The hyaluronic acid which forms a scaffold-like configuration may help to structurally stabilize the spinal cord injury site. Tracing of cells in the brain stem after injury showed much higher levels in the hydrogel treated animals compared to animals which did not receive the treatment, and approached nearly normal levels. Treated animals had higher functional scores than non-treated animals.

The work was presented at the Annual Meeting of the American Association of Neurological Surgeons in San Diego where it won the Synthes Prize for Spine Research.

“Spinal cord injury is devastating to civilian and military populations – especially to the young. There has been little progress toward paradigms of regeneration and few results that show real, sustained functional recovery,” says Dr. Preul. “We’ve been so pre-occupied with regeneration, but that is a highly complicated and difficult to define goal. This project is a synergy of neurosurgeons and bioengineers that attempts repair of the SCI lesion cavity using a tissue-engineering biomaterials approach.”

Dr. Preul says his team’s goal is to find ways to structurally allow the body to better heal itself. “In this project we did not add anything to the hyaluronic acid. It may be that adding growth factors or cells into the gel matrix may allow even better results.”

Although clinical trials are likely years off, Dr. Preul says these results show “we may be on a practical path that can give hope to the many people who suffer this sort of injury.”

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Individuals from low-income, minority backgrounds with chronic low back pain (CLBP) may be more affected due to disparities in access to treatment. Although many CLBP patients seek relief from complementary therapies such as yoga, use of these approaches are less common among minorities and individuals with lower incomes or less education.

BUSM researchers recruited adults with CLBP from two community health centers that serve racially diverse, low-income neighborhoods of Boston. They were randomly assigned to either a standardized 12-week series of hatha yoga classes or standard treatment including doctor’s visits and medications.

As part of the trial, the researchers asked participants to report their average pain intensity for the previous week, how their function is limited due to back pain, and how much pain medication they are taking. The yoga group participated in 12 weekly 75-minute classes that included postures, breathing techniques, and meditation. Classes were taught by a team of registered yoga teachers and were limited to eight participants. Home practice for 30 minutes daily was strongly encouraged. Participants were provided with an audio CD of the class, a handbook describing and depicting the exercises, a yoga mat, strap, and block.

Pain scores for the yoga participants decreased by one-third compared to the control group, which decreased by only 5 percent. Whereas pain medication use in the control group did not change, yoga participants’ use of pain medicines decreased by 80 percent. Improvement in function was also greater for yoga participants but was not statistically significant.

“Few studies of complementary therapies have targeted minority populations with low back pain” explained lead author Robert B. Saper, MD, MPH, an assistant professor of family medicine at BUSM and director of integrative medicine at Boston Medical Center. “Our pilot study showed that yoga is well-received in these communities and may be effective for reducing pain and pain medication use,” said Saper.

This study was funded by the National Center for Complementary and Alternative Medicine and the National Institutes of Health.

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Researchers have shown how an experimental drug might restore the function of nerves damaged in spinal cord injuries.

Because nerves usually are not severed in a common type of spinal cord trauma, called “compression” injuries, the drug offers hope as a possible treatment, said Riyi Shi, a professor in Purdue University’s Department of Basic Medical Sciences, School of Veterinary Medicine, Center for Paralysis Research and Weldon School of Biomedical Engineering.

“Compression is responsible for most spinal cord injuries, including many resulting in paralysis,” Shi said. “Since the nerves are not severed, this type of drug represents a potential golden opportunity to treat spinal cord injuries.”

Findings, based on experiments with guinea pig spinal cord tissue, appeared online Nov. 18 in the Journal of Neurophysiology. The work was led by Department of Basic Medical Sciences doctoral student Wenjing Sun.

Shi said the findings were made possible by the interdisciplinary nature of the work, which also involves researchers Richard Borgens, director of Purdue’s Center for Paralysis Research and the Mari Hulman George Professor of Neurology in the School of Veterinary Medicine; Stephen Byrn, the Charles B. Jordan Professor of Medicinal Chemistry, and Daniel Smith, a research assistant professor, both in the Department of Industrial and Physical Pharmacy; and Ji-Xin Cheng, an associate professor in the Weldon School of Biomedical Engineering and Department of Chemistry.

