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RARE DISORDERS & THE INTERNET
New online support groups for people with various health problems continue to proliferate. Not only are people receiving comfort from others with the same conditions, but they are learning from each other's experiences as well. By the late 1990's, most non-profit organizations had websites where people could ask questions and get immediate answers.
Nevertheless, people diagnosed with rare disease often are vulnerable to misguided assistance. While the National Institutes of Health's Office of Rare Diseases encourages people to use the internet to find information, they also warn that is dangerous to rely solely on the computer for medical advice. It is especially important to exercise caution when claims are made for unproven remedies and "miracle" cures. Too often, misleading or inaccurate information is given out that can do more harm than good. In addition, one person's experience and treatment may vary greatly from another person's experience and treatment. What may work for one individual, may not necessarily work for another. Every person is different and should be treated on an individual basis by a qualified health care provider, whether it be a conventional medical practitioner or alternative health care provider or a combination of both working together using a complementary treatment plan. The best way to use the internet is to complement the communication between health care provider and patient, not replace it.
Be wary of advertisements, newsletters, and books that offer "medical or natural" cures. Always keep in mind, anything that sounds too good to be true probably is. A good dose of healthy skepticism is good for researching information.
MoonDragon.org is a firm believer in becoming an informed consumer about your health, health care, and treatment options that may or may not be available to you as an individual, depending on each person's health issues. The information here is not meant to replace conventional or alternative health care from your practitioner, but instead offers information that you may choose to discuss with your health care provider while helping to plan a course of treatment for a specific health problem. The pages listed on the MoonDragon.org website have been researched and compiled from many resources which may include medical and natural health books and resources and journals as well as information gathered from reliable sources found on the internet. However, as research progresses and new information surfaces, some information and therapies can change over time and some may eventually become outdated. Discuss these things with your health care provider.
So... go out there and do your research and learn as much as you can about your health. Make a list of questions and concerns to discuss with your health care provider about your options specific for your situation and health issues. Be safe. Be healthy.
RARE DISORDERS & ORPHAN DISEASES OVERVIEW
Jumping Frenchmen of Maine sounds like an uproarious modern-day stage show or a new music group of some kind. But it is neither. It is actually the name of an unusual disorder that causes an extreme startle reaction to unexpected noises or sights. Though little is known about this disorder and more than 6,000 other rare, or "orphan," diseases are receiving increasing attention from the government, patient groups, and the pharmaceutical industry.
ORPHAN DISEASE DEFINITION
In the United States, an orphan disease is defined as a condition that affects fewer than 200,000 people nationwide. This includes diseases as familiar as cystic fibrosis, Lou Gehrig's disease, and Tourette syndrome, and as unfamiliar as hamburger disease, Job syndrome, and acromegaly (or gigantism). For some diseases, there are fewer than 100 known cases. Collectively, however, rare disorders affect as many as 25 million Americans, according to the National Institute of Health (NIH), and that makes these diseases, as well as finding treatments for them, a serious public health concern.
GENETICS & ENVIRONMENTAL FACTORS
New rare diseases are discovered every year. Most are inherited and caused by alterations in genetic mutations (defects in genes). Genes are pieces of DNA, part of the code that determines the traits and individual characteristics of all living things. Each human cell contains around 30,000 genes, Besides influencing features such as eye and hair color, genes also play a role in the development of diseases and in their transmission from parent to child. In addition to those with genetic causes, there are some rare diseases that can be acquired as a result of environmental and toxic conditions.
OBTAINING ACCURATE DIAGNOSIS & PROPER TREATMENT
As disparate as rare diseases are, patients share many common frustrations. For example, for 1/3 of people with a rare disease, getting an accurate diagnosis can take one to five years. And people often are so isolated that they may never know anyone else with the same disease. Patients often must travel long distances to visit the few health care providers knowledgeable about their illnesses, and the costs involved with diagnosis, treatment and other related expenses can be exorbitant.
The director of the NIH Office of Rare Diseases (ORD) has stated that in understanding health and diseases, scientists must study rare diseases that affect smaller portions of the population as readily as those, such as cancer, for which research and treatment can result in benefits to a greater number of people. He has further stated that many advances are not only the direct result of years of rare disease research, but also from the emphasis that NIH places on both basic and clinical research. The course that a rare disease takes often may represent an exaggerated form of a common disease pathway, he says, and studying one helps scientists learn about the other.
A genetic lung disease known as alpha-1-antitrypsin deficiency, for example, produces a form of emphysema that develops 10 to 30 years earlier than the more prevalent form common to smokers. Because it affects young people, it can be studied apart from any complicating factors, such as the aging process, to enhance what researchers already know about the disease.
RARE DISEASE MANAGEMENT
Many rare diseases or conditions can be difficult to diagnose and manage because in their early stages, symptoms may be absent or masked, misunderstood, or confused with other diseases. One case study involved the misdiagnosis 21 years ago of multiple sclerosis (MS) which led to a delayed and inappropriate treatment of this patient's true disease - adrenomyeloneuropathy (AMN). AMN is a milder form of adrenoleukodystrophy (ALD), one of a group of genetically determined progressive disorders known as "leukodystrophies" that affect the brain, spinal cord and peripheral nerves. This once case involving this 48 year old man raised a red flag for his health care provider when he mentioned that not only had his grandfather been diagnosed with MS - and in fact had died from it - but also that he had lost two brothers and several cousins to the same disease.
ALD affects only 1 in about 15,500 people worldwide. This was enough, however, to form an organization, The United Leukodystrophy Foundation, a voluntary health organization. According to the United Leukodystrophy Foundation (ULF), the leukodystrophies are often misdiagnosed as MS because diagnosis of neurological conditions relies on subtle and circumstantial evidence, and, even the most experienced clinical practitioners may have difficulty distinguishing between the two. Because MS is not hereditary, the patient's health care provider suspected that the disease that had befallen his family members, and now him, was not MS because of its genetic pattern of inheritance. An in-depth family history revealed that the patient and his brothers had a 50 percent chance of getting either ALD or AMN because their mother was a carried of the gene. Following his diagnosis of AMN, two more of the patient's brothers died of the disease.
For people with are rare diseases or disorder, there may be no cures, but treatments of the symptoms can help. Having the support of family and friends, patient advocacy groups, and disease associations like ULF is also helpful. Patients may have to learn to accept help form other people in the course of their treatment such as using a wheelchair or walking with a cane. They will need to realize that when they receive help from someone, it also makes the care provider feel good as well as the patient receiving the care, benefiting both in the process.
In addition to finding emotional and educational support, participating in a clinical trial may be a way to receive the most advanced care for some diseases.
FDA.gov: Inside Clinical Trials: Testing Medical Products In People
People who experience unexplained symptoms, recurrent infections, and pain that have gone undiagnosed for a long period of time might want to visit a referral center that is experienced in diagnosing patients with rare diseases. Some rare diseases do not have clearly defined treatment guidelines and require the specific skills of an expert health care provider. Be sure to go to a hospital or other clinical facility that is familiar with treating people with multiple problems.
ADOPTING THE ORPHAN DISEASE LAWS
Before the passage of rare disease laws in the United States, people diagnosed with a rare disease were denied access to effective medicines because prescription drug manufacturers rarely could make a profit from marketing drugs to such small groups. Consequently, the prescription drug industry did not adequately fund research for so called "orphan" product development. Other potential sources, such as research hospitals and universities, also lacked the capital and business expertise to develop treatments for small patient groups. Despite the urgent health need for these medicines, they came to be known as "orphans" because companies were not interested in "adopting" them.
This changed in 1983 when Congress passed the Orphan Drug Act (ODA). The ODA created financial incentives for drug and biologics manufacturers, including tax credits for costs of clinical research, government grant funding, assistance for clinical research, and a seven-year period of exclusive marketing given to the first sponsor of an orphan-designated product who obtains market approval from the Food and Drug Administration for the same indication. At the same time, federal programs at the FDA and the NIH began encouraging product development, as well as clinical research for products targeting rare diseases. Since 1983, the ODA has resulted in the development of nearly 250 orphan drugs, which now are available to treat a potential patient population of more than 12 million Americans. In contrast, the decade prior to 1983 saw fewer than 10 such products developed without government assistance. As a result, treatments are available to people with rare diseases who once had no hope for survival.
In April 2003, for example, the FDA approved the very first treatment for Fabry's disease, a serious metabolic genetic disorder that affects 1 in 40,000 American men. Fabrazyme (agalsidase beta) was approved under an accelerated or early approval policy that allows faster approval of therapies that treat serious or life-threatening illnesses. Accelerated approval can be granted when favorable results in early studies indicate outcomes that are likely to predict long-term clinical benefit. Fabrazyme, given intravenously, is a version of the human form of a natural enzyme produced by recombinant DNA technology. This replacement of the missing enzyme reduces a particular type of lipid (fat) accumulation in many types of cells, including blood vessels in the kidneys and other organs. It is believed likely that this reduction of fat deposits will prevent the development of life-threatening organ damage and have a positive health effect.
According to the FDA's Center for Biologics Evaluation & Research, a key part of the accelerated approval process involves further study of the new treatment after approval to confirm clinical benefit. In this case, FDA has worked closely with the product developer to make sure that, despite the relatively small number of patients with this disease, all reasonable steps would be pursued to make sure that researchers and developers learn more about the product's clinical benefits and long-term safety once it is on the market. Despite the success of the ODA, however, rare disease advocacy groups argue that the plight of people with orphan diseases deserves even more attention.
