February 3, 2017

Parkinson’s Disease is a chronic and progressive neurodegenerative brain disorder. Parkinson’s disease (PD) was first described by Dr. James Parkinson. Earlier, the condition was known popularly as the shaking palsy and in the medical community by its Latin equivalent, paralysis agitans. These terms are misleading, however, implying that people are paralyzed with this disorder, which is not the case. It is sometimes called idiopathic parkinsonism (the term idiopathic means that the cause is unknown), but more commonly today it is simply called Parkinson’s disease, to honor the physician who first described it.

PD is a disorder of the central nervous system, involving primarily a degeneration of certain nerve cells in deep parts of the brain called the basal ganglia, and in particular a loss of nerve cells (or neurons) in a part of the brainstem called the substantia nigra. These cells make the neuro-chemical messenger dopamine, which is partly responsible for starting a circuit of messages that coordinate normal movement. In the absence (or with substantial reduction, more than 80% of the normal level) of dopamine, the neurons in the receiving area (called dopamine receptors) in the next part of the basal ganglia circuit called the striatum are not adequately stimulated, and the result is impairment of movement with tremor, slowness, stiffness, or balance problems, among other symptoms, which will be discussed in the later section.

Nearly one million people in the US are living with Parkinson’s disease.PD occurs in roughly the same proportions in men and women, althoughthere may be a slight preponderance of affected men throughout the world.Initial symptoms may appear at any age, although under 40 is uncommon and under 20 is very rare (but it happens!). Most commonly, the first symptoms are noted in the 60’s or 70’s. The average age of onset of PD is about 59.

Causes

The exact causes of PD remain unknown, despite decades of intensive study. Many experts suggest that the disease is caused by a combination of genetic and environmental factors, which may vary from person to person.

In some people, genetic factors may play a role; in others, illness, an environmental toxin or other event may contribute to PD.

  • Genetic Factors – The vast majority of Parkinson’s cases are not directly inherited. About 15 to 25 percent of people with Parkinson’s report having a relative with the disease.

Researchers have discovered several gene mutations that can cause the disease directly, but these affect only a small number of families. Some of these mutations involve genes that play a role in dopamine cell functions. Parkinson’s has developed at an early age in individuals with mutations in genes for parkin, PINK1, LRRK2, DJ-1, and glucocerebrosidase, among others.

 

  • Environmental Factors – Several studies suggest that Parkinson’s disease may result from exposure to an environmental toxin or injury. Several factors can be linked to Parkinson’s, including rural living, well water, manganese and pesticides.

Prolonged occupational exposure to certain chemicals is associated with an elevated risk of PD. These include the insecticides permethrin and beta-hexachlorocyclohexane (beta-HCH), the herbicides paraquat and 2,4-dichlorophenoxyacetic acid and the fungicide maneb.

It is to be noted that, a simple exposure to an environmental toxin is never enough to cause Parkinson’s. Most people exposed to a toxin do not develop the disease. In fact, there is no conclusive evidence that any environmental factor, alone, can be considered a cause of the disease.

 

  • Less common causes include poisoning by carbon monoxide or manganese (a type of mineral), lesions and tumors in the brainstem, and a rare illicit drug called N-MPTP.

 

  • Drugs & Medications – Medications that can cause secondary Parkinsonism include:
    • Haloperidol* and other medications used to treat hallucinations
    • Metoclopramide (an anti-nausea medication)

 

  • Lewy bodies – Clumps of specific substances within brain cells are microscopic markers of Parkinson’s disease. These are called Lewy bodies, and researchers believe these Lewy bodies hold an important clue to the cause of Parkinson’s disease.
  • Alpha-synuclein is found within Lewy bodies – Although many substances are found within Lewy bodies, scientists believe an important one is the natural and widespread protein called alpha-synuclein (A-synuclein). It’s found in all Lewy bodies in a clumped form that cells can’t break down. This is currently an important focus among Parkinson’s disease researchers.