The researchers subjected spinal cord tissue to stresses that mimic what happens in a compression injury, which stretches nerves. Then they treated the damaged axons with 4-aminopyridine-3-methyl hydroxide.

The compound is a derivative of the drug 4-aminopyridine, used primarily as a research tool and also to manage symptoms of multiple sclerosis.

The axons of each nerve are sheathed in a thick insulating lipid layer, called myelin, which enables the transmission of signals without short circuiting, much like the insulation surrounding electrical wires. Spinal cord trauma damages the myelin sheath, exposing “fast potassium channels” that are embedded in the axons and are critical for transmitting nerve impulses.

The researchers confirmed previous circumstantial evidence suggesting injury causes the myelin insulation to recede, exposing the channels and impairing signal transmission. Laboratory and imaging techniques revealed the exposed channels in damaged axons.

The researchers also discovered that 4-aminopyridine-3-methyl hydroxide is a “potassium channel blocker,” using a sophistic laboratory technique called “patch clamp” to measure signal conduction. Findings confirmed that the compound prevents the exposed channels from leaking electrical current and enhances nerve conduction in segments of the damaged spinal cord.

The compound could make it possible to sidestep spinal cord damage by enabling axons to transmit signals as though they were still sheathed in myelin, Shi said.

Nerves transmit signals through a series of rapid electrical pulses, or “action potentials.” For proper nerve function, the time gap between pulses must be as brief as possible. However, 4-aminopyridine has been shown to lengthen the gap, or “refractory period,” between pulses. The researchers found that 4-aminopyridine-3-methyl hydroxide restores function without affecting the refractory period. As a result, the damaged nerves perform more like healthy nerves than those treated with other drugs, he said.

Another key advantage of the new compound is that it’s about 10 times more potent than 4-aminopyridine, meaning lower doses can be used to reduce the likelihood of serious side effects.

Because myelin also is damaged in multiple sclerosis, the same drug might be used to restore nerve function in people stricken with the disease, Shi said. Since the newer drug can be used in lower doses, it might be more effective than 4-aminopyridine in treating multiple sclerosis, which affects more than 350,000 people in the United States and 2 million worldwide, he said.

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Shaheen Lakhan and Marie Rowland from the Global Neuroscience Initiative Foundation, Los Angeles, USA, searched for trials evaluating the cannabis extracts delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD). According to Lakhan, “We found evidence that combined THC and CBD extracts may provide therapeutic benefit for MS spasticity symptoms”.

Spasticity, involuntary muscle tension or contraction, is a common symptom of MS. Many existing therapies for this symptom are ineffective, difficult to obtain, or associated with intolerable side effects. In this study, reported incidence of side effects from cannabis, such as intoxication, varied greatly depending on the amount of cannabis needed to effectively limit spasticity, but the researchers note that side effects were also seen in the placebo groups. They add, “Considering the distress and limitations spasticity brings to individuals with MS, it is important to carefully weigh the potential for side effects with the potential for symptom relief “.

Lakhan concludes, “The therapeutic potential of cannabinoids in MS is comprehensive and should be given considerable attention”.

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• Vitamin D Can Prevent Multiple Sclerosis (0)

There are different types of seizures, different types of epilepsy syndromes, and different causes of epilepsy. For example, both brain tumors and stroke can cause seizures and lead to chronic epilepsy. Some of the causes can be diagnosed and treated with medicines, and some require surgery.

Epilepsy treatment

The majority of epileptic seizures are controlled with drug therapy, particularly anti-convulsant drugs. The type of treatment prescribed will depend on several factors, including the type of epilepsy (focal/partial versus generalized), the frequency and severity of the seizures, the person’s age, overall health, and medical history. An accurate diagnosis of the type of epilepsy (not just the type of seizure, since most seizure types occur in different types of epilepsy) is critical to choosing the best treatment.