THE ROLE OF THE FDA
According to the director of the FDA's Office of Orphan Products Development (OOPD), a lot of people are affected and that makes it a major public health impact, and in time, they are going to see even more rare diseases requiring treatment. Because of the FDA's desire to find ways to bring orphan drugs to the marketplace, the agency established the OOPD in 1982. Its mission is to identify orphan drugs and biological products and to promote development of those that demonstrate promise for the diagnosis and treatment of rare diseases. The OOPD does this by working with the medical and research communities, professional organizations, academia, and the pharmaceutical industry, as well as rare disease groups.
Each orphan product designation request must stand on its own merit. People need to know that the approval of an orphan designation request does not change the standard regulatory requirements or the process for obtaining marketing approval. That means the product must go through the new drug approval process like any other drug. The safety of a product, and its effectiveness, also must be established through adequate and well-controlled studies.
In addition, the OOPD administers a grants program that funds clinical studies for the development of orphan products. The goal of the program is to encourage clinical development of products for use in rare diseases or conditions. The products studied can be drugs, biologics, medical devices, or medical foods.
Medical devices are not eligible for orphan designation. However, in 1996, the FDA took a major step intended to make it easier and less costly for manufacturers to bring to market medical devices for orphan diseases. The Humanitarian Device Exemption (HDE) provisions of the Safe Medical Devices Act of 1990 allow a medical device to be approved as long as manufacturers show it is safe and has probable benefit to patients with an extremely rare condition. These regulations allow approval without costly clinical studies to establish effectiveness.
To qualify for HDE approval, the device must be intended for use in the treatment or diagnosis of a disease or condition affecting fewer than 4,000 individuals per year in the United States. Humanitarian use device designation is granted to sponsors developing a medical device that targets rare disease treatment. Since October 1996, the OOPD has designated 51 humanitarian use devices, and 32 of these devices were given HDEs.
The success of the ODA has also inspired the implementation of orphan legislation outside the United States to address the treatment needs of patients worldwide who have rare diseases. Subsequent legislation has taken the study of rare diseases to even greater heights.
RESEARCH SUPPORT
Congress passed the "Rare Diseases Act of 2002," establishing a role for the ORD at the NIH in encouraging orphan disease research. The ORD provides information on rare diseases, diagnosis, and treatment. The office links investigators with research subjects and patients, identifies rare diseases where research is lagging or lacking, identifies rare disease research opportunities, and supports research in those areas.
The Rare Diseases Act authorized the expansion of national research in developing diagnostic tools and treatments for patients with rare diseases. In addition, Congress approved funding for several regional Centers of Excellence on rare diseases. The ORD makes grants to public or private nonprofit organizations to cover the cost of basic operating expenses for clinical research at these centers. These grants support training in and demonstration of diagnostic, prevention, control, and treatment methods for rare diseases.
The ORD responds to public inquiries about rare diseases, supports national and international scientific workshops, and maintains the ORD Web site and interactive rare diseases list. The workshops benefit the rare diseases community through promoting research, patient care, and disease awareness.
SUPPORT GROUPS FOR PATIENTS
Rare diseases affect so few people that information about them may be difficult to find, making the situation more traumatic and stressful. Before Congress enacted the ODA, families coping with a rare disease usually struggled alone. Support could only be found through telephone calls to other families suffering with similar diseases, and only if the names were provided by health care practitioners.
Support groups such as the National Organization for Rare Disorders (NORD) have worked aggressively in the last 20 years to draw attention to people with rare diseases, especially the lack of treatment options. Paramount in NORD's ongoing cause are efforts to promote legislation, such as the ODA, that encourages further research and continuing development of products that are necessary - and often life saving - and to provide easier access to such treatments.
Support group founders are usually individuals with personal experience with dealing with a type of disease. They develop a voluntary health organization dedicated to provider people who have these diseases, and their families, with specific information. They often provide education, advocacy, and a link between people and clinical trials and health care provider referrals. They serve as a communication network for families in matching people geographically with similar diseases.
Supporters believe that it is equally important to being informed, is being realistic. Health care professionals should not sugar coat the disease to their patients. They need to be brutally honest with their patients so that the patient can not only make informed decisions about their care options but also provide and share accurate information with other family members, especially if children are to be affected by the situation. There is more fear of the unknown, than when a person is properly informed and prepared.
The role of the support group is evolving and supporters feel that the recent trends at FDA and NIH in encouraging scientists to become involved with patient support groups has brought research even further. Supporters having had first-hand experience with the devastating effects of a rare disease can remember what it was like when there was no one at the other end of the phone line.
KEEPING INFORMED OF NEW RESEARCH & DEVELOPMENT
Individuals suffering from these are diseases and their caregivers would be well advised to stay abreast of new research as it is reported in hopes of being able to wisely choose the best combination of therapy and nutritional supplementation. Unfortunately, our knowledge on the subject of orphan diseases is limited at this time, as the research is also limited. However, everyone looks forward to information breakthroughs that can shared as they surface.
RARE DISEASES & APPROVED ORPHAN PRODUCTS
DISEASE DESCRIPTION NUMBER OF PEOPLE AFFECTED DRUG APPROVED Mucopolysaccharidosis
(MPS 1)Genetic lysosomal storage disorders caused by the body's inability to produce certain enzymes. About 200. Aldurazyme
(laronidase)Multiple Myeloma A cancer of the plasma cell. About 63,000. Velcade
(bortezomib)Lennox-Gastaut Syndrome A severe form of epilepsy (seizure disorder). About 40,000. Topamax
(topiramate)Tyrosinemia
Type 1A rare pediatric disease causing progressive liver failure and liver cancer. About 2,500 children. Orfadin
(nitisinone)Gastrointestinal Stromal Tumor
(GIST)Soft tissue sarcomas, or rare tumors, that arise from within the stomach or intestinal tract. About 15,000. Gleevec
(imatinib mesylate)Cystic Fibrosis A genetic disease that causes the body to produce abnormally thick, sticky mucus that clogs the lungs and leads to life-threatening lung infections. About 30,000. TOBI
(tobramycin)Sickle Cell Anemia A group of inherited red blood cell disorders. About 91,000. Droxia
(hydroxyurea)
FOR MORE INFORMATION
Food and Drug Administration (FDA)
Office of Orphan Products Development (HF-35)
5600 Fishers Lane
Room 6A-55
Rockville, MD 20857
(800) 300-7469
www.fda.gov/orphan/
National Institutes of Health (NIH)
Office of Rare Diseases (ORD)
6100 Executive Blvd.
Room 3B01
Bethesda, MD 20892-7518
(301) 402-4336
rarediseases.info.nih.gov
National Cancer Institute (NCI)
Cancer Information Service
(800) 4-CANCER (800-422-6237)
www.cancer.gov
The National Organization for Rare Disorders (NORD)
55 Kenosia Ave.
PO Box 1968
Danbury, CT 06813-1968
(800) 999-6673
www.rarediseases.org
The Genetic and Rare Diseases Information Center
PO Box 8126
Gaithersburg, MD 20898-8126
(888) 205-2311
TTY: (888) 205-3223
http://rarediseases.info.nih.gov/html/resources/info_cntr.html
NUTRITIONAL GUIDELINES FOR RARE ORPHAN DISEASES
In thinking about nutritional guidelines for rare orphan diseases, it may be helpful to consider the baffling symptoms, suspected causes, and possible nutritional supports appropriate for the disease. An example of this approach includes late-onset autism.
Due to the multifaceted nature of late-onset autism and the successes and failures associated with attempted treatments, it is a disease that, when studied carefully, can give hints as to the factors influencing other rare diseases.
Late-onset autism is a rare neurological condition that afflicts young children, usually between their first and fifth years. The majority of affected families report normal development during the first year or so, but these skills then disappear and new skills fail to develop. The child ceases to socialize, and verbal abilities are usually completely lost. Temper tantrums become quite common and more severe as the child no longer has the ability to communicate his or her needs. An autistic child usually becomes intolerant of certain foods as his or her digestive system becomes less functional. His or her stool and sometimes urine can become unusually putrid and his or her movements repetitive and disassociated from surroundings. The resulting stress takes its toll on the entire family.
Most clinicians believe that a cure is impossible, but some disagree and believe that a cure will soon be found. The causes of late-onset autism are debated among researchers, clinicians, and informed parents. Some believe that the mercury compound used in some vaccines is to blame. In addition, there is often a history of frequent ear infections with much antibiotic use. Some believe that an overuse of antibiotics has killed off the friendly intestinal bacteria, leaving the gut vulnerable to the antibiotic resistant, neurotoxin-producing bacterium clostridium. Other researchers suggest that, much like typical autism, there is a genetic component. In many cases, both mercury and clostridium are present. Perhaps all of these observations are correct to one degree or another. Hopefully, time and study will reveal the answers. For now, we can only guess which factors are to blame.
The affected children, whose blood tests high for mercury, are often treated with chelation therapy by licensed health care providers. Many are reporting positive results though not a complete cure. Other practitioners are concentrating on the digestive system and are attempting to bring the overgrowth of clostridium bacteria under control and, again, are reporting improvement though not a cure. Most are making dietary and nutritional changes, administering antioxidants as well as many other supplements, and are reporting improvement but still no cure. As the body of evidence grows that making nutritional and dietary changes affects this form of autism, the argument for a genetic cause weakens. If external factors are to blame, avoidance of the disease, if not a cure, is probable.