 

  • Food Allergies – Hidden food allergies and chemical sensitivities contribute to most degenerative diseases. However, in Parkinson’s disease the body generally is insensitive and does not readily react even when specifically testing for hidden allergies. Nevertheless, it has been shown that the intestinal barrier becomes increasingly inefficient with advancing age and degenerative diseases. This allows only partly digested protein fragments or peptides to enter the bloodstream and reach the brain, causing chronic Inflammation and long-term degeneration of brain cells.

 

 

  • Heavy Metals – Brain deterioration can be caused by accumulations of the heavy metals cadmium, lead and mercury. Of these, mercury is generally the greatest brain hazard, coming mainly from amalgam tooth fillings. Organic mercury compounds are strong nerve poisons, which may kill nerve cells, cause tremors and reportedly also symptoms of multiple sclerosis. Finally, iron overload, especially in inorganic form, can intensify Parkinson problems.

 

  • Aluminium-A contributing factor greatly facilitating the passage of toxic chemicals into the brain is aluminium. The brain is normally protected from undesirable chemicals in the bloodstream by a filter barrier. High aluminium levels have been shown to allow toxic chemicals to cross this barrier, which would otherwise be kept out.

 

  • Gastrointestinal Involvement – Endotoxins are toxic chemicals produced by harmful intestinal bacteria. Undesirable changes in the composition of the intestinal flora and resulting overgrowth of the small intestine with undesirable bacteria and fungi commonly results from antibiotics and other immune-suppressive drugs, from low gastric acidity and from frequently drinking alcohol.

 

Symptoms

Each person is affected differently by Parkinson’s disease and no two people will experience exactly the same symptoms. The impact of Parkinson’s disease can be unpredictable and it is common for people to have good days and bad days.

The main symptoms of Parkinson’s disease are:

  • tremor (involuntary trembling or shaking movements; the most common symptom)
  • rigidity (stiffness)
  • slowness of movement (bradykinesia)
  • balance problems
  • problems with posture (particularly a tendency to stoop forwards)

Other symptoms include –

  • Freezing
  • Micrographia – shrinkage in handwriting
  • Less Expressive Face
  • Unwanted Acceleration
  • Stooped posture, a tendency to lean forward
  • Dystonia
  • Impaired fine motor dexterity and motor coordination
  • Impaired gross motor coordination
  • Poverty of movement (decreased arm swing)
  • Akathisia
  • Speech problems, such as softness of voice or slurred speech caused by lack of muscle control
  • Difficulty swallowing
  • Sexual dysfunction
  • Cramping
  • Drooling

There are 5 stages of Parkinson’s Disease –

  • Stage 1 – Unilateral involvement only, usually with mini9mal or no functional impairment.
  • Stage 2 – Bilateral or midline involvement, without impairment of balance.
  • Stage 3 – First signs of impaired righting reflexes. This is evident as thepatient turns or is demonstrated when he or she is pushed from standing equilibrium with the feet together and eyes closed.
  • Stage 4 – Fully developed, severely disabling disease; the patient is stillable to walk and stand unassisted but is markedly incapacitated.
  • Stage 5 – Confinement to bed or wheelchair unless aided.

Treatment

Medications

There are many medications available to treat the symptoms of Parkinson’s, although none yet that actually reverse the effects of the disease.

It is common for people with PD to take a variety of these medications – all at different doses and at different times of day – in order to manage the symptoms of the disease.

These include –

  • Carbidopa/Levodopa (Sinemet) – The most potent medication for Parkinson’s is levodopa. Its development in the late 1960s represents one of the most important breakthroughs in the history of medicine. Plain levodopa produces nausea and vomiting. It is now combined with carbidopa to prevent this side effect. The well-known combined carbidopa/levodopa formulation is called Sinemet.
  • Dopamine agonists – These are the drugs that stimulate the parts of the human brain influenced by dopamine. In effect, the brain is tricked into thinking it is receiving the dopamine it needs. The two most commonly prescribed oral pill agonists in the US are pramipexole (Mirapex) and ropinirole (Requip). A third, rotigotine transdermal system (Neupro), was recently re-approved after several years of being off the market. Bromocriptine (Parlodel® ) is available, but is less commonly used.
  • Anticholinergics – Anticholinergics can be helpful for tremor and may ease dystonia associated with wearing-off or peak-dose effect. They have little effect on other symptoms of Parkinson’s. The drugs in this class include trihexyphenidyl (Artane),benztropinemesylate (Cogentin) and procyclidine (no longer available in the US), among others.
  • MAO-B inhibitors — Selegilinealso called deprenyl, with trade names Eldepryl and Zelapar and rasagiline (Azilect) — block an enzyme in the brain that breaks down levodopa. These drugs have a modest effect in suppressing the symptoms of Parkinson’s.

