HOMEBOUND LAW WOULD BENEFIT MILLIONS

"Every ounce of energy I have is being consumed by being here today, but I would much rather be here than confined to home waiting to die. Please give me and thousands like me the opportunity to forget about our disabilities and enjoy life as you have the freedom to do."

David Jayne receives home health care from Medicare. Photo by Atlanta Journal-Constitution

These are the words of David Jayne of Rex, Ga., a man severely affected by ALS. His May 16 speech — conveyed by voice synthesizer to a Capitol Hill audience of members of Congress and disability advocates — asked for support of the Homebound Clarification Act of 2001 (H.R. 1490).

Jayne is a long-term survivor of ALS whose Medicare home health battle was instrumental in the measure's reintroduction in Congress. Endorsed by MDA, the measure would benefit 3.5 million Medicare recipients who receive home health care, including people with ALS and other neuromuscular disorders.

The act broadens the definition of "homebound" for people receiving Medicare-covered services in the home. Current law requires recipients to remain in their homes except for infrequent absences of generally short duration.

Attending the briefing on behalf of MDA were Anne Kennedy, health care services coordinator at the Association's Fairfax, Va., district office, and Luis Baez, a member of the MDA National Task Force on Public Awareness. Other speakers included the law's co-sponsors, Reps. Edward Markey, D-Mass., and Chris Smith, R-N.J.

Jayne became a visible symbol for the Homebound Clarification Act last year when he successfully challenged the policy of both his home health agency and Medicare.

A law known as BIPA passed late last year allows recipients of Medicare in-home benefits to attend religious services and adult day-care programs, in addition to going out for medical services. H.R. 1490 would still require that recipients have a "normal inability to leave home." However, the frequency, purpose and duration of excursions wouldn't be counted against eligibility for Medicare's in-home services.

"Today new technology and positive attitudes toward people with disabilities, which are embodied in the Americans with Disabilities Act and promoted by MDA, help make it possible for thousands of individuals with disabilities to have complete access to community life," read a recent statement of support from MDA's national task force.

The Homebound Clarification Act is endorsed by some 30 disability organizations, including MDA. By early June, the measure had 46 congressional co-sponsors, and backers are seeking more.

You can support the bill by writing or calling your congressional representative. Contact information can be found at www.house.gov.

For updates on the legislation's progress, visit www.als-mda.org, or the Web site of the National Coalition to Amend the Medicare Homebound Restriction for Americans with Significant Chronic Illness (NCAHB), www.amendhomeboundpolicy.homestead.com. 

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ALS CHAT: THE POSSIBILITIES ARE ENDLESS

Internet users can go to MDA's new ALS Web site at www.als-mda.org and click on the Chat option to find out what ALS-related MDA chat sessions are in the offing.

Several directors of MDA/ALS research and clinical centers across the country have agreed to lead a series of online discussions about ALS that will begin in October. Some chats will focus on ALS research being conducted at the centers while other sessions will explore quality-of-life issues such as ventilation, caregiving, nutrition and exercise.

David Jayne, longtime advocate on issues important to people with ALS, has agreed to host an MDA chat on the ALS Division Web site, on July 24, called "Issues That Matter." (See "Homebound Law Would Benefit Millions")

In May, a monthly session on a wide range of ALS topics debuted on MDA's ALS site, co-hosted by Dave Gilbert and Elissa Edson. Gilbert (chat name "dgals") has ALS and serves as an MDA Task Force on Public Awareness member in Connecticut. Edson (chat name "woof") is MDA health care services coordinator in Glastonbury, Conn.

This discussion is open to anyone interested in ALS. The next session will be held from 2:30 to 4:30 p.m. EDT on June 21.

MDA is looking for people with ALS as well as family members and caregivers who may be interested in serving as hosts for new chats. Those with ideas for new ALS-related chats should contact the MDAchat administrator at mdachat@mdausa.org, or fill out a new chat group application form in the chat area to initiate the process.

Those who want to participate in MDA chats can register on the Web site, at no cost. And, if you're otherwise engaged at the time of an important MDA chat, you can find out what was said and by whom by checking out the chat transcript section.

At the bottom of the ALS chat page is a link to MDA's complete chat calendar. This page at www.mda.org/chat/calendar.html features chats on such subjects as careers, parenting, and service dogs — and a number of Spanish-language chats. In addition, this month MDA inaugurated a new Spanish Web site at www.mdaenespanol.org featuring chats, publications and news in Spanish. 