Late-onset autism is a disease where there are, in addition to chelation therapy, four primary areas of support that have shown some degree of success and perhaps can be applied where fighting other very difficult and rare diseases.
- Gastrointestinal support.
- Neurological support.
- Cardiovascular support.
- Immune system support.
GENERAL RULES FOR COMBATING RARE DISEASES
Some general rules to consider when combating many diseases:
1. Start with the gastrointestinal tract. This should include digestive enzymes and probiotics. Care must be taken when giving digestive enzymes. Too much can result in a partial digestion of the stomach lining itself, resulting in severe inflammation, especially with small children. Digestive enzymes and probiotics and guidance for their use are available from:Healthy Alternatives, Inc.
10458 Moe Hall Road NW
Garfield, MN 56332
888-362-0401
www.healthyalternatives.com
2. Provide the necessary nutritional supplements for neurological support. Digestive inflammation results in the consumption of excessive quantities of seratonin. Serotonin is an inflammation mediator as well as being essential for emotional stability. Neurological stress consumes excessive quantities on gamma-aminobutyric acid (GABA). GABA acts as a stabilizer by inhibiting neurological overreaction. Vitamin B-12, in the methylcobalamin form, aids in the building and healing of nerve cells.
The following formula includes the precursors for the production of GABA, serotonin, and other supporting nutrients, and is available under the brand name GabaMax from:NeuroScience Inc.
373 280th Street
Osceola, WI 54020
877-729-6784
www.neurorelief.com
GABAMax Product Description
GabaMax includes the following ingredients:
- N-Acetyltyrosine.
- 5-Hydroxytryptophan (5-HTP).
- Theanine.
- L-Glutamine.
- Taurine.
- Vitamin B-6.
- Folic Acid.
- Vitamin C.
- Magnesium Glycinate.
GabaMax should be taken as directed on the label. In addition, 5,000 mcg (1,000 mcg for small children) of Vitamin B-12 in the form of methylcobalamin works well with the above formula to help heal nerve damage and is available from:Healthy Morning - A Natural Apothecary
P.O. Box 67
Woodville, MA 01784
508-728-6223
www.healthymorning.com
AndAerobic Life Industries, Inc.
2800 E. Chambers Street, Suite 700
Phoenix, AZ 85040
800-798-0707
www.aerobiclife.com
GABAMax Products From Online Stores:
Bayho.com: GABAMax Supplement, 90 Caps
AcuAtlanta.com: GABAMax Supplement, 90 Caps
Methylcobalamin B-12 Products For Amazon.com:
3. Provide support for the cardiovascular system. There are many of the rare diseases where the circulatory system is so compromised that nutrients have great difficulty finding their way to the areas in desperate need of them. Therefore, supplements that target the circulatory system may help.
One formula that should be considered is Aerobic Life Heart Formula by Aerobic Life Industries (listed above). This formula helps to strengthen and increase circulation while reducing inflammation of the arteries and capillaries of the cardiovascular system, making the delivery of nutrients to affected areas more efficient.
Aerobic Life Heart Formula From Online Stores:
VitaminLife.com: Aerobic Life Heart Formula
4. Strengthen the immune system to help combat microbes that may attack during times of weakness. There is also some suspicion that a few of the orphan disease are virally induced.
Many rare disease are known to be of genetic origin, and in many cases there is evidence that even they may respond positively to sound nutrition. The diseases that follow may be caused by problems in some or all of the above areas. You will find notes for each that suggest different combinations of treatments that could help to alleviate their symptoms and/or severity.
ACUTE DISSEMINATED ENCEPHALOMYLITIS
Acute disseminated encephalomyelitis (ADE) is characterized by inflammation of the brain and spinal cord caused by damage to the myelin sheath - the fatty insulator of the brain's nerve fibers. Both viral and bacterial infection can be associated with ADE. It can also arise as a complication of inoculation or vaccination. The onset of ADE is sudden and symptoms vary from person to person. They can include:
- Headaches.
- Delirium.
- Lethargy.
- Coma.
- Seizures.
- Stiff neck.
- Fever.
- Ataxia.
- Optic neuritis.
- Transverse myelitis.
- Vomiting.
- Weight loss.
In some cases, a limb or an entire side of the body can become paralyzed. ADE strikes children more often ' than adults.
CONSIDERATIONS
The treatment of ADE typically includes the use of corticosteroid medications plus symptom-relieving and supportive measures.
The prognosis for people with ADE varies. Some patients achieve complete or nearly complete recovery, while others continue to suffer residual symptoms. In severe cases, the disorder can prove fatal. If diagnosed early and treated promptly, however, the prognosis for ADE disorder is generally good.
For nutritional recommendations, see Neurological Support (#2 Above) and the links below.
FOR MORE INFORMATION
NINDS: Acute Disseminated Encephalomyelitis Information
Wikipedia: Acute Disseminated Encephalomyelitis
E-Medicine-WebMD: Acute Disseminated Encephalomyelitis Article
MyDailyApple Acute Disseminated Encephalomyelitis (ADEM)
The Encephalitis Center at Johns Hopkins
Neuroimmunological Lessons Learned from Acute Disseminated Encephalomyelitis
Fulminant Acute Disseminated Encephalomyelitis NOROL BIL D 18: 1 , 2001
Encephalitis Information - Acute Disseminated Encephalomyelitis (ADEM)
Encephalitis Global
The Contact a Family Directory - Acute Disseminated Encephalomyelitis
ADEM support group
ADEM Discussion Forum
Myelitis.org: Obstetric Issues - TM, ADEM, NMO
From the 2008 Rare Neuroimmunologic Disorders Symposium
Acute Disseminated Encephalomyelitis (ADEM)
Benjamin Greenberg, MD, MHS
Johns Hopkins University, Baltimore, MD
View Video 27 minFrom the 2008 Rare Neuroimmunologic Disorders Symposium
Pediatric TM as different from CIDP, and pediatric ADEM
Gregory Barnes, MD, Ph. D
Vanderbilt University, TN
Presentation Handout
View Video 35 minFrom the 2006 Rare Neuroimmunologic Disorders Symposium
Acute Disseminated Encephalomyelitis (ADEM)
Anita Venkataramana, MBBS
Thomas O. Crawford, MD
View VideoFrom the 2004 Rare Neuroimmunologic Disorders Symposium
Acute Disseminated Encephalomyelitis (ADEM)
David Irani, MD
Assistant Professor of Neurology
Co-Director, Johns Hopkins Transverse Myelopathy Center (JHTMC)
Johns Hopkins University School of Medicine
Handouts 500Kb
View Video 34 minsFrom the 2004 Rare Neuroimmunologic Disorders Symposium
Recognizing pediatric TM from CIDP and pediatric ADEM
Gregory Barnes, MD, University of Kentucky, KY
View Video 29 minsFrom the 2nd Transverse Myelitis Symposium, July 2001
Lessons from ADEM/Acute Leukoencephalopathies
David Irani, MD
Assistant Professor of Neurology
Co-Director, Johns Hopkins Transverse Myelopathy Center (JHTMC)
Johns Hopkins University School of Medicine
View Handouts 308KB
View Video 26 minutes plus 7 minute Q & A
View Slideshow 298KB
AGNOSIA
Agnosia, means a loss of knowledge or non-knowledge, is a rare disorder characterized by the inability to recognize familiar objects or people, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. Agnosia can be limited to one sense such as hearing or vision. For example, a person may have difficulty identifying a sound as a cough or recognizing an object as a cup. The case made famous in neurologist Oliver Sack's popular book The Man Who Mistook His Wife For A Hat (Touchstone, 1998) was one of a man with visual agnosia.
This disorder can be caused by stroke or brain injury, dementia, or other neurological disorders, or hereditary. It can become debilitating and compromise the quality of life. Agnosia typically affects specific brain areas in the occipital, occipitotemporal border, or parietal lobes, areas of the brain that are important for processing and integrating information received through vision and other senses. People with agnosia may retain cognitive abilities in other areas. Some forms of agnosia have been found to genetic. Agnosias have been identified in people with autism and a range of agnosias can be present as symptoms commonly associated with autism.
TYPES OF AGNOSIA
Alexia: Inability to recognize text.
Amusia or Receptive amusia: Is agnosia for music. It involves loss of the ability to recognize musical notes, rhythms, and intervals and the inability to experience music as musical.
Anosognosia: This is the inability to gain feedback about one's own condition and can be confused with lack of insight but is caused by problems in the feedback mechanisms in the brain. It is caused by neurological damage and can occur in connection with a range of neurological impairments but is most commonly referred to in cases of paralysis following stroke. Those with Anosognosia with multiple impairments may even be aware of some of their impairments but completely unable to perceive others.
Apperceptive Agnosia: Patients are unable to distinguish visual shapes and so have trouble recognizing, copying, or discriminating between different visual stimuli. Unlike patients suffering from associative agnosia, those with apperceptive agnosia are unable to copy images.
Apraxia: Is a form of motor (body) agnosia involving the neurological loss of ability to map out physical actions in order to repeat them in functional activities. It is a form of body-disconnectedness and takes several different forms; Speech-Apraxia in which ability to speak is impaired, Limb-Kinetic Apraxia in which there is a loss of hand or finger dexterity and can extend to the voluntary use of limbs, Ideomotor Apraxia in which the gestures of others cannot be easily replicated and cannot execute goal-directed movements, Ideational Apraxia in which one cannot work out which actions to initiate and struggles to plan and discriminate between potential gestures, Apraxia of Gait in which co-ordination of leg actions is problematic such as kicking a ball, Constructional Apraxia in which a person cannot co-ordinate the construction of objects or draw pictures or follow a design, Oculomotor Apraxia in which the ability to control visual tracking is impaired and Buccofacial Apraxia in which skilled use of the lips, mouth and tongue is impaired.
