ALS Research Roundup

Stem cells injected into spinal cord slow ALS progression in rats

Nicholas Maragakis led a research team that found transplantation into the spinal cord of cells called glial-restricted precursors increased survival time and slowed disease progression in ALS rats.

Scientists at Johns Hopkins School of Medicine in Baltimore and Invitrogen Corp in Carlsbad, Calif., have shown that specialized stem cells known as glial-restricted precursors, or GRPs, can slow disease progression and prolong survival in rats engineered to have a disease that closely mimics human ALS.

The team published its findings online Oct. 19 in Nature Neuroscience. MDA supported the principal investigator, Nicholas Maragakis at Johns Hopkins, for this work.  Jeffrey Rothstein, a longtime MDA grantee and director of MDA’s ALS Center at that institution, was also a collaborator on the project.

The investigators injected the GRPs, a type of immature nervous-system support cell, into the area of the cervical (upper) spinal cord associated with respiratory function, targeting motor neurons (nerve cells that activate muscle) responsible for stimulating the diaphragm. Approximately one-third of the transplanted cells survived through end-stage disease (when the rats were about 170 days old) and, of those, nearly 90 percent differentiated, or matured, into astrocytes, a type of support cell in the nervous system. No damage to the spinal cord, including cyst or tumor formation, was observed.

Rats that received the GRPs lived 16.9 days longer than those that received a placebo. They also showed slower disease progression than the placebo-treated rats did, with longer preservation of respiratory and front-leg function, and motor neuron loss was slowed.

Data from the study indicates the transplanted cells continued to produce a protein that clears the potentially toxic chemical glutamate from the vicinity of nerve cells. Other therapeutic benefits of the GRPs, investigators note, could include a protective effect caused by the release of neurotrophic factors (proteins responsible for the growth and survival of neurons) and reduction of inflammation.

Third IGF1 trial shows no benefit

In a recently completed third trial of insulin-like growth factor 1 (IGF1) in people with ALS, investigators found the protein did not slow the progression of weakness, prolong survival or change the rate of functional deterioration.

Results were announced Nov. 5 at the 19th International Symposium on ALS/MND in Birmingham, United Kingdom.

A total of 330 participants from 21 centers were randomly selected to receive under-the-skin injections of either IGF1 or a placebo (inert substance) twice daily. Neither the participants nor the investigators knew who received which.

Measurements of muscle testing scores, survival rates and ALS Functional Rating Scale-Revised (ALSFRS-R) revealed no differences between the treatment and placebo groups.

However, this may not mean the end of IGF1-based treatment development. For more on the potential for this substance, see “IGF1: Failure or Success as an ALS Therapy?”

Surgeon reports on diaphragm pacing in ALS

A diaphragm pacing system, such as this NeuRx DPS, uses electrodes to rhythmically stimulate the diaphragm. Illustration courtesy of Synapse Biomedical

Raymond Onders, director of minimally invasive surgery at University Hospitals Case Medical Center in Cleveland, presented data at the 19th International Symposium on ALS on 88 ALS patients who were involved in trials of an implanted diaphragm pacing system. The symposium was held in Birmingham, United Kingdom, Nov. 3-5. (For more on this meeting, see www.mndassociation.org.)

Onders said diaphragm pacing appears to be well tolerated by people with ALS and to slow respiratory deterioration in this disease. The diaphragm is a major respiratory muscle located under the rib cage.

A diaphragm pacing system uses surgically implanted electrodes in the diaphragm to cause regular, rhythmic muscle contractions. It works similarly to a cardiac pacemaker, which regulates the heartbeat.

The goal of diaphragm pacing, which can be used in combination with noninvasive positive pressure ventilation, is to help maintain respiratory function artificially while preserving as many remaining muscle fibers in the diaphragm as possible.

Onders presented results from a pilot study of 16 patients who received pacing systems and a second, larger study of 72 who got the devices.

In the long-term follow-up of the pilot study, patients with declining respiratory capacity during the lead-in period showed a slower rate of decline after receiving the implanted pacing system, said Onders, who holds the Margaret and Walter Remen Chair in Surgical Innovation at Case. He also said the respiratory items on the ALS Functional Rating Scale did not decline despite deteriorating scores overall.

In summarizing results from all trial participants who received diaphragm pacing systems, Onders noted that some have had the device for as long as two years and that so far no one has been unable to tolerate it. All 26 patients who received a pacing system and also had a gastrostomy (feeding) tube were alive 30 days after pacer insertion, and 83 percent were alive after a year.