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NEW GENE IMPLICATED IN FAMILIAL ALS

Heart Gene May Be Link

In a new study, researchers investigating the genetics of cardiovascular disease may have stumbled upon a previously unknown genetic risk factor for ALS.

Defects in the SOD1 gene — the only known cause of ALS — account for just 2 percent of all ALS cases, leaving scientists to speculate about what causes the remaining 98 percent of cases. But the new study suggests that defects in a gene called VEGF could emerge as another cause of the disease.

The VEGF gene produces vascular endothelial growth factor, a protein that normally enhances the formation and function of blood vessels. When cells in the body are subjected to oxygen deprivation (a phenomenon called hypoxia), they respond by boosting their production of VEGF protein, thus improving local blood flow and oxygen supply.

Recent data have shown that a poor VEGF response — the persistence of low VEGF levels during hypoxia — might contribute to heart disease in humans.

That link between VEGF and heart disease caught the attention of Peter Carmeliet, who heads a cardiovascular research group at the Flanders Interuniversity Institute for Biotechnology in Belgium. To find out whether a poor VEGF response would cause heart disease in mice, Carmeliet and his group deleted a region of the mouse VEGF gene that acts like a hypoxia sensor.

As anticipated, the mutant mice showed a poor VEGF response. But unexpectedly, they also developed a condition similar to ALS.

The study appears in the June issue of Nature Genetics, along with commentary by ALS expert and MDA research grantee Don Cleveland, who's at the Ludwig Institute for Cancer Research in La Jolla, Calif.

In the commentary, Cleveland suggests that defects in the VEGF gene might account for cases of familial (inherited) ALS that aren't linked to the SOD1 gene. Cleveland also speculates that defects in VEGF regulation — genetic or otherwise — might even contribute to sporadic (noninherited) ALS.

Mutant VEGF mice develop a late-onset disease with many of the same microscopic signs of motor neuron destruction seen in people with ALS and in mutant SOD1 mice.

But how does the VEGF response — once thought to mainly control cardiovascular health — also affect motor neuron health? The mutant VEGF mice have signs of low blood flow in neuronal tissues, suggesting that oxygen deprivation contributes to motor neuron death in the mice. Also, it turns out that VEGF has a direct survival-promoting effect on isolated motor neurons.

It's now up to scientists to determine whether VEGF has similar effects in humans. In his commentary, Cleveland predicts that Carmeliet's results will "provoke a rapid search" for VEGF defects in people with either sporadic or familial ALS. 

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First Look Suggests Some Benefit From CoQ10

In a nine-month study of six people with ALS conducted at the Eleanor & Lou Gehrig MDA/ALS Center at Columbia-Presbyterian Medical Center in New York, investigators found that high-dose, orally administered coenzyme Q10 might be beneficial in preserving motor units in the disease. Because of the positive trends, researchers are planning a larger study.

A motor unit consists of a motor neuron (muscle-controlling nerve cell) and the muscle cells it controls. Coenzyme Q10 plays a role in the mitochondria, the energy-producing units of cells. It also functions as an antioxidant, a chemical that can help detoxify potentially damaging free radicals.

A person with ALS usually loses about 50 percent of existing motor units over a six-month period, said Clifton Gooch, a neurophysiologist who heads the Electromyography Laboratory at Columbia-Presbyterian. Motor unit numbers are estimated by measurements taken from surface electrodes placed on the skin, noted Sheila Hayes, a physical therapist who was part of the study team.

Hayes said that of the six people who remained throughout the study, three showed minimal gains in their motor unit numbers, and the other three had losses of 16 percent, 23 percent and 38 percent, respectively.

"Because of the small number of patients, one cannot draw firm conclusions from these results, but there were positive trends," Hayes said. She noted that people tolerated well the high doses used in the study — 600 milligrams a day. No symptoms or laboratory value changes were attributed to the drug.

The study data were presented at the 11th International Symposium on ALS/Motor Neuron Disease in Arhus, Denmark, in December. Funding was provided by Solgar Laboratories, which manufactures coQ10.