Associative Agnosia: Patients can describe visual scenes and classes of objects but still fail to recognize them. They may, for example, know that a fork is something you eat with but may mistake it for a spoon. Patients suffering from associative agnosia are still able to reproduce an image through copying.
Auditory Agnosia: With Auditory Agnosia there is difficulty distinguishing environmental and non-verbal auditory cues including difficulty distinguishing speech from non-speech sounds even though hearing is usually normal.
Autotopagnosia: Is associated with the inability to orient parts of the body, and is often caused by a lesion in the parietal part of the posterior thalmic radiations.
Color Agnosia: Refers to the inability to recognize a color, while being able to perceive or distinguish it.
Cortical Deafness: Refers to people who do not perceive any auditory information but whose hearing is intact.
Finger Agnosia: Is the inability to distinguish the fingers on the hand. It is present in lesions of the dominant parietal lobe, and is a component of Gerstmann syndrome.
Form Agnosia: Patients perceive only parts of details, not the whole object.
Integrative Agnosia: This is where one has the ability to recognize elements of something but yet be unable to integrate these elements together into comprehensible perceptual wholes.
Mirror Agnosia: One of the symptoms of Hemispatial neglect. Patients with Hemispatial neglect were placed so that an object was in their neglected visual field but a mirror reflecting that object was visible in their non-neglected field. Patients could not acknowledge the existence of objects in the neglected field and so attempted to reach into the mirror to grasp the object.
Pain Agnosia: Also referred to as Analgesia, this is the difficulty perceiving and processing pain; thought to underpin some forms of self injury.
Phonagnosia: Is the inability to recognize familiar voices, even though the hearer can understand the words used.
Prosopagnosia: Also known as face-blindness and facial agnosia: Patients cannot consciously recognize familiar faces, sometimes even including their own. This is often misperceived as an inability to remember names.
Semantic Agnosia: Those with this form of agnosia are effectively 'object blind' until they use non-visual sensory systems to recognize the object. For example, feeling, tapping, smelling, rocking or flicking the object, may trigger realization of its semantics (meaning).
Simultanagnosia: Patients can recognize objects or details in their visual field, but only one at a time. They cannot make out the scene they belong to or make out a whole image out of the details. They literally cannot see the forest for the trees. Simultanagnosia is a common symptom of Balint's syndrome.
Social Emotional Agnosia: Sometimes referred to as Expressive Agnosia, this is a form of agnosia in which the person is unable to perceive facial expression, body language and intonation, rendering them unable to non-verbally perceive people's emotions and limiting that aspect of social interaction.
Somatosensory Agnosia: Or Astereognosia is connected to tactile sense - that is, touch. Patient finds it difficult to recognize objects by touch based on its texture, size and weight. However, they may be able to describe it verbally or recognize same kind of objects from pictures or draw pictures of them. Thought to be connected to lesions or damage in somatosensory cortex.
Tactile Agnosia: Impaired ability to recognize or identify objects by touch alone.
Time Agnosia: Is the loss of comprehension of the succession and duration of events.
Topographical Agnosia: This is a form of visual agnosia in which a person cannot rely on visual cues to guide them directionally due to the inability to recognize objects. Nevertheless, they may still have an excellent capacity to describe the visual layout of the same place.
Verbal Auditory Agnosia: This presents as a form of meaning 'deafness' in which hearing is intact but there is significant difficulty recognizing spoken words as semantically meaningful.
Visual Agnosia: Is associated with lesions of the left occipital lobe and temporal lobes. Many types of visual agnosia involve the inability to recognize objects.
Visual Verbal Agnosia: This is where the difficulty comprehending the meaning of words effects comprehension of the written word. The capacity to read is usually intact but the comprehension of what is read will be impaired.
CONSIDERATIONS
The primary cause of agnosia must first be established in order to determine how best to treat symptoms.
For nutritional recommendations, see the links below.
FOR MORE INFORMATION
Wikipedia: Agnosia
Psychnet-UK: Agnosia
NINDS: Agnosia Information Page
Healthline: Agnosia Information
ALPHA-1 ANTITRYPSIN DEFICIENCY
Alpha-1 antitrypsin deficiency is a genetic disease characterized by a lack of the protein alpha-1 antitrypsin in the liver. This substance is used to break down enzymes in various organs of the body. The disease can lead to hepatitis and cirrhosis, or scarring, of the liver. In addition, alpha-1 antitrypsin also protects the lungs from irritants in conjunction with an enzyme released by white blood cells. A person deficient in alpha-1 antitrypsin is therefore much more susceptible to lung disease, especially emphysema.
Alpha-1 antitrypsin deficiency most commonly appears in newborn infants and is characterized by jaundice, swelling of the abdomen, and poor feeding. However, the disease may also develop in late childhood or even in adulthood. In such cases, symptoms may include:
- Fatigue.
- Poor appetite.
- Swelling of the abdomen and legs.
- Abnormal liver test results.
CONSIDERATIONS
There is no current cure for alpha-1 antitrypsin deficiency. Treatment aims to control abnormalities and to provide the liver with essential nutrients. Multiple vitamin supplements plus Vitamins E, D, and K are typically prescribed. Phenobarbitol or cholestyramine is prescribed for jaundice.
Only 1/4 of people who develop this disorder actually go on to develop cirrhosis of the liver. The remaining 3/4 never develop serious liver disease beyond the newborn period.
For nutritional recommendations, see the links below.
FOR MORE INFORMATION
Alpha-1 Antitrpysin Deficiency Association
Wikipedia: Alpha-1 Antitrypsin Deficiency
NIH Genetics Home Reference: Alpha-1 Antitrypsin Deficiency
MedicineNet: Alpha-1 Antitrypsin Deficiency (A-1ATD)
NIH MedlinePlus: Alpha-1 Antitrypsin Deficiency
Alpha-1 Foundation
American Liver Foundation: Alpha-1 Antitrypsin Deficiency
Genome.gov: Learning About Alpha-1 Antitrypsin Deficiency (AATD)
ATAXIA
People with ataxia experience a failure of muscle control in their arms and legs, resulting in a lack of balance and coordination or a disturbance of gait. This can occur if parts of the nervous system that control movement care damaged. While the term ataxia is primarily used to describe this set of symptoms, it is sometimes also used to refer to a family of disorders.
Most disorders that result in ataxia cause cells in the part of the brain called the cerebellum to degenerate, or atrophy. Sometimes the spine is also affected. While the phrases cerebellar degeneration and spinocerebellar degeneration are used to describe changes that have taken place in a person's nervous system, neither term constitutes a specific diagnosis. Cerebellar and spinocerebellar degeneration can have many different causes. The age of onset of any resulting ataxia varies depending on the underlying cause of the degeneration. Among the more common inherited ataxias are Friedreich's ataxia and Machado-Joseph disease.
Friedreich's ataxia is an inherited disease that causes progressive damage to the nervous system, resulting in symptoms to heart disease. Symptoms usually begin between the ages of 5 and 15, but appear as early as 18 months or as late as 30 years of age. The first symptom is usually difficulty in walking. The ataxia gradually worsens and slowly spreads to the arms and then the trunk. Foot deformities such as clubfoot, flexion (involuntary bending) of the toes, hammertoes, or foot inversion (turning in of the foot) may be early signs. Rapid, involuntary rhythmic movements of the eyeball are common. Most people with Friedreich's ataxia develop acoliosis (a side-ways curvature of the spine), which, if severe, may impair breathing. Other symptoms include chest pain, shortness of breath, and heart palpitations.
Machado-Joseph disease (MJD), also called spinocerebellar ataxia type 3, is a rare hereditary ataxia. The disease is characterized by clumsiness and weakness in the arms and legs, spasticity, a staggering lurching gait easily mistaken for drunkenness, difficulty with speech and swallowing, involuntary eye movements, double vision, and frequent urination. Some people suffer from dystoria, or sustained muscle contractions that cause twisting of the body and limbs, repetitive movements, abnormal postures, and/or rigidity - symptoms similar to those of Parkinson's disease. Others have twitching of the face or tongue, or peculiar bulging eyes. In Machado-Joseph disease, degeneration of cells in an area of the brain called the hind-brain leads to deficits in movement. The hind-brain includes the cerebellum, the brain stem, and the upper part of the spinal cord. MJD is an inherited, autosomal dominant disease, which means that if a child inherits one copy of the defective gene from either parent, the child will develop symptoms of the disease. People with a defective gene have a 50 percent chance of passing the mutation on to their children. The severity of the disease is related to the age of onset, with earlier onset associated with a more severe form of the disease. Symptoms can begin any time between early adolescence and about 70 years of age. MJD is also a progressive disease, meaning that symptoms get worse with time. Life expectancy ranges from the midthirties for those with severe forms of MJD to a normal life expectancy for those with mild forms. For those who die early from the disease, the cause of death is often aspiration pneumonia, which can occur if fluids or other materials are inhaled into the lungs and cannot be cleared away.
In addition to being a result of heredity, ataxia also can be acquired. Conditions that can cause acquired ataxia include stroke, multiple sclerosis, tumors, alcoholism, peripheral neuropathy, metabolic disorders, and vitamin deficiencies.