 

Alternative Treatment

  • Vitamin E – Vitamin E can fight damage in the brain caused by free radicals, and has been suggested to lower the risk of PD. But taking vitamin E alone did not seem to have the same effect. More studies are needed to know whether there is any real benefit. Vitamin E supplements can increase the risk of bleeding, especially if you also take blood thinners, such as warfarin (Coumadin), clopidogrel (Plavix), or aspirin. Selenium is an antioxidant that works with vitamin E. It also helps to increase circulation and tissue oxygenation, thereby limiting damage to nerve cells.
  • Gamma-aminobutyric acid (GABA) is an amino acid that acts as a neurotransmitter. It helps both to strengthen and relax the nervous system.
  • Acidophilus and bifidobacteria are friendly bacteria that ensure a healthy gastrointestinal tract. Probiotics are especially helpful for preventing constipation, which is often a problem for people with Parkinson’s disease.
  • Alpha-lipoic acid is an antioxidant that also helps to “recharge” other antioxidants in the body.
  • Calcium and magnesium are imperative for maintaining a healthy nervous system.
  • Coenzyme Q10 is an oxygenating antioxidant that helps prevent free-radical damage and important for cell renewal.
  • Evening primrose oil and flaxseed oil contain valuable essential fatty acids (EFAs), which are often deficient in people with Parkinson’s disease.
  • Green-foods supplements supply chlorophyll and important trace minerals.
  • Marine alginate concentrate and N-acetylcysteine may help in the process of chelating (binding to) heavy metals in the body so that they can be excreted.
  • Nicotinamide adenine dinucleotide hydrogren (NADH) is an enzyme that helps to improve neurotransmitter function.
  • Phosphatidylserine is a type of lipid important for normal brain function and the effective transmission of nerve impulses. Low levels of phosphatidylserine are associated with Parkinson’s disease.
  • Soy Lecithin is rich in phosphatidylcholine. Choline is a vital building block for acetylcholine.
  • Pine-bark and grape-seed extracts fight free-radical damage and have anti-inflammatory properties. Many people consider Parkinson’s disease to be a consequence of degeneration of nerve cells due to free-radical damage.
  • The B vitamins are very important for brain and nerve function.
  • Vitamin C and the bioflavonoids are powerful antioxidants that fight free radicals.
  • Creatine– Some studies suggest that taking creatine, an amino acid that helps supply energy to muscles, may help slow progression of Parkinson’s among people who are in the early stages, and who do not need medication to control symptoms.
  • Exercise – Exercising may increase your muscle strength, flexibility and balance. Exercise can also improve your well-being and reduce depression or anxiety.
    • Massage. Massage therapy can reduce muscle tension and promote relaxation. These services, however, are rarely covered by health insurance.
    • Acupuncture. During an acupuncture session, a trained practitioner inserts tiny needles into many specific points on the body, which may reduce the pain.
    • Tai chi. An ancient form of Chinese exercise, tai chi employs slow, flowing motions that may improve flexibility, balance and muscle strength. Tai chi may also prevent falls. Several forms of tai chi are tailored for people of any age or physical condition.
    • Yoga. In yoga, gentle stretching movements and poses may increase theflexibility and balance.
    • Alexander technique. This technique — which focuses on muscle posture, balance and thinking about how you use muscles — may reduce muscle tension and pain.
    • Meditation. In meditation, body quietly reflects and focuses on mind, on an idea or image. Meditation may reduce stress and pain and improve the sense of well-being.
    • Music or art therapy. Music or art therapy may help to relax. Music therapy helps some people with Parkinson’s disease to improve their walking and speech. Participating in art therapy, such as painting or ceramics, may improve the mood.