"This encourages us to organize a larger, double-blind, placebo-controlled trial of high-dose coQ10 in patients with ALS," said neurologist and study team member Salvatore DiMauro, an MDA research grantee. Planning for such a study is under way. 

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WHAT CAUSES ALS?

It's More Than Motor Neurons ...

A new study suggests that motor neurons — the muscle-controlling nerve cells that waste away in ALS — can't be the only cells that contribute to the disease.

While it's clear that motor neuron degeneration gives rise to the progressive muscle weakness that occurs in ALS, researchers have long speculated that other cell types might be essential players in the disease process. Guy Rouleau, an MDA grantee at McGill University and the Montreal General Hospital Research Institute in Canada, decided to test that idea by putting a new twist on a mouse model of familial ALS (FALS).

FALS is caused by mutant versions of the SOD1 gene — a gene that's normally turned on (activated) not just in motor neurons but in most cell types. Previous studies have shown that FALS-linked SOD1 genes have a toxic gain of function: When the mutant SOD1 is mixed into the genetic makeup of mice, the mice develop ALS, even if they have their own normal SOD1.

In the new study, Rouleau created mice carrying an FALS-linked SOD1 gene that could only turn on in motor neurons. (The mice still had normal SOD1 in all of their cells.)

To Rouleau's surprise, those mice didn't develop ALS. In the May 15 issue of the Journal of Neuroscience, he reports that the mice remained healthy throughout life, with no evidence of muscle weakness or motor neuron degeneration.

There are two possible explanations for the lack of disease in the mice, Rouleau says. One possibility is that the mutant SOD1 wasn't produced at high enough levels to have a toxic effect on the motor neurons. But the more interesting possibility is that mutant SOD1 toxicity in motor neurons alone isn't sufficient to cause ALS.

"This suggests that there's a very important interaction between motor neurons and other cells [in ALS]," says Rouleau.

Cells called astrocytes are especially likely to play a role in ALS, he says. It's known that astrocytes normally protect motor neurons from overstimulation by vacuuming up excess levels of the stimulatory chemical glutamate, and one theory holds that defective astrocytes contribute to ALS by allowing a toxic buildup of glutamate. Consistent with that theory, ALS is often associated with a decrease in glutamate uptake by astrocytes, and an increase in astrocyte growth called astrocytosis.

Last year, a group of researchers created mice with an FALS-linked SOD1 gene that could only turn on in astrocytes. While these mice didn't develop ALS, they did develop astrocytosis.

A combination of defects in astrocytes and motor neurons might be necessary to trigger full-blown ALS, Rouleau says. 

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Protein Clumps May Be Guilty in ALS

Clumps (aggregates) of proteins often observed in the motor neurons of people with ALS may not be innocent bystanders in the disease, but instead may play a role in causing it, implies a report in the May 25 issue of the journal Science.

Experts disagree about the role of such protein clumps, which are common in many neurodegenerative disorders. Some observers have suggested that clumps and tangles of proteins could be beneficial, while others have suggested they may be neutral, and still others have said that they're probably harmful. (See "Solving the SOD1 Puzzle," The ALS Newsletter, vol. 6, no. 1; and "Why Motor Neurons Die" vol. 4, no. 6.)

The new report, by Neil Bence, Roopal Sampat and Ron Kopito of the Department of Biological Sciences at Stanford (California) University, suggests that these clumps may play a key role in either starting or perpetuating cellular destruction in various neurodegenerative disorders, such as Alzheimer's disease. It doesn't specifically mention ALS.

Protein clumps in cells, the researchers say, may preoccupy a cellular garbage-disposal mechanism called the ubiquitin-proteasome system that normally rids the cell of damaged or malformed proteins before they can do any harm. The protein clumps found in many diseases (including ALS) may overwhelm the detoxification system, leaving malformed proteins free to wreak havoc while the disposal system is busy with the clumps, the researchers suggest.

The investigators tested the system by adding two different proteins known to lead to aggregates — an abnormal protein found in Huntington's disease and another one found in cystic fibrosis.

In a genetic form of ALS (not specifically addressed in the report), abnormal SOD1 protein appears to lead to protein aggregates. For some reason, such clumps are also seen in some people with sporadic ALS, in which SOD1 is theoretically normal.

More research needs to be done to confirm or refute these findings with respect to ALS. 

