. An artificial neural connection that bridges the lost pathway and connects brain to spinal circuits has potential to ameliorate the functional loss. Yukio Nishimura, Associate Professor of the National Institute for Physiological Sciences, Japan, and Eberhard Fetz, Professor and Steve Perlmuter, Research Associate Professor at the University of Washington, United States investigated the effects of introducing a novel artificial neural connection which bridged a spinal cord lesion in a paretic monkey. This allowed the monkey to electrically stimulate the spinal cord through volitionally controlled brain activity and thereby to restore volitional control of the paretic hand. This study demonstrates that artificial neural connections can compensate for interrupted descending pathways and promote volitional control of upper limb movement after damage of neural pathways such as spinal cord injury or stroke. The study will be published online in Frontiers in Neural Circuits on April 11.
"The important point is that individuals who are paralyzed want to be able to move their own bodies by their own will. This study was different from what other research groups have done up to now; we didn’t use any prosthetic limbs like robotic arms to replace the original arm. What’s new is that we have been able to use this artificial neuronal connection bypassing the lesion site to restore volitional control of the subject’s own paretic arm. I think that for lesions of the corticospinal pathway this might even have a better chance of becoming a real prosthetic treatment rather than the sort of robotic devices that have been developed recently", Associate professor Nishimura said.
Getting a grip on hand function: Discovering key spinal cord circuits
Professor and neurosurgeon Dr. Rob Brownstone and postdoctoral fellow Dr. Tuan Bui have identified the spinal cord circuit that controls the hands’ ability to grasp.
The world’s leading neuroscience journal, Neuron, published the breakthrough finding in its latest issue.
The researchers have found that a certain population of neurons in the spinal cord — called the dI3 interneurons — assess information from sensory neurons in the hands and then send the appropriate signals to motor neurons in the spinal cord, and hence to the muscles, to control the hands’ grip.
Importance of hand-grip control
“This circuit allows us to subtly and unconsciously adjust our grasp so we apply the right amount of force to whatever we’re holding,” says Dr. Brownstone, a professor in the Department of Medical Neurosciences and the Division of Neurosurgery. “This mechanism is disrupted in spinal cord injuries, which can completely eliminate the ability to grasp, and in neurodegenerative diseases like Alzheimer’s disease, which can lead to an uncontrollable reflexive grasp such that people grab and can’t let go of what they touch.”
Impaired hand function has a devastating effect on people’s independence and ability to function in daily life. As Dr. Brownstone points out, people with quadriplegia ranked hand function as their number-one priority, when asked in a 2004 survey which function they would most want to recover if they could. They rated hand function well above trunk stability, walking, sexual function, bladder and bowel control, and normal sensation.
An unexpected finding
Drs. Brownstone and Bui were testing a spinal cord circuit for its role in the rhythmic pattern of walking, when they found it controlled hand grip instead. “The mice with this circuit disrupted were walking just fine, but I found it was unusually easy to remove them from their cages,” recounts Dr. Bui. “Mice will usually grab onto the cage wires when you go take them out, so this really got us thinking.”
While Dr. Bui was pondering the meaning of this unexpected observation in the lab, Dr. Brownstone was in his neurosurgery clinic, assessing a patient who was unable to control her grasp. “When she took my hand, she was unable to let go,” he recalls. “I had to peel her fingers off one by one to release my hand.”
As they compared notes, Drs. Brownstone and Dr. Bui quickly realized they had come across the circuit that controls hand grasp. Struck by the implications of their observations, they embarked on a series of experiments — with collaborators, including Dr. Tom Jessell at Columbia University in New York City — which validated the finding.
A path to future treatments
Now that the researchers have identified the specific spinal cord circuit that controls hand grip, they can go on to find targets for potential treatments for impaired hand function. “It’s possible that a neurotransmitter or other agent could be delivered to the spinal cord to correct the faulty circuit,” notes Dr. Brownstone. “It could be a complex strategy, but understanding is always the first step.”
Dr. Brownstone is a Tier 1 Canada Research Chair in spinal cord circuits. His research is also supported through grants from the Canadian Institutes of Health Research. Dr. Bui is a key member of Dr. Brownstone’s research team in the Motor Control Lab at Dalhousie University, where they are identifying the neural circuits that control our ability to walk and move in coordinated ways. Their ultimate goal is to identify targets for therapies to restore lost motor function and control in people with spinal cord injuries and other neurological diseases.