 

As Parkinson’s disease is a long-term condition and symptoms worsen over time, it is important to treat it on time.

 

 

References –

www.parkinson.org

http://www.pdf.org/en/parkinson_otc_meds

http://www.parkinson.org/understanding-parkinsons/treatment/complementary-treatment

http://www.mayoclinic.org/diseases-conditions/parkinsons-disease/basics/causes/con-20028488

http://bodyandhealth.canada.com/channel_condition_info_details.asp?channel_id=2046&disease_id=102&relation_id=33685

http://www.brainandspine.org.uk/parkinsons-disease

http://parkinsonsresource.org/wp-content/uploads/2012/01/The-FIVE-Stages-of-Parkinsons-Disease.pdf

https://ethnomed.org/patient-education/neurological-conditions/parkinsons/Parkinsons%20Disease%20Overview.pdf

Posted in DEGENERATIVE
February 3, 2017

Osteoporosis is a disease in which bones become fragile and weak, leading to an increased risk of fractures (broken bones). People with osteoporosis can experience a fracture even after a slight bump, or a fall from standing height, in the course of daily activities.

Osteoporosis comes from ‘osteo’ meaning bone and the Greek word ‘por’ (passage) i.e. porous bone. Normal bone is composed of a mixture of calcium and other minerals such as magnesium and phosphate. It is also made up of collagen (protein), which forms the structural framework of bone. Osteoporosis occurs when there is a loss of mineral from bone mainly in the form of calcium as well as architectural loss of normal bone structure. The loss of mineral content of the bone is referred to as a loss of bone mineral density in the bone.

The 3 types of bone cells are osteoblasts, osteoclasts, and osteocytes. The osteocytes function as “mechanostats”, sensing the degree of micro-damage and triggering remodeling in areas of stress and strain, thus allowing continual renewal, repair, and replacement of bone. This process of remodeling maintains bone strength.

Osteoporosis has no signs or symptoms until a fracture occurs – this is why it is often called a ‘silent disease’. Fractures due to osteoporosis occur most commonly at sites such as the wrist, upper arm, pelvis, hip and spine, and can result in severe pain, significant disability and even death.

About 54 million Americans have osteoporosis and low bone mass, placing them at increased risk for osteoporosis. Studies suggest that approximately one in two women and up to one in four men age 50 and older will break a bone due to osteoporosis.

Causes

Genetic Factors – Bone health can be strongly inherited so consider your family history of osteoporosis. It is important to note if anyone in your family (particularly parents or siblings) has ever been diagnosed with osteoporosis, broken a bone from a minor fall or rapidly lost height. These can indicate low bone density.

Medical History – Certain conditions and medications can impact on your bone health. Corticosteroids – commonly used for asthma, rheumatoid arthritis and other inflammatory conditions Low hormone levels – in women: early menopause; in men: low testosterone Thyroid conditions – over active thyroid or parathyroid Conditions leading to malabsorption eg: coeliac disease, inflammatory bowel disease Some chronic diseases eg: rheumatoid arthritis, chronic liver or kidney disease Some medicines for breast cancer, prostate cancer, epilepsy and some antidepressants.

Calcium and Vitamin D Level – Low calcium intake – adults require 1,000 mg per day (preferably through diet) which increases to 1,300 mg per day for women over 50 and men over 70 Low vitamin D levels – a lack of sun exposure can mean you are not getting enough vitamin D which your body needs to absorb calcium.

Gender

Women are more at risk of developing osteoporosis than men because the hormone changes that occur in the menopause directly affect bone density.

The female hormone oestrogen is essential for healthy bones. After the menopause (when monthly periods stop), oestrogen levels fall. This can lead to a rapid decrease in bone density.

In most cases, the cause of osteoporosis in men is unknown. However, there’s a link to the male hormone testosterone, which helps keep the bones healthy.

Risk factors – Many hormones in the body can affect the process of bone turnover. If you have a condition of the hormone-producing glands, you may have a higher risk of developing osteoporosis.