Onders said he believes diaphragm pacing systems can be safely implanted and utilized in ALS patients and have a positive effect on diaphragm function.

Hans Katzberg in the Department of Neurology & Neurological Sciences at Stanford (Calif.) University has an MDA grant to study the effect of diaphragm pacing on sleep quality in people with ALS.

What happens first in ALS could influence treatment development

Damage to muscle fibers may play an earlier and larger role in ALS than previously believed, according to a multinational team of researchers coordinated by MDA grantee Antonio Musaro at the University of Rome (Italy).

The findings of these investigators, published in the Nov. 5 issue of Cell Metabolism, contradict an assumption that ALS researchers have made for decades, which is that the primary targets in the disease process are muscle-controlling nerve cells called motor neurons in the spinal cord and brain.

The new conclusions, if confirmed, would be a positive development for ALS researchers and patients, because muscle tissue is more accessible than the spinal cord or brain and would be easier to reach with therapeutic substances.

Nerve and muscle fibers interact at the neuromuscular junction. New research suggests damage to muscle fibers may play an earlier and larger role in ALS than previously realized.

However, in a study partially funded by MDA that was published in Proceedings of the National Academy of Sciences in 2006, Timothy Miller and colleagues showed that partially blocking the effects of an ALS-causing genetic mutation in mice in muscle alone, while leaving the mutation in motor neurons, did not slow the course of the disease.

These investigators interpreted their findings to mean that muscle does not play an important role in ALS, at least in the form caused by mutations in the SOD1 gene, and that the problem is primarily one of motor neuron damage.

But in their new paper, Gabriella Dobrowolny and colleagues (coordinated by Musaro) report having conducted different experiments, and they come to different conclusions about these earlier findings.

In their experiments, the Musaro group found that when mice were genetically engineered to express mutated SOD1 genes and produce a toxic form of the SOD1 protein in skeletal muscles alone, they developed severe muscle wasting without any loss of motor neurons.

The muscle fibers with the mutated SOD1 genes sustained damage to their protective membranes, showed a change in metabolic activity, and didn’t function normally, the investigators say.

“The results of this study challenge the accepted dogma that motor neuron degeneration ... is the primary cause of muscle atrophy [wasting],” they note.

They say their findings don’t necessarily contradict the report from Miller and co-workers. Instead, they speculate, the reason that group didn’t see any slowing of the ALS disease process after blocking mutated SOD1 in muscle tissue is that the SOD1 wasn’t blocked completely and therefore continued to exert its toxic effect on muscle fibers.

They further speculate that toxic signals originating from skeletal muscle fibers may compromise the nerve-to-muscle connections. Damage to these connections, known as neuromuscular junctions, could, in this new way of looking at ALS, contribute to the loss of motor neurons.

“Taken together,” Musaro said, “these results support the redefinition of ALS as a multisystem disease in which in structural, physiological and metabolic alterations in different cell types — muscle cells, motor neurons and motor-neuron support cells — may act synergistically to exacerbate the disease.” He added that, from a therapeutic point of view, “perhaps the most powerful future approach would be to target both spinal cord and muscle.”

VEGF-B saves nerve cells, lengthens life in ALS rats

A protein called VEGF-B (vascular endothelial growth factor B) protects nerve cells that control muscle action and prolongs the lives of ALS rats, an MDA-supported research team has found.

MDA grantee Peter Carmeliet at the Flanders Institute for Biotechnology at the University of Leuven (Belgium) coordinated the team, which announced its findings in the Oct. 15 issue of the Journal of Neuroscience.

Earlier work by Carmeliet and colleagues has shown that a structurally similar protein, VEGF (vascular endothelial growth factor, which encourages the growth of blood vessels), also has the ability to protect these nerve cells, called motor neurons. However, concerns about the potential for this protein to cause excessive proliferation of blood vessels has limited its development as a neuroprotective agent.

This spring, Xuri Li at the National Institutes of Health, and colleagues, found that VEGF-B, which comes from a gene different from the VEGF gene, also has potent cell-protecting properties in the nervous system. Despite its similar name, they found, it doesn’t cause growth of new blood vessels. Li’s group found VEGF-B minimized damage to the optic nerve, retina and brain in mice with injuries to these areas.