CONSIDERATIONS
There is no cure for hereditary ataxias. If the ataxia is caused by another condition, that underlying condition is treated first. For example, ataxia caused by a metabolic disorder may be treated with medications and a controlled diet. vitamin deficiency is treated with vitamin therapy. A variety of drugs may be used to treat gait and swallowing disorders. Physical therapy can strengthen muscles, while devices or appliances can assist in walking and other activities of daily life. The prognosis for individuals with ataxia and cerebellar / spinocerebellar degeneration varies depending on its underlying cause.
There is currently no effective cure or treatment for Friedreich's ataxia. However, many symptoms and accompanying complications can be treated to help individuals maintain optimal functioning as long as possible. Diabetes and heart problems such as foot deformities and scoliosis can be treated with braces or surgery. Physical therapy may prolong the use of the arms and legs. Generally, however, a person with Friedreich's ataxia requires a wheelchair, and in later stages of the disease, he or she is likely to become completely incapacitated. If significant heart disease is involved, a person with Friedreich's ataxia is likely to die in early adulthood, but some who have less severe symptoms live much longer.
MJD is incurable, but some symptoms of the disease can be treated. For people whose symptoms include Parkinsonian features, levodopa therapy can help for many years.
Treatment with antispasmodic drugs, such as baclofen (Lioresal), can help reduce spasticity. Physiotherapy can help people cope with disability associated with gait problems. Physical aids, such as walkers and wheelchairs, can assist with everyday activities. Other problems, such as sleep disturbances, cramps, and urinary dysfunction, can be treated with medications and medical care.
For nutritional recommendations, see Neurological Support (#2 Above) and the following links.
FOR MORE INFORMATION
Wikipedia: Ataxia
National Ataxia Foundation
Mayo Clinic: Ataxia
NINDS: Ataxias & Cerebellar or Spinocerebellar Degeneration Information Page
A-T Children's Project
National Cancer Institute: Ataxia Telangiectasia Fact Sheet
MDVU.org: Pediatric Movement Disorders - Ataxia
Friedreich's Ataxia - Symptoms, Treatment & Prevention
GeneClinics.org: Hereditary Ataxia Overview
MDA: Friedreich's Ataxia (FA)
Ataxia MJD Research Project: About Machado-Joseph Disease
BELL'S PALSY
Bell's palsy is the result of damage to the seventh cranial nerve and is characterized by weakness and paralysis of one side of the face. Currently, 40,000 Americans develop Bell's palsy each year. Although it can strike anyone at any age, pregnant women and people who have diabetes, influenza, or a cold or other respiratory ailment are particularly susceptible to the disorder. The facial paralysis usually leads to an inability to close the eye on the affected side. Other symptoms may include:
- Pain.
- Tearing.
- Drooling.
- Hypersensitivity to sound in the affected ear.
- Impairment in taste.
Many cases of Bell's palsy are believed to be caused by viruses, especially those in the herpes family such as the herpes simplex virus, which causes cold sores.
CONSIDERATIONS
Steroid drugs can be effective in treating Bell's palsy. A combination of the antiviral medication acyclovir (Zovirax) and the corticosteroid prednisone (Deltasone and others) may be effective in improving facial function. Some treatments focus on keeping the affected eye moist during the night.
The prognosis for people with Bell's palsy is very good. Although the condition is troublesome and even possibly alarming, for most, the condition improves within 2 weeks whether it is treated or not. About 80 percent enjoy a complete recovery within 3 months. There are some cases in which symptoms may last longer, or never fully disappear, but these are the minority.
For nutritional recommendations, see Neurological Support (#2 above), and add 500-1,000 mg L-Lysine daily.
FOR MORE INFORMATION
Wikipedia: Bell's Palsy
Bell's Palsy InfoSite & Forums
NINDS: Bell's Palsy Information Page
Mayo Clinic: Bell's Palsy
Bell's Palsy Network - Support & Information
Neurology Channel: Bell's Palsy
BINSWANGER'S DISEASE
Binswanger's disease is a rare form of dementia, a loss of certain types of brain function. This disorder is sometimes known as subcortical dementia. It is most common in people over the age of 60.
The mental disability characteristic of Binswanger's disease includes memory loss caused by the presence of cerebrovascular lesions in the deep white matter of the brain, cognitive problems, and mood changes. These problems are associated with tiny areas of tissue damage or death - multiple strokes, in effect - that occur deep within the brain's white matter (nerve cells) and that are probably due to severe high blood pressure and blood vessel disease in the head and neck.
In addition to mental symptoms, people with Binswanger's disease are often found to have blood abnormalities and heart valve disorders, and they can become incontinent, experience clumsiness, and develop difficulty with walking, speech, and physical activity in general. The ability to show normal facial expressions may become limited as well. For some people, symptoms progress steadily once they start; for others, symptoms may seem to come and go as people experience strokes followed by partial recovery.
CONSIDERATIONS
There is no known cure and no specific treatment recommended for all people with Binswanger's disease. Drug therapy may be used to control blood pressure, depression, and heart arrhythmias.
For nutritional recommendations, see Gastrointestinal Support (#1 Above), Neurological Support (#2 Above) and the following links.
FOR MORE INFORMATION
NINDS: Binswanger's Disease Information Page
Wikipedia: Binswanger's Disease
MedicineNet: Binswanger's Disease
BROWN-SEQUARD SYNDROME
This is a rare neurological condition that leads to weakness or paralysis affecting one side of the body, accompanied by a loss of sensation on the opposite side. These problems are associated with a lesion in the spinal cord that in turn may be the result of a spinal cord tumor, injury to the back or neck, a blocked blood vessel causing ischemia (oxygen deprivation) to the area, or an underlying disease such as tuberculosis or multiple sclerosis.
CONSIDERATIONS
The prognosis for people with Brown-Sequard syndrome depends on the underlying cause. Treatment therefore usually focuses on identifying and, if possible, removing the cause. Early treatment with high doses of steroids may be beneficial as well.
For nutritional recommendations, see Neurological Support (#2 above) and the links below.
FOR MORE INFORMATION
Wikipedia: Brown-Sequard Syndrome
NINDS: Brown-Sequard Syndrome Information Page
DYSTONIA
People with dystonia experience sustained, simultaneous muscle contractions that force affected body parts into abnormal and sometimes painful postures and movements.
Dystonia is actually not a single disorder, but a category of them, usually divided into 2 types: Primary dystonia, which occurs on its own and has no known cause; and secondary dystonias, which are caused by some underlying problem, such as Parkinson's disease, a brain tumor, or stroke.
CONSIDERATIONS
A variety of treatments, among them drug therapy, surgery, and physical therapy (including biofeedback), have been used for dystonias. These measures are useful for some people, helping to reduce pain and muscle spasms, although overall the results are decidedly mixed and a certain amount of trial and error can be involved.
A relatively new treatment for dystonia involves the use of a brain implant. A system called the Activa dystonia therapy system, which has already been used to treat Parkinson's disease and essential tremor, consists of electrodes and a deep brain neurostimulator. The electrodes are implanted into the brain and connected by wires under the skin to the neurostimulator, which is implanted in the chest. The neurostimulator sends a constant stream of tiny electrical pulses to the brain to suppress symptoms. If both sides of the brain are affected, it is necessary to use 2 separate systems, one in each side of the brain. A person with the implant touches a handheld magnet over the neurotransmitter to switch the device on and off. This system is manufactured by Medtronic Inc.
For nutritional recommendations, see Neurological Support (#2 above) and the following links.
FOR MORE INFORMATION
Wikipedia: Dystonia
Dystonia Foundation - Medical Research & Support
MedlinePlus: Dystonia
MedicineNet: Dystonia
MayoClinic: Dystonia
NINDS: Dystonias Information Page
FABRY'S DISEASE
Fabry's disease (also known as Anderson-Fabry disease, Angiokeratoma corporis diffusum, Ruiter-Pompen-Wyers syndrome, Ceramide trihexosidosis, and Sweeley-Klionsky disease) is a X-linked recessive (inherited) lysosomal storage disease. It is a lipid storage disorder resulting from a deficiency of the enzyme ceramids trihexasidase that is involved in the biodegradation of fats. Because of the enzyme deficiency, there is an insufficient breakdown of lipids, which build up in the body. This leads to a number of problems. Symptoms include:
- Burning sensations in the hands and feet that progressively worsen with hot weather and exercise or when one has a fever.
- Reddish-purple, raised blemishes (angiokeratomas) on the skin. These are tiny, painless papules that appear on any region of the body but are predominant on the thighs, buttocks, lower abdomen, and groin (the bikini area).
- Eye manifestations like cloudiness of the cornea (cornea verticillata, also known as vortex keratopahty) are found in some boys with this disorder.
- Symptoms are typically first experienced in early childhood and can be difficult to understand. Misdiagnosis sometimes occurs with this disease. Manifestations of the disease usually increase in number and severity as an individual ages.
As people with Fabry's grow older:
- They become susceptible to heart attack and stroke due to impaired circulation. Cardiac complications occur when Gb3 builds up in different heart cells, heart related effects worsen with age and may lead to increased risk of heart disease. Cerebrovascular effects lead to an increased risk of stroke.
- Eventually, the kidneys are affected, and dialysis or transplantation may be required. Kidney complications are a common and serious effect of the disease, renal insufficiency and renal failure may worse throughout life.
- Some people also develop gastrointestinal difficulties in which frequent bowel movements occur shortly after eating, including nausea and diarrhea
- Other symptoms include an inability or decreased ability to sweat, fatigue, and ringing in the ears (tinnitus).