There are many drugs available to treat epilepsy, including:

Phenytoin (Dilantin® or Phenytek®)
Phenobarbital
Carbamazepine (Tegretol® or Carbatrol®)
Primidone (Mysoline®)
Ethosuximide (Zarontin®)
Valproic acid (Depakene®)
Divalproex (Depakote®, Depakote ER®)
Diazepam (Valium®) and related medications such as clonazepam (Klonopin®), and clorazepate (Tranxene®)
Felbamate (Felbatol®)
Gabapentin (Neuronti-n®)
Lamotrigine (Lamictal®)
Tiagabine (Gabitril®)
Topiramate (Topamax®)
Levetiracetam (Keppra®)
Zonisamide (Zonegran®)
Pregabalin (Lyrica®)
In general, for a given type of epilepsy there are only minor differences among appropriate drugs. The choice is most often based on other factors specific to each patient, such as which side effects can be tolerated and which delivery method is acceptable.

Although the different types of epilepsy vary greatly, in general, medicines can control seizures in about 70 percent of epilepsy patients.

It might take several months before the best drug and dosage are determined for you. During this adjustment period, you might be monitored with frequent blood tests. It is very important to keep your follow-up appointments with your doctor and the laboratory to minimize your risk for serious side effects and to prevent complications.

When seizures continue despite treatment for epilepsy, it might be because the episodes thought to be seizures are non-epileptic. In such cases, you should get a second opinion from a specialist and undergo EEG-video monitoring so the diagnosis can be re-evaluated. In specialized centers, about 15 percent to 20 percent of patients referred for persistent, refractory or intractable seizures ultimately prove to have non-epileptic conditions instead.

What are the side effects of epilepsy medicine?

As is true of all drugs, the drugs used to treat epilepsy have side effects. The occurrence of side effects depends on the dose, type of medicine, and length of treatment. The side effects worsen with higher doses but tend to be less severe with time as the body adjusts to the medicine. Anti-epileptic drugs are usually started at lower doses and increased gradually to make this adjustment easier.

Side effects of epilepsy drugs can include blurry or double vision, fatigue, sleepiness, unsteadiness, stomach upset, skin rashes, low blood cell counts, liver problems, swelling of the gums, hair loss, weight gain, and tremor.

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During the study, UV light released gamma aminobutyric acid (GABA) from the “caged” compound carbonyl amino butanoic acid (BC204). GABA then decreased the abnormal electrical activity in the CA1 area of the brain. Results of this study have considerable potential in treating focal epilepsy in humans. Details of this study are available in the January 2010 issue of Epilepsia, a journal published by Wiley-Blackwell on behalf of the International League Against Epilepsy.

Focal (or partial) epilepsy is very common in both adults and can occur in children. It is caused by an abnormality in a localized area of the brain resulting from such conditions as stroke, trauma, or infections. Up to one-third of epileptic patients fail to respond to conventional medical therapies and are subject to toxic effects from antiepileptic drugs (AEDs). While surgery has benefited some patients with focal epilepsy, a substantial number of patients do not experience a complete remission after operation, prompting researchers to investigate alternative treatments.

Steven Rothman, M.D., and colleagues conducted experiments with UV LEDs to control seizure-like activity in rodent brain slices. Population spikes in CA1 (which reflect the discharge of a population of neurons) were elicited by delivering constant current pulses through a microelectrode placed in the CA3 brain area. Researchers induced seizure-like activity by adding the convulsant, 4-aminopyridine (4-AP; 100 µM) and removing magnesium from the fluid solution outside the cells. Caged GABA, BC204, was perfused into the preparation for at least 30 minutes prior to the first illumination.

When population spikes were measured (as a reflection of tissue excitability), the research team found that illumination of control slices with up to 200 mA LED current had no effect on peak amplitudes. Addition of BC204 (30 µM) and illumination using as little as 50 mA LED current produced a statistically significant reduction of the peak of the population spike. More important, BC204 (10 µM) significantly reduced the slice spikes and bursting induced by the 4-AP and low magnesium.