Now, Carmeliet and colleagues have found an infusion of VEGF-B into the spinal fluid of ALS rats protected nerve cells and prolonged life by an average of 15 days compared to survival for untreated ALS rats, a difference considered significant. VEGF-B treatment appears safer than treatment with VEGF, since it didn’t cause blood-vessel growth or leakiness in brain membranes, which are concerns with VEGF.

ALS rats treated with VEGF-B also maintained the ability to stay on a rotating rod 11 days longer than the untreated rats did, but this difference was not considered statistically significant.

“Overall, delivery of VEGF-B may offer therapeutic opportunities for neurodegenerative diseases that develop spontaneously,” the researchers say.

ALS Clinical Research Network project selection under way

Five MDA/ALS Centers will participate in the new ALS Clinical Research Network. A study of blood lipid levels in ALS is among the proposed projects.

Investigators from the five centers that comprise the ALS-focused aspect of MDA’s new Clinical Research Network have begun selecting and prioritizing projects. (See “ALS to be a major focus,” October 2008.)

Among them is a study of hyperlipidemia (raised levels of fatty molecules, or “lipids,” in the blood) as a predictor of disease progression.

Results from a French study, published in March 2008 in the journal Neurology, suggested that elevated levels of lipids in the blood, known to be risk factors for cardiovascular disease, actually may be a good thing in ALS. (See “Does a high serum cholesterol level increase survival time in ALS?”, May 2008.)

Also spurring interest in hyperlipidemia and ALS is a possible connection between the use of cholesterol-lowering “statin” medications such as atorvastatin (Lipitor), lovastatin (Mevacor), simvastatin (Zocor) and others, and an elevated risk of developing ALS. This possible association was the focus of a 2007 report from the World Health Organization.

On the other hand, studies have shown evidence of inflammation in the spinal cords of ALS patients, and statins are known to have anti-inflammatory properties. At the Methodist Neurological Institute in Houston, atorvastatin is being investigated in a clinical trial for its potential to positively affect the course of ALS.

Other ALS projects identified by the investigators as priorities include the development of meaningful measures for use in clinical trials, and development of a system to select, design and perform studies on treatments in phase 2 clinical trials.

Teva to test blocker of AMPA receptors in large-scale trial

Teva Pharmaceutical Industries, a global pharmaceutical company based in Petach Tikva, Israel, is conducting a multicenter, one-year study of an experimental oral drug called talampanel, in which two doses of the drug will be compared to a placebo in people with ALS.

Teva is seeking approximately 100 participants for study at seven U.S. sites and some 400 additional participants from other countries.

Talampanel blocks AMPA receptors, molecular docking sites for glutamate, a potentially toxic nervous-system chemical. In an earlier, small study, there were indications that people who took talampanel did better on the ALS Functional Rating Scale than those who took a placebo.

This new, larger study will assess safety and effectiveness of talampanel in ALS and is open to adults who have ALS symptoms that began no more than three years before their screening visit; who are not using any assisted ventilation; don’t have a gastrostomy tube; and meet other criteria. Contact Mary Lou Watson at SUNY Upstate Medical University in Syracuse, N.Y., at (315) 464-5004.

IGF1: Failure or Success as an ALS Therapy?

By Amy Labbe

Genes encased in adeno-associated virus (AAV) delivery vehicles are injected into muscle. From there they can travel through the nerve fiber to the nervous system.

In a recently completed clinical trial for insulin-like growth factor 1 (IGF1) in ALS, (See “Third IGF1 trial,” ), investigators found the protein did not slow the progression of weakness, prolong survival or slow functional deterioration in people with ALS.

In spite of these results, IGF1 may yet have a future in treating ALS.

Studies in the 1990s showed conflicting results

The naturally occurring protein IGF1 plays an important role in human growth and development. It also belongs to a group of chemicals called “neurotrophic factors,” which contribute to the growth and survival of neurons (nerve cells).

As a potential therapy, IGF1 was developed under the brand name Myotrophin by the pharmaceutical company Cephalon of Frazer, Pa., and its partner Chiron of Emeryville, Calif.

Two human clinical trials of Myotrophin, delivered by subcutaneous (under the skin) injection in ALS patients in the 1990s, demonstrated inconclusive results. The first study, in North America, suggested a beneficial effect as measured by the Appel ALS rating scale, which measures loss of function over time. A large European study, however, failed to demonstrate benefit; in addition, more deaths occurred among patients who received the drug than in those who received a placebo.