- Fabry's disease may also have ocular involvement, such as the presence of corneal verticillata in the basal layers of the epithelium, conjunctival aneurysms, and spoke-like cataracts. Papilloedema, macular edema, optic atrophy and retinal vascular dilation may also be present.
This serious genetic disorder affects about 1 in 40,000 men. Though it is believed that fewer women suffer the most serious consequences of the disease, they also can be seriously affected. People with Fabry's disease usually survive into adulthood. However,they have a higher than normal risk of heart attack, stroke, and kidney damage.
CONSIDERATIONS
Treatment includes therapy with anti-seizure medications such as carbamazepine (Tegretol) and phenytoin (Dilantin) for pain in the hands and feet, and nutritional replacement products such as Lipisorb or digestive medications such as metoclopramide (Reglan) to control gastrointestinal hyperactivity.
Until recently, treatment of Fabry disease targeted the symptomatic effects. Recent studies show that enzyme replacement is effective therapy. It is currently being treated at the cellular level using galsidase alpha (Replagal) and Agalsidase beta (Fabrazyme), a version of the human form of the missing enzyme produced by recombinant DNA technology, has now been approved to treat Fabry's disease. The cost of these drugs is problematic (approximately $170,000 US a year/patient) and remains a barrier to many patients in some countries. Enzyme replacement therapy (typically infused every two weeks) may be performed in the patient's home by the patients themselves. When given intravenously, this replacement enzyme reduces a particular type of fat accumulation in many types of cells, including blood vessels in the kidneys and other organs. It is believed that this reduction of fat deposition will prevent the development of life-threatening organ damage. Enzyme replacement therapy is not a cure, and must be infused recurrently for maximum benefit.
For nutritional recommendations, see Gastrointestinal Support (#1 above) and Cardiovascular Support (#3 above) and the following links.
FOR MORE INFORMATION
Wikipedia: Fabry's Disease
E-Medicine: Fabry's Disease
NCBI: Fabry's Disease
MedicineNet: Fabry's Disease
Fabry Community: Fabry Disease Information
NINDS: Fabry's Disease Information Page
HEMORRHAGIC COLITIS (HAMBURGER DISEASE)
Hemorrhagic colitis is a gastrointestinal illness caused primarily by a particular strain of bacteria known as Escherichia coli (E. coli) O157:H7. It is actually a type of food poisoning.
In fact, it is also known as "hamburger disease" or "barbecue season syndrome" because outbreaks often are due to consuming grilled hamburger and other beef products that have not been thoroughly or properly cooked or handled.
While other types of E. coli are common in the gastrointestinal tract of healthy people, the O157:H7 strain normally is not. This strain of bacteria produces extremely potent toxins which are the main cause of the symptoms related to the gastrointestinal illness. The most common symptoms of E. coli O157:H7 colitis include:
- Diarrhea (often with blood in the stools).
- Severe abdominal cramps.
- Vomiting.
These symptoms usually start within 24 hours of consuming contaminated food, but can take as long as 2 days to appear, and can continue for as long as two weeks. Some individuals develop fever as well with the infection.
People can get hamburger disease at any age; however, young children, older adults, and those with weakened immune systems tend to develop severe symptoms. Thousands of people become infected each year, with many local outbreaks reported in Canada, Japan, the United States, and Europe.
E. coli O157:H7 bacteria infects the intestines of cattle and, less frequently, the gastrointestinal tracts of other animals. Typically carried in feces, it can contaminate the meat during and after slaughtering. In addition to beef, these bacteria are associated with consuming unpasteurized milk and cheese and using contaminated water sources. The infection is highly contagious. Once someone has eaten contaminated food, hamburger disease can pass from person-to-person by hand-to-mouth contact. Poor hand-washing and improper food handling are factors that lead to the spread of these bacteria.
CONSIDERATIONS
While E. coli bacteria can be killed with antibiotics, the toxins they produce - and that cause the illness - remain unaffected and there is no evidence that these drugs do anything to relieve symptoms or shorten the illness in most cases. Treatment for hemorrhagic colitis therefore focuses on supporting the affected individual, trying to ease symptoms, and taking measures to prevent the spread of the infection.
If complications develop, hospitalization may be required so that proper care can be administered.
Once hemorrhagic colitis is contracted, antibiotics must be taken. However, a nutritional and probiotic regimen can help prevent contraction and/or restore friendly bacteria after completing antibiotics.
For nutritional recommendations, see Gastrointestinal Support (#1 above) and the following links.
FOR MORE INFORMATION
The Parent Report: Food Poisoning: How To Prevent Hamburger Disease - Infant Nutrition Article
MedicineNet: E. Coli O157:H7 Information
HEREDITARY FRUCTOSE INTOLERANCE
Hereditary fructose intolerance (HFI) is an inherited disorder characterized by the inability to digest fructose, or fruit sugar. In people with HFI, the enzyme fructose-1-phosphate aldolase is deficient, resulting in an accumulation of fructose-1-phosphate in the liver, kidneys, and small intestine. Symptoms include:
- Severe abdominal pain.
- Vomiting.
- Dehydration.
- Convulsions due to low blood sugar.
- Extreme thirst.
- Excessive urination.
- Sweating.
- Loss of appetite.
- Stunted growth.
Acute symptoms are made worse by the consumption of anything containing fruit sugar. If untreated, HFI can result in coma or death.
CONSIDERATIONS
Early treatment, primarily the adoption of a fructose-free diet, leads to a normal length and quality of life. Otherwise, the disorder can lead to serious and permanent damage to the liver and kidneys, and eventually death.
Adhering to a diet with no fructose in it can be difficult in today's world. We encounter fructose not only in natural fruits, fruit juices, and some vegetables, but also in a vast array of processed food products. High-fructose corn syrup, for example, is one of the most common additives listed on food product labels, and it is present not only in foods that taste sweet. It may be worthwhile to consult a qualified nutritionist or dietitian who can help with this task.
For nutritional recommendations, see Gastrointestinal Support (#1 above) and and the following links.
FOR MORE INFORMATION
Wikipedia: Hereditary Fructose Intolerance
E-Medicine: Hereditary Fructose Intolerance
NLM: Hereditary Fructose Intolerance
Health A To Z: Hereditary Fructose Intolerance
Mayo Clinic: Fructose Intolerance - Which Foods Should I Avoid
WrongDiagnosis: Hereditary Fructose Intolerance: Professional Guide
HYPERIMMUNOGLOBULIN E (HYPER-IGE) SYNDROME (JOB SYNDROME)
Hyper-IgE syndrome, or Job syndrome, is an immunodeficiency syndrome characterized by recurrent bacterial (staphylococcal) infections, particularly of the skin, and markedly elevated levels of a natural immune-system protein, immunoglobulin E (IgE). Experts suspect that the origin is genetic. The term - Job syndrome - named for the Bibical figure who was afflicted with boils - arose because one of the symptoms of this syndrome is recurrent skin abscesses. The staphylococcus infection may involve the skin, lungs, joints, and other sites. Decreased bone density and frequent fractures are common. Signs of allergies, such as eczema, asthma, and runny nose, are sometimes present.
CONSIDERATIONS
There is no known cure for Job syndrome. Treatment consists of intermittent or continuous antibiotics. Trimethoprim / sulfamethoxazole, a combination antibiotic, is particularly effective in treating infection.
FOR MORE INFORMATION
Wikipedia: Fabry's Disease
E-Medicine: Hyperimmunoglobulinemia E (Job) Syndrome
MedLinePlus: Hyper IgE Syndrome (Job Syndrome)
Science Daily: Job's Syndrome Cause Identified
IMMUNOLOGIC THROMBOCYTOPENIC PURPURA
Immunologic thrombocytopenic purpura (ITP) is a disorder of the blood that leads to low levels of platelets, which are essential for normal clotting activity. This can be due to problems with platelet production, abnormal destruction of platelets, or other factors. The main symptom is abnormal bleeding, which can be manifested as acchymosis (bruising) and petechiea (tiny red dots on the skin or mucous membranes). In some instances, bleeding from the nose, gums, digestive, or urinary tracts may also occur. In rare cases, there is bleeding within the brain.
Some cases of ITP are also caused by drugs. Others are associated with infection, pregnancy, or immune disorders such as systemic lupus erythematosus. About half of all cases are classified as idiopathic, meaning that there is no known underlying cause.
Acute, or temporary, thrombocytopenia purpura is most commonly seen in young children. Boys and girls are equally affected. Symptoms often, but do not necessarily, follow a viral infection. About 85 percent of children recover within one year, and the problem does not return. Thrombocytopenic purpura is considered chronic if it lasts for more than 6 months. Adults more often have the chronic form of the disorder and females, in this case, are affected 2 to 3 times more than males.
CONSIDERATIONS
If use of a drug is the cause of the thrombocytopenia, standard treatment involves discontinuing the drug's use. Infection, if present, is treated vigorously, since control of the infection can return the platelet count to normal.
The treatment of idiopathic thrombocytopenic purpura is determined by the severity of the symptoms. In some cases, no therapy is needed. In most cases, drugs that alter the immune system's attack on the platelets are prescribed. These include corticosteroids such as prednisone (Deltasone and others) and/or intravenous infusions of immune globulin. Another treatment that usually results in an increased number of platelets is removal of the spleen, the organ that destroys antibody-coated platelets. Other drugs, such as vincreistine, azathioprine (Imuran), danazol (Danocrine), cyclophosphamide (Cytoxan), and cyclosporine (Sandimmune), are prescribed only for people with severe cases for which other treatments have not shown benefit, because these drugs have potentially harmful side effects.