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STUDY OF EMOTIONAL CHANGES STILL OPEN

Avanir Pharmaceuticals of San Diego has added eight more locations for its trial of the drug AVP-923, designed to help control unwanted laughing and crying that sometimes occurs because of neurological dysfunction in ALS. (See "Avanir Launches Trial," The ALS Newsletter, vol. 5, no. 6, December 2000.) In addition, most of the original locations are still recruiting participants.

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ADAPTIVE FUN IN THE SUN

If you have ALS, the right adaptive sports or recreation program, or an accessible state or national park, may be able to help you get outside for a while this summer, while supporting your physical needs.

Some private organizations located across the United States offer organized outdoor fun for people with disabilities. These accessible facilities, with specially trained staff members, can accommodate people who use power wheelchairs or those who need full transfer assistance.

For example, Disabled Sports USA has many affiliates across the country, each specializing in certain activities. At Donner Memorial State Park in northern California, the organization offers a program adapted for people who use power wheelchairs; those who want to water ski or jet ski must be able to wear life vests, right themselves in the water and breathe on their own. The adventurous can use water skis specially outfitted with a secure seat comparable to that of a wheelchair.

At the National Sports Center for the Disabled in Winter Park, Colo., prospective participants are screened by telephone for their interest in and suitability for adapted programs in sailing, horseback riding, fishing and rafting.

While many places that offer adapted activities have recreational aides who also are trained to provide general assistance to people with physical disabilities, they generally expect people who need personal assistant services to provide their own or to pay extra for them.

Prices for activities vary from well under $100 per person per day to the low hundreds per day with additional attendant service.

If you prefer a less structured approach or a less strenuous excursion, you may choose day trips or camping at state or national parks, which offer a variety of outdoor choices amid spectacular settings.

At Yellowstone National Park, natural hot springs and geysers are the main attraction, and the Old Faithful area has accessible lodging, food service, camping and parking. In other areas of the park, visitors can find accessible fishing and wheelchair rental. Yellowstone offers a visitor's guide to accessible features.

At Acadia National Park on the rocky coast of Maine, campers can register at Blackwoods Camp-ground without leaving their cars, and some campsites have paved pathways leading to grills, picnic tables, water, restrooms and the amphitheater. And you can take in a view you'll always remember from the comfort of your own vehicle, driving the steep, winding road up to the top of 1,500-foot Cadillac Mountain, which overlooks the village of Bar Harbor and lovely coastal islands in Frenchman Bay.

Whichever of the hundreds of wildlife refuges, monuments, recreation areas, parks or historic sites you choose, the National Park Service offers its free Golden Access Passport to people with documented permanent disabilities. The pass entitles holders to free lifetime admission to facilities and 50 percent off camping, parking and more.

A recreation program, vacation or camping excursion should be chosen in consultation with your physician, and your plans should take into account your medical needs, level of ability and stamina.

To find out more about the accessibility of a national park near you, go to www.nps.gov/parks.html, and from the drop-down menu, select the park of your choice. From there, select "travel basics," then scroll down to "accessibility."

For detailed information on state-run outdoor facilities, contact your state park or conservation department. Other resources include:

Disabled Sports USA
www.dsusa.org (301) 217-0960

Disability Travel and Recreation Resources
www.makoa.org/travel.htm

Easy Access, the Sierra Club Guide
to National Parks for People with Disabilities,
by Wendy Roth and Michael Tompane

National Ability Center
www.nationalabilitycenter.org

National Center on Accessibility
www.indiana.edu/~nca/outdoor/outdoor.htm

National Park Service
www.nps.gov
(202) 208-6843

National Sports Center for the Disabled
www.nscd.org
(970) 726-1540

Wilderness Inquiry
www.wildernessinquiry.com
(800) 728-0719 

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VENTILATION STORY DRAWS READER RESPONSES

In response to "Noninvasive Ventilation Can't Sustain Life Indefinitely in ALS" (vol. 6, no. 2), we received a few comments taking issue with Hiroshi Mitsumoto's cautions about long-term use of noninvasive ventilation (NIV) in ALS. The story was a report of a study published in Muscle & Nerve which found that use of noninvasive ventilation may hasten decline of respiratory muscles over time. Mitsumoto, director of the Eleanor & Lou Gehrig MDA/ALS Center at Columbia University's Neurological Institute in New York, was an author of the study. The article wasn't meant to provide medical advice — only to report on a study.