“We were left with one ‘good’ study and one ‘failed’ study — with the latter possibly due to unequal baseline stratification of patients — and a third study was truly needed,” said neurologist Stanley Appel, director of MDA’s ALS Center at the Methodist Neurological Institute in Houston (and creator of the Appel ALS rating scale).

Results from ‘tie-breaker’ trial negative

Cephalon provided the drug for the recent third and “tie-breaking” trial, in which IGF1 again showed no benefit in people with ALS.

Appel noted the protein still may have potential if administered differently, such as by viral-vector or stem cell delivery, but, he said, “This trial settles the question as to whether injection of IGF1 in this form has a significant clinical benefit.”

Down, but perhaps not out

The possibility that IGF1 may yet provide some benefit in ALS might depend on tweaking the protein’s structure or changing the method of delivery. 

One structural variation of IGF1 that has garnered a significant amount of interest is Iplex, a combination of IGF1 and binding protein 3 manufactured by Insmed of Richmond, Va. (In the body, IGF1 connects to binding proteins that prolong its usefulness and help deliver it to target tissues.) Iplex, like IGF1, is administered via subcutaneous injection.

Although it’s being studied in myotonic muscular dystrophy, Iplex never has been rigorously tested in ALS, and there currently is no evidence to support its use in ALS.

Delivery as gene therapy

Another possible IGF1 approach that may yield greater success in reaching the nervous system (brain and spinal cord) is gene therapy.

One proposed method involves encasing genes for IGF1 in adeno-associated viral (AAV) delivery vehicles and injecting them into muscle, from which they can travel to the nervous system.

In 2003, Jeffrey Rothstein, director of the MDA/ALS Center at Johns Hopkins University in Baltimore, and colleagues, demonstrated the feasibility and benefit of this strategy in animals. Mice with an ALS-like disease survived a median 37 days longer than untreated animals with the same disease after IGF1 gene therapy.

Brian Kaspar at Nationwide Children’s Hospital in Columbus, Ohio, also has shown that AAV delivery of IGF1 to the spinal cord can lengthen survival in mice with a disease resembling ALS. Kaspar currently has MDA support to further develop IGF1 gene therapy.

The road ahead

The differences between injecting the IGF1 protein subcutaneously, as was done in the three IGF1 human clinical trials, and injecting a modified version of it or delivering it via gene therapy, may be the differences between failure and success for IGF1 in ALS.

The field has come a long way since Myotrophin was first developed. At that time, researchers believed the large protein molecule might somehow reach the ALS-affected nervous system (which it didn’t do) or that its positive effect on muscle fibers might maintain patients’ strength in the face of nerve-cell destruction (another false hope).

Gulf War Syndrome Report May Have ALS Implications
“… the first page in the next chapter of investigations”

Above photo of unidentified soldier from iStockphoto

by Margaret Wahl

On Nov. 17, the Research Advisory Committee on Gulf War Veterans’ Illnesses released a 454-page report linking exposure to nervous-system toxins with the development of illness in Gulf War veterans.

Gulf War illness, or syndrome, which this report describes as a collection of symptoms typically including persistent memory and concentration problems, chronic headaches, widespread pain and gastrointestinal problems, affects at least 25 percent of the 697,000 U.S. veterans who served in the 1990-1991 Gulf War.

This syndrome is not ALS. However, the report also notes that veterans of the Gulf War have significantly higher rates of ALS and brain cancer than other veterans. The links, if any, among these conditions are unknown.

The advisory committee, made up of experts from several academic institutions and government agencies, stated in its report that “evidence strongly and consistently indicates that two Gulf War neurotoxic exposures are causally associated with Gulf War illness: 1) use of pyridostigmine bromide (PB) pills, given to protect troops from effects of nerve agents, and 2) pesticide use during deployment.”

These chemicals cause an abnormal and potentially toxic elevation of the chemical acetylcholine in parts of the nervous system and at the junction of nerve and muscle fibers. They’ve previously been suspected as possible culprits in the development of ALS in veterans of the Gulf War, in conjunction with genetic factors that interfere with the body’s ability to handle these substances.

Denise Figlewicz, who had MDA support for several ALS-related research projects at the University of Rochester (N.Y.) and the University of Michigan between 1994 and 2006, was part of a research group that in 2006 found that variants in the genes for the PON1 and the PON2 enzymes (known to help detoxify chemicals) were associated with ALS in a Polish population.