  • Hormone-related conditions that can trigger osteoporosis include:
  • hyperthyroidism (overactive thyroid gland)
  • disorders of the adrenal glands, such as Cushing’s syndrome
  • reduced amounts of sex hormones (oestrogen and testosterone)
  • disorders of the pituitary gland
  • hyperparathyroidism (overactivity of the parathyroid glands)

Lifestyle choices – Some bad habits can increase your risk of osteoporosis. Examples include –

  • Sedentary lifestyle – People who spend a lot of time sitting have a higher risk of osteoporosis than do those who are more active. Any weight-bearing exercise and activities that promote balance and good posture are beneficial for your bones, but walking, running, jumping, dancing and weightlifting seem particularly helpful.
  • Excessive alcohol consumption. Regular consumption of more than two alcoholic drinks a day increases your risk of osteoporosis.
  • Tobacco use – The exact role tobacco plays in osteoporosis isn’t clearly understood, but it has been shown that tobacco use contributes to weak bones.

Symptoms

There are often no warning signs or symptoms until a minor fall or a sudden impact causes a bone fracture. Healthy bones should be able to withstand a fall from standing height, so a bone that breaks in these circumstances is known as a fragility fracture.

The most common injuries in people with osteoporosis are:

  • wrist fractures
  • hip fractures
  • fractures of the spinal bones (vertebrae)

Sometimes a cough or sneeze can cause a rib fracture or the partial collapse of one of the bones of the spine. In older people, a fractured bone can be serious and result in long-term disability. For example, a hip fracture may lead to long-term mobility problems. Although a fracture is the first sign of osteoporosis, some older people develop the characteristic stooping (bent forward). It happens when the bones in the spine have fractured, making it difficult to support the weight of the body.

Treatment

Medications – Treatment recommendations are based on an estimate of your risk of breaking a bone in the next 10 years using information such as the bone density test. If the risk is not high, treatment might not include medication and might focus instead on lifestyle, safety and modifying risk factors for bone loss.

For both men and women at increased risk of fracture, the most widely prescribed osteoporosis medications are bisphosphonates. Examples include –

  • Alendronate (Fosamax)
  • Risedronate (Actonel, Atelvia)
  • Ibandronate (Boniva)
  • Zoledronic acid (Reclast)

Side effects include nausea, abdominal pain, difficulty swallowing, and the risk of an inflamed esophagus or esophageal ulcers. These are less likely to occur if the medicine is taken properly. Intravenous forms of bisphosphonates don’t cause stomach upset. Bisphosphonates have the potential to affect the jawbone. Osteonecrosis of the jaw is a rare condition that can occur after a tooth extraction in which a section of jawbone dies and deteriorates. You should have a recent dental examination before starting bisphosphonates.

Hormone-related therapy – Estrogen, especially when started soon after menopause, can help maintain bone density. However, estrogen therapy can increase a woman’s risk of blood clots, endometrial cancer, breast cancer and possibly heart disease. Therefore, estrogen is typically used for bone health only if menopausal symptoms also require treatment.

 