“Our strongly positive results, in an epilepsy model far more severe than the naturally occurring disease, suggest that this technique could translate to human epilepsy,” said Dr. Rothman. Researchers believe that a programmable pump could deliver the caged GABA into the subarachnoid space over the epileptic area of the brain. UV LEDs could then be responsively activated to release GABA, using techniques similar to those used for cortical stimulation units that are currently in clinical trials.

The researchers are optimistic that an LED-based implantable device is feasible. “Optical stimulation would be a far more rapid delivery method than any mechanical device for direct administration of drug into the brain and would not subject patients to toxic doses of medication or irreversible brain damage from epilepsy resections,” concluded Dr. Rothman.

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Active duty military personnel in war zones also experience severe brain injury as a result of blasts from the explosion of makeshift bombs or improvised explosive devices.

The study will take place over five years and will be led by Michael Rogawski, professor and chair of the Department of Neurology in the UC Davis School of Medicine, who is highly regarded for developing new drug treatments for patients with epilepsy.

“Allopregnanolone has never been tested in humans with brain injuries but it has been shown to be effective in animal models,” Rogawski said. “We believe that this approach can provide patients with improved survival and cognition and better overall neurological outcomes. We also will be looking to see if it prevents the development of post-traumatic epilepsy.”

“Post-traumatic epilepsy is a major complication of traumatic brain injury that is associated with psychosocial disability and may be a contributing factor to premature death after head injury,” Rogawski said. “The incidence of post-traumatic epilepsy is 10 to 15 percent for adults with severe brain injuries and has been as high as 50 percent in the military.”

Allopregnanolone is a steroid that protects against seizures and brain injury. It is produced in the body from the female sex hormone progesterone. Recently, progesterone has been studied and found promising for treating brain injury in humans. But it is difficult to formulate and administer and produces hormonal side effects, Rogawski said. In animals, allopregnanolone is more potent than progesterone in treating traumatic brain injury and it does not have progesterone’s hormonal activity, he said.

Whether from car crashes or the explosion of bombs in war-torn countries, more than 1.4 million Americans suffer head injuries each year and 50,000 people die from them, according to the U.S. Centers for Disease Control and Prevention. More than 5 million people – about 2 percent of the population – are left with long-term or lifelong disabilities as a result of traumatic brain injury.

All 18- to 59-year-old patients with severe blunt or penetrating head trauma seen in the UC Davis Medical Center emergency department will be approached to participate in the clinical trial. Patients who enroll will receive either allopregnanolone or a placebo within hours of a brain injury and at regular intervals over a five-day period.

Researchers hope to enroll 136 male and female patients to determine whether receiving the drug minimizes brain damage, reduces or eliminates post-traumatic epileptic seizures, and improves patients’ psychological functioning and overall quality of life.

UC Davis will manufacture allopregnanolone through the UC Davis Institute for Regenerative Cures’ Good Manufacturing Practices Facility directed by Gerhard Bauer, an assistant professor of hematology and oncology. Kate Marusina of the National Institutes of Health (NIH)-funded Clinical Translational Science Center is assisting with Food and Drug Administration regulatory filings.

“This is a unique study because UC Davis is sponsoring the trial and is also manufacturing the drug to be used in the clinical trial,” Rogawski said.

Joanne Natale, associate professor of pediatrics, designed the study with Rogawski. Other study researchers will include Nathan Kuppermann, professor and chair of emergency medicine, Paul Muizelaar, professor and chair of neurological surgery, and Kathleen Baynes, professor of neurology, all of UC Davis.

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“The incidence of individuals with a mathematics learning disability is between 6 – 7% of the population.” Sidney Groffman OD, MA, FCOVD, Professor Emeritus at SUNY College of Optometry, author of the article published in the December 2009 issue of Optometry & Vision Development, also says, “This is unfortunate because math skills are of prime importance in everyday life enabling us to understand number concepts and do calculations.”