Phase 1 ALS trial is first to test antisense treatment of neurodegenerative disease
The initial clinical trial of a novel approach to treating amyotrophic lateral sclerosis (ALS) – blocking production of a mutant protein that causes an inherited form of the progressive neurodegenerative disease – may be a first step towards a new era in the treatment of such disorders. Investigators from Massachusetts General Hospital (MGH) and Washington University School of Medicine report that infusion of an antisense oligonucleotide against SOD1, the first gene to be associated with familial ALS, had no serious adverse effects and the drug was successfully distributed thoughout the central nervous system.
"This therapy directly targets the cause of this form of ALS – a mutation in SOD1, which was originally discovered here at the MGH by my mentor Robert Brown," says Merit Cudkowicz, MD, chief of Neurology at MGH and senior author of the report in Lancet Neurology, which has been released online. “It’s very exciting that we have reached a stage when we can start clinical trials against this type of ALS.”
ALS causes the death of motor neurons in the brain and spinal cord, stopping transmission of neural signals to nerve fibers and leading to weakness, paralysis and usually death from respiratory failure. Only 10 percent of ALS cases are inherited, and mutations in SOD1 – which produce an aberrant, toxic form of the protein – account for about 20 percent of familial cases. Although that first SOD1 mutation was identified 20 years ago by the team lead by Brown – who is now professor and chief of Neurology at the University of Massachusetts Medical School – a technology that directly addresses such mutations became available only recently.
The current study, the first author of which is Timothy Miller, MD, PhD, of Washington University, used what are called antisense oligonucleotides – small, single-stranded DNA or RNA molecules that prevent production of a protein by binding to its messenger RNA. While antisense medications have been tested against several types of disease, this was the first trial in a neurological disorder, making the assurance of safety – a primary goal of a phase 1 study – particular important. Studies in animal models led by Miller and others found that the experimental antisense drug used in this trial reduced expression of mutated and nonmutated SOD1 and slowed the progression of ALS.
Conducted at the MGH, Washington University, Johns Hopkins University and the Methodist Neurological Institute in Houston, the trial enrolled a total of 21 patients with SOD1 familial ALS. Four sequential groups of participants received spinal infusions over an 11-hour period of the antisense drug or a placebo, with the active drug being administered at one of four dosage levels. Since participants in one group were free to join a subsequent group more than 60 days later, seven received two infusions and two received a total of three.
Some of the participants reported the type of adverse effects typically associated with spinal infusions – headache and back pain – with no difference between the active drug and placebo groups. Participants who receive subsequent infusions reported fewer adverse effects. Cerebrospinal fluid samples taken immediately after infusion revealed the presence of the antisense oligonucleotidein all participants receiving the drug at levels close to what was predicted based on animal studies. Analysis of spinal cord samples from one participant who had later died from ALS found drug levels highest at the site of the infusion and lowest at the furthest point and suggested that prior estimates of how long the drug would persist in the spinal cord were accurate.
Cudkowicz notes that the next step will be a larger study to address long-term safety and take a first look at the effectiveness of antisense treatment against ALS “This is a very important step forward for neurodegenerative disorders in general,” she explains. “There are other ALS gene mutations that antisense technology may be useful against. There also is an ongoing study of a different oligonucleotide against spinal muscular atrophy, and ongoing preclinical studies in Huntington’s disease, myotonic dystrophy and other neurological disorders are in development.
"The first person with ALS that I cared for had SOD1 ALS," she adds, "and I promised her a commitment to finding a treatment for this form of the disease. It’s so gratifying to finally be at the stage of knowledge where we can start testing this treatment in patients with SOD1 ALS. We also hope that this treatment may apply to the broader population of patient with sporadic ALS." Cudkowicz is the Julieanne Dorn Professor of Neurology at Harvard Medical School.
(Source: massgeneral.org)
New Hope for Reversing the Effects of Spinal Cord Injury
Walking is the obvious goal for individuals who have a chronic spinal cord injury, but it is not the only one. Regaining sensation and continence control also are important goals that can positively impact an individual’s quality of life. New hope for reversing the effects of spinal cord injury may be found in a combination of stem cell therapy and physical therapy as reported in Cell Transplantation by scientists at the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School.
“Our phase one/two clinical trial had one goal: to give patients who have no other treatment options some hope,” said Hatem E. Sabaawy, MD, PhD, an assistant professor of medicine in the molecular and regenerative medicine program at Robert Wood Johnson Medical School. “Early findings have concluded that we have met our goal and can improve the quality of life for individuals with spinal cord injuries by providing a safe treatment that restores some neurological function.”