This article adds to the conflicting information and misinformation reaching the ALS patient concerning respiratory care. Broad statements such as Dr. Mitsumoto's comment that BiPAP and other NIV systems are "not an answer" for long-term survival are simply incorrect. I am now in my sixth year of nasal ventilation and doing fine in a stabilized condition. Mitsumoto is incorrect, in my opinion, when he states that NIV won't be effective indefinitely in ALS.

Ed White
Fredericksburg, Texas

The question regarding whether it may be "worse" to provide NIV doesn't seem to be of much concern in ALS. The statement that pulmonary function declined over time despite the use of NIV is misleading, as this will occur as part of the disease process of ALS, regardless of the use of assisted ventilation, whether it be noninvasive or via trach. It is not the assisted breathing device causing the deconditioning of muscles, but ALS.

Pulmonary function will always deteriorate in time, so why not give the patient an extension of life and a better quality of life in any way possible? Although NIV cannot be used by every ALS patient, it can be a very effective long-term option.

Carolyn Moore, licensed vocational nurse
Blanco, Texas

Noninvasive ventilation can be delivered via mask.

MDA's The ALS Newsletter is one of the best informational resources today for people with ALS. Nowadays, with the growing number of ALS ventilator users, the newsletter provides up-to-date and accurate information for making the best life choices.

Until the 1990s, people with ALS used tracheostomy ventilation, usually as a result of emergency hospitalization and decision making. This unplanned outcome often resulted in unwanted, long-term ventilator-dependent survival, with progressive immobility, substantial care and high costs. In recent years, however, the use of nasal ventilation has steadily increased and is currently the treatment of choice for respiratory insufficiency associated with ALS.

Pamela A. Cazzolli, R.N.
ALS Clinical Nurse Consultant
Canton, Ohio

I agree [with Dr. Mitsumoto] that tracheostomy ventilation provides the best long-term survival for people with ALS who are engaged in living, want to continue and have the needed resources. But usually noninvasive ventilation is used first if possible.

Until a larger, well-designed, prospective [looking forward] clinical trial is done, I do not think that people with ALS should worry about the speculation that nocturnal NIV may decondition the respiratory muscles.

I strongly agree with Dr. Mitsumoto's emphasis that attention to safety is critically important when using mechanical ventilation for 20 to 24 hours a day.

Many people with ALS are quite satisfied with the quality of life and survival benefit from NIV and do not want to ever go on to tracheostomy. An advance directive should be used to formalize one's goals and preferences.

Edward Anthony Oppenheimer, M.D.
Pulmonary specialist
University of California, Los Angeles

Reply from Hiroshi Mitsumoto:

There is no doubt that noninvasive, positive-pressure ventilation (NPPV) is the first line of treatment for respiratory symptoms that occur during the course of ALS, including frequent awakening due to nocturnal respiratory problems.

We were in fact one of the first physician groups to start using NPPV for patients with ALS in the 1980s. Our experience therefore allows us to recognize the promise, as well as the limitations,of NPPV.

Now, in the era of evidence-based medicine, what we need is "class 1" evidence (based on prospective — following people through time — and controlled studies) that NPPV really prolongs survival and improves quality of life. Such evidence is not only important for medical practice but also strongly influences insurance carriers.

At present, there is only class 2 evidence, which is based on retrospective (looking back at patient histories) studies to support NPPV in ALS. Therefore, the use of NPPV is recommended as a guideline but not yet as a standard of care.

Obviously, the more we understand the effects and mechanisms of NPPV on respiratory muscles, the greater will be our ability to effectively use NPPV for patients with ALS.

Hiroshi Mitsumoto, M.D.
Professor of Neurology
Columbia University Neurological Institute, New York  

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AS YOU GIVETH . . .

After a lifetime of serving others, Sister Monica LaFleur of the Sisters of Charity of the Incarnate Word is now receiving care herself. Her career as an educator and historian had spanned nearly four decades when she first experienced unusual symptoms in 1999. In January 2000, she learned they were the result of ALS, and in May of that year she retired.

Sister Monica has received services at the MDA clinic in Houston. She's also attended the local MDA/ALS support group and obtained advice on equipment such as BiPAP and feeding tube.