In 2008, MDA grantee Guy Rouleau at the University of Montreal and colleagues published findings showing that genetic variants in the PON genes are associated with ALS in France and Quebec.

Figlewicz notes that several additional studies also have found associations between ALS development and PON gene variants that may make PON enzymes less effective, but no two studies have fingered the same PON variant.

“It’s a mystery that still needs to be unraveled,” she says, adding that more research is needed to probe the possible connections between Gulf War illness, ALS, toxic exposures and PON gene and enzyme variations.

“There are many unanswered questions, but after reading this report on Gulf War illness, I don’t think anybody would say to stop this area of research because there’s nothing there. In fact, the credible identification of two causative factors for GWI represents the first page in the next chapter of investigations.”

The Research Advisory Committee on Gulf War Veterans’ Illnesses report can be seen at www1.va.gov/RAC-GWVI.

Tips for Helping Your Caregiver Cope

by Kathy Wechsler

A tense caregiving relationship can be difficult for everyone involved.

Although the focus often is on the person with ALS, sometimes caregivers also need help dealing with their feelings and learning new skills, including how to ask for help from others, says Elizabeth Etigson, a licensed professional clinical counselor who facilitates the MDA/ALS support group in Albuquerque, N.M., and has a private practice, Purple Turtle Counseling.

Below are some tips for addressing common complaints from caregivers and improving the caregiver/care receiver relationship.

“I can’t do everything myself!”

Caregivers often feel overwhelmed and as if everyone is pulling them in different directions, Etigson says.

One solution is better organization. Hold regular meetings to discuss what tasks need to be done and assign a variety of people to do them — family members, friends, neighbors, hired professionals and acquaintances who have offered to help. If a task must be done by the caregiver, can someone else pick up one of the caregiver’s other responsibilities? Be ready to reach for the task list whenever people say, “Let me know if there’s anything I can do to help.”

“I never have time for myself!”

If caregivers don’t take time off every now and then, resentment can start to build and may spill over onto their loved ones. To avoid burnout, caregivers must learn to take periods of time for themselves, whether it’s a weekend away or short breaks to get a massage, go to the gym, take a nap, phone a friend, walk the mall or read a book.

Sometimes caregivers feel guilty about being away from their loved ones, so they put their own needs aside. Care receivers must address these feelings of guilt, urges Etigson, and let caregivers know they want them to take breaks and ask for help when needed.

“What happens if I get hurt?”

Many caregivers worry about the possibility of hurting themselves, especially during transfers, and not being able to care for their loved ones any longer. This concern needs to be addressed before problems arise, especially as caregivers age.

Again, getting some help is a good way to solve this problem. Another solution is to have occupational therapists evaluate transfers and suggest ways to make them safer, says Etigson. Patient lifts (like a Hoyer lift) take the risk and physical strain out of transfers. For their own well-being, all caregivers should consider using lifts for transfers. Care receivers can help by being willing to accept this different form of transfer.

“I don’t feel appreciated!”

Sometimes discomfort or bad days make it hard for care receivers to show gratitude. But it’s important to let caregivers know that their hard work hasn’t gone unnoticed.

Never underestimate the value of a smile and a “thank you.” Etigson also suggests writing a letter of appreciation or simply acknowledging the situation in a humorous way: “‘I know I’m a pain in the butt sometimes, and I really thank you for hanging in there with me.’”

Look Ma! No Hands!
Head mouse, virtual clickers provide hands-free computer access

by Alyssa Quintero

Kristen Sauer, who’s had ALS for eight years, uses the SmartNav and her laptop to run a successful home business, pay her family’s bills, communicate via e-mail and much more.

Hand and arm weakness can make it fatiguing and frustrating to use a computer’s conventional keyboard and mouse. So, why not try using your head?

For some with ALS, a head mouse, or head tracker, provides an effective way to maintain communication and computer access. These devices typically are used in conjunction with specialized communication software, onscreen keyboards and mouse-clicking solutions.

Staying connected

For Kristen Sauer of Waupin, Wis., computer access is crucial to maintaining her home-based business, communicating with family and friends, and other activities.

The SmartNav AT package provides a complete hands-free computer solution — including built-in onscreen keyboard and mouse-clicking capabilities — to people who are unable to use a traditional keyboard and mouse.