Dr. Dominck Maino, editor of Optometry & Vision Development says that in this article, “Dr. Groffman goes on to review a particular ability called subitizing. This is a basic skill which has been known to be a precursor of math skills.” Dr. Groffman has helped to develop a subitizing vision therapy computer program that has been designed and based upon theories and experimental data appropriate for improving math skills. It consists of a diagnostic test and four therapy programs. This paper reviews subitizing and how members of the College of Optometrists in Vision Development can use this computer program to help their patients.

In this same issue of Optometry & Vision Development, Drs. Burkhart Fischer and Klaus Hartnegg of the Centre of Neuroscience, Optomotor Laboratory, of the University of Freiburg, present their research on instability of fixation and children with dyslexia. They note that “Dyslexic subjects have higher incidence of fixation instabilities as compared with their corresponding age group. The percentage of affected subjects was 25% for the binocular instability independent of age. Daily practice improves binocular fixation by 55%, with simple stability improving by 19%. To the extent that the binocular vision instability causes dynamic problems of stereo-vision (3D vision), the trained subjects have less and shorter periods of double images arriving at cortical levels of visual processing. This in turn makes it easier for them to identify letters and short sequences of letters with the result of fewer problems in reading.”

And finally, researchers at Western University of Health Sciences, College of Optometry, the Jules Stein Eye Institute, UCLA, and the Southern California College of Optometry, Drs. Chris Chase, Chinatsu Tosha, Eric Borsting, and William Ridder have noted that the Conlon survey is a useful tool to identify students with near work vision problems that negatively affect academic/school performance or are associated with eye focusing problems.

About Optometry & Vision Development

Optometry & Vision Development (OVD) is a peer-reviewed open access journal indexed in the online Directory of Open Access Journals.

About COVD

The College of Optometrists in Vision Development (COVD) is an international, non-profit optometric membership organization that provides education, evaluation, and board certification programs in behavioral and developmental vision care, optometric vision therapy, and visual rehabilitation. The organization is comprised of doctors of optometry, vision therapists and other vision specialists.

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The researchers say the findings support further investigation of the drug, decitabine, as a first-line treatment for these patients, who have limited treatment options.

Almost two-thirds of AML patients over age 65 do not receive treatment for the disease because standard therapy can be risky and often is ineffective. On average, such patients survive only 1.7 months after diagnosis.

“Older leukemia patients don’t have good treatment options because the chemotherapy and stem cell transplants that we commonly use for younger patients are often too toxic for them,” says lead author Amanda F. Cashen, M.D., assistant professor of medicine in the Division of Oncology and a bone marrow transplant specialist with the Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine.

“Furthermore, the biology of acute leukemia in the older patient population is different, making their response rate lower, their risk of relapse higher and their cure rates lower,” she says. “So we definitely need new therapies in that patient population — treatments that are going to be both better tolerated and more effective.”

The study, to be published in an upcoming issue of the Journal of Clinical Oncology and now available on-line, was conducted at three sites: Washington University School of Medicine; the University of California, Los Angeles; and the City of Hope National Medical Center in Duarte, Calif. The researchers tested decitabine in 55 AML patients with an average age of 74 years.

Decitabine can increase the activity of genes that have been silenced in cancer cells. It works by reducing the amount of DNA that is marked with a chemical tag called a methyl group. Scientists think that the excess methylation found in cancer cells inactivates genes that normally suppress tumor development.

All patients received the same decitabine dose for five consecutive days every four weeks until their disease stopped responding to the drug and began progressing or until an adverse event occurred to prevent further participation. By comparison to standard chemotherapy and stem cell transplantation, the treatment was considered a low-intensity treatment and was more tolerable for elderly patients, especially those with accompanying medical problems.

In 24 percent of the study participants, blood counts and bone marrow returned to normal, which is considered a complete response. It took 4.5 cycles of decitabine treatment on average to achieve a complete response. In those with a complete response, average survival time was 14 months. For all study participants, average survival time was 7.7 months.

Treatment-related adverse events included low blood counts (red cells, white cells and platelets), infection, fever and fatigue. Almost half of the study participants had at least one serious adverse event. Seven patients discontinued treatment, and three patients died as the result of adverse events.