Except in certain situations, such as internal bleeding and preparation for surgery, platelet transfusions usually are not beneficial and are seldom performed. Because all therapies can have risks, it is important that over-treatment based solely on platelet counts rather than symptoms be avoided.
In some instances, lifestyle adjustments may help to prevent bleeding due to injury. These would include using protective gear such as helmets and avoiding contact sports if there are symptoms or if platelet counts are less than 50,000 mm3. Otherwise, most people can carry on normal activities, but final decisions about activity should be made in consultation with a hematologist (a practitioner who specializes in blood disorders).
For nutritional recommendations, see the links below.
FOR MORE INFORMATION
Wikipedia: Idiopathic Thrombocytopenia Purpura
E-Medicine: Immune Thrombocytopenic Purpura
WrongDiagosis: Immune Thrombocytopenic Purpura
Mayo Clinic: Idiopathic Thrombocytopenic Purpura
Current Oncology: Drug-Induced Immune Thrombocytopenic Purpura
Scripps.edu: Adult Chronic Immune Thrombocytopenic Purpura
Annals of Internal Medicine: Therapy For Adults With Refractory Chronic Immune Thrombocytopenia Purpura
LEUKODYSTROPHIES
Leukodystrophy refers to progressive degeneration of white matter of the brain due to imperfect growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fiber. Myelin is a complex substance made up of at least 10 different compounds. The leukodystrophies are a group of disorders that are caused by genetic defects in how myelin produces or metabolizes these chemicals. Each of the leukodystrophies is the result of a defect in the gene that controls only one of these chemicals.
The most common symptom of a leukodystrophy disease is a gradual decline in the functioning of an infant or child who previously appeared well. There may be a progressive loss in body tone, movements, gait, speech, ability to eat, vision, hearing, and behavior. There is often a slow-down in mental and physical development. Symptoms vary according to the specific type of leukodystrophy, and may be difficult to recognize in the early stages of the disease.
The prognosis and recommended treatment for most of the leukodystrophies is symptomatic and supportive, and may include medications, physical, occupational, and speech therapies, and nutritional, educational, and recreational programs. Bone-marrow transplantation is showing promise for some. The prognosis for leukodystrophies varies according to the specific type of leukodystrophy. Some important types of leukodystrophy include adrenoleukodystrophy (ALD), Alexander disease, Canavan disease, Krabbe disease, metachronmatic leukodystrophy (MLD), and Pelizaeus-Merzbacher disease (PMD).
ADRENOLEUKODYSTROPHY
People with adrenoleukodystrophy (ALD) accumulate high levels of compounds known as saturated very-long-chain fatty acids (VLCFA) in the brain and parts of the adrenal glands because they do not produce the enzyme that breaks down these fatty acids in a normal manner. The loss of myelin and the progressive dysfunction of the adrenal glands are the primary characteristics of ALD.
There are main subtypes of ALD. The most common is the X-linked form (X-ALD), which involves an abnormal gene located on the X-chromosome; and neonatal ALD, which is caused by defective genes that are not located on the X-chromosome. The distinction between the tow makes a significant difference because women who have two X-chromosomes while men only have one, lacking the protection of a second, normal X-chromosome (it is highly unlikely for both of a woman's X-chromosomes to be defective), men are generally more severely affected by the disease - although a mild form of ALD is occasionally seen in women who are carriers of the disorder. Symptoms include:
- Progressive stiffness.
- Weakness or paralysis of the lower limbs.
- Ataxia.
- Excessive muscle tone.
- Mild peripheral neuropathy.
- Urinary problems.
In contrast, neonatal ALD can affect either male or female babies, with symptoms including:
- Mental retardation.
- Facial abnormalities.
- Seizures.
- Retinal degeneration.
- Weak muscle tone.
- Enlarged liver.
- Adrenal dysfunction.
This form usually is present from birth and progresses rapidly.
The onset of X-ALD, on the other hand, can occur either in childhood or adulthood. The childhood form, with symptoms usually starting between the ages of 4 and 10 years, is the more severe. The most common symptoms are usually behavioral changes such as:
- Abnormal withdrawal or aggression.
- Poor memory.
- Poor school performance.
Other symptoms include:
- Visual loss.
- Learning disabilities.
- Seizures.
- Poorly articulated speech.
- Difficulty swallowing.
- Deafness.
- Disturbances of gait and coordination.
- Fatigue.
- Intermittent vomiting.
- Increased skin pigmentation.
- Progressive dementia.
In the milder adult-onset form, which typically begins between the ages of 21 and 35, symptoms may include:
- Progressive stiffness.
- Weakness or paralysis of the lower limbs
- Ataxia (disturbances in coordination and motor function).
Although adult-onset ALD progresses more slowly than the classic childhood form, it can also result in deterioration of brain function.
CONSIDERATIONS
Adrenal function must be tested periodically in all patients with ALD. Treatment with adrenal hormones can be lifesaving.
Symptomatic and supportive treatments for ALD include physical therapy, psychological support, and special education.
Some evidence suggests that administering a mixture of oleic acid and euric acid, known as Lorenzo's oil (and made famous in the movie by that name), to boys with X-ALD can reduce or delay the appearance of symptoms.
Bone marrow transplants can provide long-term benefit for boys who have early evidence of X-ALD, but the procedure carries substantial and serious risks, and is not recommended for those whose symptoms are already severe or who have the adult-onset or neonatal forms.
The administration of the omega-3 essential fatty acid docosahexaenoic acid (DHA) may help some infants and children with neonatal ALD.
The overall prognosis for people with ALD is generally poor because of the progressive neurological deterioration it causes. Death usually occurs within 1 to 10 years after the onset of symptoms.
For nutritional recommendations, see the links below.
FOR MORE INFORMATION
Wikipedia: Adrenoleukodystrophy
United Leukodystrophy Foundation: X-Linked Adrenoleukodystrophy
Bio-Medicine: Leukodystrophy
Adrenoleukodystrophy (ALD) Foundation
WebMD: Adrenoleukodystrophy
The AMN-ALD Community Pages Support For Families
Human & Scientific Story of Adrenoleukodystrophy
MCW HealthLink: Adrenoleukodystrophy
MERALGIA PARESTHETICA
Meralgia paresthetica is a disorder characterized by tingling, numbness, and burning pain in the outer side of the thigh. The disorder is also known as Bernhardt-Roth syndrome and lateral femoral cutaneous nerve entrapment".
Meralgia paresthetica is caused by compression of the lateral femoral cutaneous nerve, which transmits sensation from the outer thigh to nerves in the spinal cord, as it exits the pelvis. The disorder occurs in men more than women, and is generally found in middle-aged or overweight individuals. Affected individuals often complain that the symptoms worsen after walking or standing, and that the skin is sensitive to touch. Meralgia paresthetica disorder is associated with wearing clothing that is too tight, as well as with pregnancy, diabetes, and obesity.
RECOMMENDATIONS
If you are overweight, lose the extra pounds.
Try wearing looser clothing.
Avoid standing or walking for prolonged periods of time. Also avoid any position that places pressure on the outer thigh.
CONSIDERATIONS
Gabapentin (Neurontin) and other medications may be prescribed to help alleviate symptoms.
In very few cases in which pain is persistent or severe, surgical intervention to relieve pressure may be needed. Surgery is not always successful, however.
Meralgia paresthetica usually eases or disappears after treatment. In some cases, the disorder simply goes away on its own.
For other nutritional recommendations, see Neurological Support (#2 above) and the following links.
FOR MORE INFORMATION
Wikipedia: Meralgia Paresthetica
E-Medicine: Meralgia Paresthetica
MedScape: Treatment For Meralgia Paresthetica
MedicineNet: Meralgia Paresthetica
Health Scout: Meralgia Paresthetica
NINDS: Meralgia Paresthetica Information Page
MULTIPLE SYSTEM ATROPHY WITH ORTHOSTATIC HYPOTENSION
See Orthostatic Hypotension (below) in the next section.
ORTHOSTATIC HYPOTENSION
Orthostatic hypotension is a sudden decrease in blood pressure when a person stands upright. Other known names for this disorders are postural hypotension and Bradbury-Eggleston syndrome. The condition may be caused by a decreased amount of blood in the body resulting from excessive use of diuretics, vasodilators, or other types of drugs. Dehydration and prolonged bed rest can also cause orthostatic hypotension. Symptoms appear upon standing (the more suddenly one stands, the more serious the problem) and generally include dizziness, light-headedness, blurred vision, and syncope or temporary loss of consciousness.
Other diseases are sometimes associated with the disorder, including Addison's disease, atherosclerosis, diabetes, and certain neurological disorders like-multiple system as Shy-Drager syndrome, multiple system atrophy with orthostatic hypotension is a progressive disorder of the central and autonomic nervous systems that is characterized by orthostatic hypotension - an excessive drop in blood pressure when standing up, causing dizziness and fainting. Multiple nervous system atrophy can occur without orthostatic hypotension, but is very rare.
The disorder is classified into 3 types:1. The Parkinsonian-type, which include symptoms similar to those of Parkinson's disease, such as slow movement, stiff muscles, and tremor.
2. The cerebellar-type, which causes problems with coordination and speech.
3. The combined-type, which includes symptoms of both Parkinsonism and cerebellar failure.
Problems with urinary incontinence, constipation, and sexual impotence in men occur early in the course of the disease. Other symptoms may include:
- Generalized weakness.