Seven years ago, when ALS made it difficult and exhausting to use a standard mouse and keyboard, Sauer, 32, put her money on the SmartNav ($499), a hands-free mouse solution manufactured by NaturalPoint (www.naturalpoint.com).

“Using a computer the conventional way can be very taxing,” Sauer wrote via e-mail. “My shoulders, wrists and back would ache after a short time. The SmartNav took the exhaustion and pain away, and I could enjoy the computer again! I wouldn’t be able to use a computer at all without it.”

Sauer, who has no functional movement from the shoulders down, relies on the SmartNav 3 AT package for complete computer control. A small infrared camera mounts to the top of Sauer’s Windows-based laptop (about 2 feet away) and a paper-thin reflective dot attaches to her eyeglasses; she moves her head, and the cursor moves to the desired location. Cursor speed is adjustable, and less than an inch of head movement is enough to move it across the screen.

It sounds simple, but the head mouse itself is only one part of the equation. A head mouse can move the cursor around the screen — but that’s it. To achieve complete hands-free computer access, users usually require two other components — an onscreen keyboard for typing and a secondary clicking solution to make selections.

Making it work

Sauer uses an onscreen keyboard called OnScreen ($119) from RJ Cooper and Associates (www.rjcooper.com). It has a WordComplete feature that attempts to complete the word being typed based on your commonly used words. (In contrast, word prediction attempts to type ahead based on what the user already has typed.)

Typing a letter or e-mail with the onscreen keyboard takes longer than using a regular keyboard, but “it isn’t bad with practice,” Sauer said.

Sauer also uses the SmartNav software’s built-in dwell-clicking toolbar for making right and left mouse clicks. For example, when surfing the Internet, she just points to move the cursor to the desired location, dwells (lingers in one spot), and the head mouse clicks to select. (The SmartNav’s dwell time is adjustable.)

The dwell-clicker has all the capabilities of a mouse, including allowing the user to drag objects around the screen. Sauer simply selects the “drag object” button and moves her head in the direction she wants the object to go. Then she holds her head still for a fraction of a second to release the drag option.
“I know it sounds complicated, but it very quickly becomes second nature,” she reported.

A variety of uses
With her laptop and SmartNav, Sauer:

•   runs a home business putting VHS tapes, 8mm reels, pictures and slides on DVDs;

•   maintains the books for her husband’s electrical business;

•   helps her son with homework and school projects;

•   pays her family’s bills and shops online;

•   uses an Internet relay service to make phone calls;

•   controls the television, VCR, DVD player and satellite dish;

•   communicates via e-mail with family, friends and medical experts; and

•   corresponds with people with ALS and caregivers in online support groups and chats.

“The SmartNav has made a huge difference,” Sauer said. “I use it to make phone calls, which allows me to be home alone, and I can call if I need anything or if there’s an emergency. And, without the SmartNav, running my business wouldn’t be possible. I wouldn’t be able to edit photos and video, design the DVD covers and labels, or communicate with my clients.”

In addition, Sauer sometimes uses the text-to-speech software installed on her laptop, although her DynaVox V is her primary speech-generating device.

“I have separate devices because if my laptop gets a virus or breaks down, I’m not left without a speech device,” Sauer explained. “And, the DynaVox V doesn’t have enough power to run the software for my DVD business.”

Unfortunately, SmartNav isn’t compatible with her DynaVox V software, so she uses TrackerPro ($995, manufactured by Madentec) to operate the DynaVox, along with the OnScreen software and a dwell-clicking solution.

The TrackerPro doesn’t require additional software to work, but Sauer sees that as a drawback. For example, if she needs to adjust the TrackerPro’s cursor speed, all she can do is make the standard Windows mouse adjustments.

Sauer said she prefers the SmartNav over the TrackerPro because it allows better fine-tuning of the cursor speed, and requires much less effort to move the cursor.

“I can’t imagine life without the SmartNav,” Sauer emphasized. “I would be limited to watching the world go by. Instead, I can communicate with others and be productive.”

To learn more about the new SmartNav 4, which includes built-in dwell-clicking software and virtual onscreen keyboard for an all-in-one AT package, visit www.naturalpoint.com, or call (888) 865-5535. NaturalPoint also offers a SmartNav 4 upgrade discount to previous customers.

Stay tuned: In the February issue, ALSN will explore AbleNet’s revolutionary Impulse computer access device with Bluetooth technology.