“We have to wait for the results of further trials of decitabine to have a better estimate of the response rate and survival outcome compared to other low intensity options for older adults,” Cashen says. “This study can’t definitively establish decitabine’s role for treating older adults with AML, but it certainly excites us to study it more.”

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Gleevec, one of the first targeted cancer therapies with wide success in CML patients, destroys most leukemic cells in the body, but in most patients, some cancerous cells remain and are measurable with sensitive molecular tests. These remaining cells are a source of relapse, according to the investigators, especially if Gleevec therapy is stopped.

In a pilot study published in Clinical Cancer Research, the Johns Hopkins investigators used a vaccine made from CML cells irradiated to halt their cancerous potential and genetically altered to produce an immune system stimulator called GM-CSF. The treated cells also carry molecules, called antigens, specific to CML cells, which prime the immune system to recognize and kill circulating CML cells. The team cautions that their results are very preliminary and they cannot yet rule out other reasons for success.

The study vaccine was given to 19 CML patients with measurable cancer cells, despite taking Gleevec for at least one year. A series of 10 skin injections were given every three weeks for a total of four times. After a median of 72 months of follow-up, the number of remaining cancer cells declined in 13 patients, 12 of whom reached their lowest levels of residual cancer cells. In seven patients, CML became completely undetectable. Because the study was conducted in a limited number of patients and not compared with other therapies, the researchers warn they cannot be sure that the responses were a result of the vaccine.

“We want to get rid of every last cancer cell in the body, and using cancer vaccines may be a good way to mop up residual disease,” says Hyam Levitsky, M.D., professor of oncology, medicine and urology at the Johns Hopkins Kimmel Cancer Center. More research to confirm and expand the results is needed, Levitsky said.

The investigators will be testing blood samples taken from the study patients to identify the precise antigens that the immune system is recognizing. With this information, they will tailor their vaccine for additional studies that monitor immune response more precisely.

Patients receiving the trial vaccine experienced relatively few side effects that included injection site pain and swelling, occasional muscle aches and mild fevers.

According to the investigators, most patients with CML will need to remain on Gleevec therapy for the rest of their lives. More than 90 percent of them will achieve remission, but about 10 to 15 percent of patients cannot tolerate the drug long term. “Often patients have low blood cell counts, fluid retention, significant nausea and other gastrointestinal problems,” says B. Douglas Smith, M.D., associate professor of oncology at the Johns Hopkins Kimmel Cancer Center. Secondary therapies, including dasatinib and nilotinib, also have many side effects.

Another common side effect of Gleevec, says Smith, is fatigue. “Patients often tell me that they feel about 80 to 90 percent of what they should, and over time, this may have a big impact on their quality of life,” he says.

Gleevec also cannot be taken during pregnancy, and since one-third of CML patients are in their 20s and 30s, many patients hoping to start families would like to discontinue taking it.

“Ultimately, should this vaccine approach prove to be successful, the ability to get patients off lifelong Gleevec therapy would be a significant advance,” says Levitsky.

The research was funded by the National Institutes of Health.

Study contributors include Yvette Kasamon, Jeanne Kowalski, Christopher Gocke, Kathleen Murphy, Hua-Ling Tsai, Lu Qin, Christina Chia, Barbara Biedrzycki, and Richard Jones from Johns Hopkins; Carole Miller from St. Agnes Hospital; Elizabeth Garrett-Mayer from the Medical University of South Carolina; and Thomas Harding and Guang Haun Tu from Cell Genesys, Inc.

Under a licensing agreement between BioSante Pharmaceuticals Inc. and the Johns Hopkins University, Dr. Levitsky is entitled to a share of milestone payments and a share of royalty received by the University on sales of GVAX. Dr. Levitsky previously served as a paid consultant to Cell Genesys, which has since been acquired by BioSante Pharmaceuticals Inc. The terms of this arrangement are being managed by the Johns Hopkins University in accordance with its conflict-of-interest policies.

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