Anne Swisher, MDA program services director in Houston, has become acquainted with Sister Monica and many of the other convent members. Swisher describes her as "a very gentle person with a great sense of humor. She's just a very caring person. She's part of a big family birthwise and adoptionwise" (as a convent member).

Sister Monica was born in 1928, 25 miles north of Lafayette, La., one of 10 children. She remains in contact with her siblings and receives monthly visits from her birth sisters.

To interview Sister Monica, who doesn't speak, we e-mailed questions to St. Placidus Director of Nursing Anne McVey, who relayed the questions to Sister Monica, who answered in longhand. Special thanks to Anne McVey for facilitating the interview.

A member of Houston's Villa de Matel (named for the congregation's founder), Sister Monica recently helped to dedicate the Heritage Center, the congregation's new archives building. An educator by vocation, she joined the order in 1946. She taught and served as principal and superintendent, grades K-8, for the Diocese of Houston and Galveston for 26 years. For 12 more she worked as archivist (historian) for the congregation of the Sisters of Charity of the Incarnate Word.

Having lost the ability to speak, she misses her role in sharing the events of the day with other members of her community. With assistance, she still goes to mass each morning and participates in a regular exercise group, but her days contain much more silent reflection and prayer.

After years of serving others, she's now receiving others' service, yet she has no complaints. She says, "I get the best. My congregation provides all needs."  

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MDA OPENS TWO NEW ALS CENTERS IN ARIZONA

St. Joseph's Hospital in Phoenix and the Neurology Clinic of the University of Arizona Health Sciences Center in Tucson have been designated as the sites of the newest MDA/ALS research and clinical centers. The new centers — the 23rd and 24th such facilities to receive the MDA/ALS designation — were announced during a recent Perspective on ALS seminar in Tucson, sponsored by MDA's ALS Division.

The comprehensive, multidisciplinary facilities are expected to serve more than 150 people in Arizona with ALS.

The UA Neurology Clinic, at 707 N. Alvernon Way, Suite 201, houses the Tucson center, operating under the direction of Valerie Cwik, UA assistant professor of neurology. Cwik heads a team that offers a multidisciplinary approach to ALS treatment. The center provides ALS patients with care from physicians, a nurse coordinator, a physical therapist, an occupational therapist, a speech therapist and a genetic counselor.

In addition to its clinical services for patients, Cwik's team also conducts ongoing ALS research. To schedule an appointment, call (520) 694-8888. For other inquiries about the center, call (520) 694-1450.

The director of the new Phoenix center, called the MDA/ALS Neuromuscular Research Center, is Kumaraswamy Sivakumar. The center provides ALS patients with care from physicians, a nurse coordinator, a physical therapist, an occupational therapist, a speech therapist and a genetic counselor. Because of its affiliation with St. Joseph's Hospital, the Phoenix center will also feature a pulmonologist, a cardiologist and a gastroenterologist — all on-site.

Sivakumar's team also conducts ALS research. The facility is located at 240 W. Thomas Road, and can be reached by calling (602) 406-6360.

For a complete list of MDA/ALS centers, see The ALS Newsletter, vol. 6, no. 1, or go to www.als-mda.org.  

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HELP FIGHT ALS TODAY AND TOMORROW

Many people who know the devastating effects of ALS are providing lasting support for MDA's battle against the disease. Through your will, you can designate a gift to MDA earmarked to support ALS research or services.

To give what remains of your estate after other bequests have been satisfied, just include the following language in your will:

"I give, devise and bequeath all (or a specified fraction of) the rest, residue and remainder of my estate, whether real or personal, of every kind and description, and wherever situated, to Muscular Dystrophy Association Inc., a New York not-for-profit corporation having its principal office at 3300 East Sunrise Drive, Tucson, Arizona, 85718-3208, for its program of research and services related to amyotrophic lateral sclerosis."

To give a dollar amount or percentage of your estate:

"I give, devise and bequeath the sum of $________ (or ________ percent of my estate) to Muscular Dystrophy Association Inc., a New York not-for-profit corporation having its principal office at 3300 East Sunrise Drive, Tucson, Arizona, 85718-3208, for its program of research and services related to amyotrophic lateral sclerosis."

Your attorney or financial adviser can help you work out the details of a bequest to MDA's ALS Division. For more information, call MDA's Planned Giving Department at (800) 572-1717. 

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