- Double vision or other vision problems.
- Difficulty breathing & swallowing.
- Sleep disturbances.
- Decreased sweating.
The disease can take years to diagnose because its features resemble those of so many other health problems.
CONSIDERATIONS
If orthostatic hypotension is caused by hypovolemia (a decreased amount of blood in the body) due to medications, the disorder may be reversed by adjusting the dosage or by discontinuing the medication.
If the condition is caused by prolonged bed rest, simply sitting up with increasing frequency each day may yield some improvement.
In some cases, physical counter pressure such as elastic hose or whole-body inflatable suits may be required.
Dehydration is treated with salt and fluids.
The prognosis for most people with orthostatic hypotension depends on the underlying cause.
There is no cure for multiple system atrophy with orthostatic hypotension. Treatment is aimed at controlling symptoms. The medication carbidopa/levodopa (Sinemet), which is used for treating Parkinson's disease, may improve the general sense of well-being. Other medications that elevate blood pressure while standing are often used, but these can also cause high blood pressure while lying down.
People with multiple system atrophy with orthostatic hypotension should sleep with their heads elevated. Those who have breathing and swallowing difficulty may need to use an artificial breathing or feeding tube.
The prognosis for individuals with multiple system atrophy with orthostatic hypotension is poor. People usually die within 7 to 10 years after the onset of symptoms. A problems with the respiratory system is the most common cause of death.
For other nutritional recommendations, see Neurological Support (#2 above) and the following links.
FOR MORE INFORMATION
Wikipedia: Orthostatic Hypotension
E-Medicine: Orthostatic Hypotension
Dizziness & Balance: Orthostatic Hypotension
MedHelp: Hypotension Links
About Health Disease: Tilt Table Testing
NINDS: Orthostatic Hypotension Information Page
PHENYLKETONURIA
Phenylketonuria (PKU) is an inherited error of metabolism caused by a deficiency of the enzyme phenylalanine hydroxylase, which is responsible for processing the essential amino acid phenylalanine. Lack of the enzyme results in the buildup of phenylalanine in the body, which over time can lead to mental retardation, organ damage, abnormal posture, and in some cases, severely compromised pregnancy. Symptoms in affected infants include:
- Drowsiness.
- Lethargy.
- Difficulty feeding.
- Light eyes.
- Light pigmentation in hair and skin.
- A rash similar to eczema may develop.
If left untreated, PKU can develop into severe mental retardation, and also can cause neurological symptoms, such as seizures, hyperactivity, clumsy walking, unusual posture, aggressive behavior or psychiatric disturbances. Fortunately, the problem is detectable through blood tests within the first days of life. Screening for PKU is part of routine testing recommended for newborns in many states.
CONSIDERATIONS
If treated properly with a carefully controlled phenylalanine-restricted diet, mental retardation can be prevented. Among the things that people with PKU absolutely cannot consume are products containing the artificial sweetener aspartame (found in Equal, NutraSweet and many processed food products), which has as one of its components the amino acid phenylalanine.
For other nutritional recommendations, see Neurological Support (#2 above) and the following links.
FOR MORE INFORMATION
Wikipedia: Phenylketonuria (PKU)
PKU.com: Online Resource & Community
National PKU News
MedHelp: Phenylketonuria (PKU)
March of Dimes: PKU (Phenylketonuria)
WebMD: Phenylketonuria - PKU Test
NLM-NIH: Phenylketonuria
MedicineNet: Phenylketonuria
PKU World Link: International Organization
PIRIFORMIS SYNDROME
Piriformis syndrome is a rare neuromuscular disorder that occurs when the piriformis muscle (a narrow muscle located deep in the buttocks) compresses or irritates the sciatic nerve, the largest nerve in the body. As with sciatica, caused by a herniated or ruptured disc, compression of the sciatic nerve causes pain, frequently described as tingling or numbness, in the buttocks and along the nerve, often extending down the leg. The pain may worsen with prolonged periods of sitting, or by climbing stairs, walking, or running.
CONSIDERATIONS
Treatment generally begins with stretching and massage. Anti-inflammatory drugs may be prescribed.
It may be advisable to stop, or at least take a break from, physical activities that aggravate the problem.
The prognosis for piriformis syndrome is good. Once symptoms are addressed, individuals can usually resume their normal activities. In some cases, exercise regimens may need to be modified in order to reduce the likelihood of recurrence or worsening symptoms.
For other nutritional recommendations, see Neurological Support (#2 above) and the following links.
FOR MORE INFORMATION
Wikipedia: Piriformis Syndrome
About Orthopedics: Piriformis Syndrome
National PKU News
The Stretching Handbook: Piriformis Syndrome & Effective Piriformis Stretches
E-Medicine: Piriformis Syndrome
BodyBuildingForYou: Piriformis Syndrome (Sciatic Pain)
E-Medicine: Sports - Piriformis Syndrome Article
Orthogate.org: Piriformis Syndrome
POSTURAL TACHYCARDIA SYNDROME
People who suffer with postural tachycardia syndrome (POTS) experience a pulse rate that is too fast when they stand. Symptoms include:
- Rapid heartbeat.
- Light-headedness with prolonged standing.
- Headache.
- Chronic fatigue.
- Chest pain.
The underlying cause or causes of POTS usually cannot be identified, but the disorder is not thought to progress to heart disease.
CONSIDERATIONS
The severity of symptoms usually determines the course of treatment for POTS. Individuals with the disorder are usually advised to increase their fluid and salt intake. Body stockings may provide some relief. Drug therapy, with fludrocortisone, beta-blockers, midodrine (Pro-Amatine, a drug used to treat low blood pressure), or clonidine (Catapres, which is used to treat high blood pressure), can be beneficial. Physical exercise, especially calf muscle resistance training, also may help.
Some people with postural tachycardia syndrome may require and benefit from insertion of a cardiac pacemaker.
The prognosis for people with POTS varies. Many individuals improve with one or more of the treatments outlined above, although severe POTS can be disabling for years.
For other nutritional recommendations, see Neurological Support (#2 above) and the following links.
FOR MORE INFORMATION
Wikipedia: Postural Tachycardia Syndrome
Knol: Postural Tachycardia Syndrome
NINDS: Postural Tachycardia Syndrome Information Page
REFSUM DISEASE
Refsum disease is a hereditary disorder of fat metabolism caused by the deficiency of an enzyme that breaks down phytanic acid, a type of fatty acid. The result is an abnormal accumulation of phytanic acid in blood plasma and body tissues. Phytanic acid is not made in the human body. It comes from consuming dairy products, beef, lamb, and some seafood.
Symptoms of the disorder may include:
- Visual impairment.
- Peripheral neuropathy (damage to nerves that can cause pain, tingling, burning and other sensations in the extremities).
- Ataxia (disturbances in coordination and motor function).
- Impaired hearing.
- Bone and skin changes.
Other symptoms may also occur:
- Nystagmus (rapid, involuntary to-and-fro eye movements).
- Anosmia (Loss of the sense of smell).
- Ichthyosis (dry, rough, scaly skin).
The onset of Refsum disease varies from early childhood to age 50, however, symptoms usually appear by the age of 20. The disorder affects both males and females.
RECOMMENDATIONS
Strictly limit or avoid consumption of foods that contain phytanic acid, including dairy products, beef and lamb, fatty fist such as tuna, cod and haddock. The body also converts phytol, a substance found in green leafy vegetables, to phytanic acid, so limiting them may be helpful as well.
CONSIDERATIONS
In addition to making dietary changes, plasmapheresis (the removal and reinfusion of blood plasma) may be required periodically to manage Refsum disease.
The prognosis for individuals with Refsum disease varies. With treatment, symptoms of peripheral neuropathy and ichthyosis generally disappear. However, while treatment may forestall further deterioration of vision and hearing, it cannot undo damage to vision and hearing that may have occurred.
For nutritional recommendations, see Gastrointestinal Support (#1 above) and and the following links.
FOR MORE INFORMATION
Wikipedia: Refsum's Disease
E-Medicine: Refsum Disease Article
RefsumDisease.org: Adult Refsum's Disease Information
NINDS: Refsum's Disease
The Pacifier: Infantile Refsum's Disease
E-Medicine: Diseases of Tetrapyrrole Metabolism - Refsum Disease
TOURETTE SYNDROME
Tourette syndrome (TS) is an inherited neurological disorder distinguished by repeated involuntary movements and uncontrolled vocal sounds called tics. There may be facial tics and eye-blinking, head-jerking, neck-stretching, foot-stomping, body twisting and bending, throat-clearing, coughing, sniffing, and grunting, yelping, barking, or shouting noises. Tics can be suppressed for a short time, but when stress increases, eventually a tic will escape. In limited cases, such tics can include the compulsive use of inappropriate words and phrases.
The onset of TS generally appears before the age of 18, and the majority of cases are mild.
CONSIDERATIONS
Medication is available to control tics that interfere with daily functioning, but the majority of people with TS require no medication.
There is no cure for Tourette syndrome. However, while TS is generally a chronic lifelong condition, it does not get progressively worse. In fact, many people find that their symptoms improve as they mature.
For other nutritional recommendations, see Neurological Support (#2 above) and the following links.
FOR MORE INFORMATION
Wikipedia: Tourette Syndrome
Tourette Syndrome Association: TSA Home Page
TouretteSyndrome.net: Tourette Syndrome Plus
NINDS: Tourette Syndrome
MedLine Plus: Tourette Syndrome
Mayo Clinic: Tourette Syndrome
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