Dr. Sabaawy led a clinical trial that included 70 patients who had cervical or thoracic spinal cord injuries and were previously treated for at least six months without response. The patients were randomized into two groups, both of which were given physical therapy treatment. One of the groups also received stem cells derived from their own bone marrow injected near the injury site. Using the American Spinal Injury Association Impairment (AIS) Scale, patients received neurological and physical evaluations monthly for 18 months to determine if sensory and motor functions improved.
“Of primary importance, there was a notable absence of side effects in patients treated with stem cells during the course of our investigation,” added Dr. Sabaawy, who also is a resident member of The Cancer Institute of New Jersey at Robert Wood Johnson Medical School.
None of the patients in the control group who received only physical therapy showed any improvement in sensory or motor function during the same time frame. Although the scale of injuries differed, all patients who were treated with a combination of bone-marrow derived stem cells and physical therapy responded to tactile and sensory stimuli as early as 4 weeks into the study. After 12 weeks, they experienced improvements in sensation and muscle strength, which was associated with enhanced potency and improved bladder and bowel control that eventually allowed patients to live catheter-free. Patients who showed improvement based on the AIS scale also were able to sit up and turn in their beds.
“Since the emergence of stem cells as a potential therapy for spinal cord injury, scientists have diligently sought the best application for using their regenerating properties to improve a patient’s mobility,” said Joseph R. Bertino, MD, University Professor of medicine and pharmacology, interim director, Stem Cell Institute of New Jersey and chief scientific officer at The Cancer Institute of New Jersey. “Dr. Sabaawy’s discovery that treatment is more successful when stem cell therapy is combined with physical therapy could provide a remarkable, and hopefully sustainable, improvement in the overall quality of life for patients with spinal cord injury.”
At the end of 18 months, 23 of the 50 patients who received both physical therapy and stem cell therapy showed a significant improvement of at least 10 points on the AIS scale. Several were able to walk with assistance. In addition, more gains were made in motor skill control by patients with thoracic spinal cord injuries, suggesting that patients with thoracic spinal cord injuries may respond better to the combined treatment.
Dr. Sabaawy however cautioned that more studies are needed with a larger number of patients to test different cell dose levels and intervals at which stem cell therapy should be delivered.
“Although a cure for spinal cord injury does not yet exist, it is clear that the regenerative and secretory properties of bone-marrow derived stem cells can improve symptoms of paralysis in some patients when coupled with the current standard of care that physical therapy provides,” said Dr. Sabaawy. “We will continue monitoring our patients for long-term safety effects of stem cell therapy and work to expand our research through a phase two clinical trial that can be conducted at multiple centers nationwide and internationally.”
(Image courtesy: University of Alberta, Faculty of Rehabilitation Medicine)
Human brain treats prosthetic devices as part of the body
People with spinal cord injuries show strong association of wheelchairs as part of their body, not extension of immobile limbs injuries.
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.
(Image: University of Miami)
Reflex control could improve walking after incomplete spinal injuries
A training regimen to adjust the body’s motor reflexes may help improve mobility for some people with incomplete spinal cord injuries, according to a study supported by the National Institutes of Health.
During training, the participants were instructed to suppress a knee jerk-like reflex elicited by a small shock to the leg. Those who were able to calm hyperactive reflexes – a common effect of spinal cord injuries – saw improvements in their walking.
The study was led by Aiko Thompson, Ph.D., and Jonathan Wolpaw, M.D., both of whom hold appointments at the New York state Department of Health and the State University of New York in Albany, and at Columbia University in New York City. The study took place at Helen Hayes Hospital in West Haverstraw, N. Y. It was funded in part by NIH’s National Institute of Neurological Disorders and Stroke (NINDS), and published in the Journal of Neuroscience.
"People tend to think of reflexes as fixed, but in reality, normal movement requires constant fine tuning of reflexes by the brain. Loss of that fine-tuning is an important part of the disability that comes with a spinal cord injury," said Dr. Wolpaw, a research physician and professor at the Wadsworth Center, the state health department’s public health laboratory.
When the brain makes a decision to move, it sends signals that travel through the spinal cord to the appropriate muscles. Spinal reflexes – controlled by local circuits of nerve cells in the spinal cord – provide a way for the body to react and move quickly without a conscious decision from the brain. “They enable you to jerk your hand away from a hot stove before you’ve registered the pain and experienced severe burns,” Dr. Wolpaw said. “The brain can gradually enhance or suppress reflexes as needed,” he said.