Alternative Treatment

Supplements

  • Calcium is the most abundant mineral in the human body. It is well recognized for its importance in the development of bones and teeth and has many other functions as well. The ability of calcium supplements to “maintain good bone health and reduce the high risk of osteoporosis later in life” is one of the few health label claims allowed by the U.S. Food and Drug Administration.
  • Magnesium is the second most common mineral in the body, after calcium. Magnesium is important for many metabolic processes, including building bone, forming adenosine triphosphate, and absorbing calcium. Dietary sources of magnesium include nuts, whole grains, dark green vegetables, fish, meat, and legumes. Magnesium is often deficient in the standard American diet, due to low consumption of foods containing this nutrient, as well as soil depletion from commercial farming practices such as overcropping.
  • Vitamin D is essential for the formation and maintenance of bone tissue, due to its involvement in several complex mechanisms, including the regulation of calcium and phosphorous absorption. If vitamin D levels are low, parathyroid hormone (PTH) increases and triggers osteoclasts to release calcium into the blood via bone readsorption. If this process continues over time, it weakens bone and leads to osteoporosis. In addition, vitamin D stimulates intestinal epithelial cells to synthesize calcium-binding proteins that support the absorption of calcium in the blood.
  • Boron is ubiquitous throughout the human body, with the highest concentrations found in the bones and dental enamel. Although there is currently no RDA for it, boron appears to be indispensable for healthy bone function, possibly because of its effects on reducing the excretion and absorption of calcium, magnesium, and phosphorus.
  • The mineral strontium is a powerful agent in the treatment and prevention of osteoporosis. Strontium is a naturally occurring mineral present in water and food. Trace amounts of strontium are found in the human skeleton, where it is adsorbed at the matrix crystal surface of bones.
  • Research supports the positive effects of soy isoflavones on reducing the risk of developing osteoporosis. Diets high in soy may decrease bone reabsorption in postmenopausal women. Although ipriflavone, a semi-synthetic flavone comparable to genistein and daidzein found in soy foods, was ineffective in restoring bone density in rats, it modulated IGF-I (insulin growth factor I), which is linked to bone mineral density, and increased bone remodeling through several mechanisms.
  • Vitamin K is a fat-soluble vitamin known for its effect in blood clotting, which it accomplishes by regulating the coagulation cascade via its ability to bind calcium ions (Ca2+), among other mechanisms. Three known vitamin K–dependent proteins have been isolated in bone: MGP (matrix Gla protein), protein S, and osteocalcin. One of vitamin K’s roles in helping to maintain healthy bone mass is linked to its importance in the formation of osteocalcin by osteoblasts. The synthesis of osteocalcin requires both vitamin D and vitamin K.
  • Omega-3 fatty acids is proven way to improve cardiovascular health, Omega-3 fatty acids have also shown some benefit to those with rheumatoid arthritis, reducing morning stiffness and joint swelling
  • Traditional Chinese Medicine (TCM) and acupuncture: TCM has been proven over thousands of years to help treat many different physical ailments. Based on herbs (usually brewed into tea or soup), TCM can improve how your body uses calcium, which in turn helps bone health.

 

References

http://www.osteoporosis.org.au/about-osteoporosis

http://www.medicinenet.com/osteoporosis/page2.htm

http://www.mayoclinic.org/diseases-conditions/osteoporosis/basics/risk-factors/con-20019924

http://www.choosingwisely.org/patient-resources/bone-density-tests/

http://nof.org/learn

http://womenshealth.gov/publications/our-publications/fact-sheet/osteoporosis.pdf

http://menopauseandu.ca/documents/OsteoporosisinMenopause2014.pdf

http://share.iofbonehealth.org/WOD/2013/patient-brochure/WOD13-patient_brochure.pdf

Posted in DEGENERATIVE
February 3, 2017

Ostoepenia is a condition characterized by a decreased density of bone, which leads to bone weakening and an increased risk of breaking the bone (fracture). “Osteo” means bone and “penia” indicates a state of being low in quantity. Therefore, the term osteopenia refers to a bone density which is somewhat less, but not excessively less, than a “standard” young person (someone in their mid to late 20s) of the same gender.

Osteopenia and osteoporosis are related conditions. The difference between osteopenia and osteoporosis is that in osteopenia the bone loss is not as severe as in osteoporosis. That means someone with osteopenia is more likely to fracture a bone than someone with a normal bone density but is less likely to fracture a bone than someone with osteoporosis. Osteopenia increases your risk of developing osteoporosis and is considered a precursor to osteoporosis.

Bone mineral density refers to the measure of the amount of mineral in bones, which determines the strength of the bones. As the mineral density decreases, the bones become thinner and more vulnerable to fractures. This happens when the balance between formation and loss of bone is lost. It indicates weakening of the bones which can eventually lead to osteoporosis. But this does not mean that every person diagnosed with osteopenia necessarily develops osteoporosis. It can lead to osteoporosis only if it is not treated at the right time.

Osteopenia is generally seen in women, though it does occur in men. The bones become thinner and weaker as one grows older. It is observed that after menopause, women are more prone to osteopenia. This is because the production of the hormone, estrogen, reduces after menopause. Estrogen is necessary for having strong and dense bones. There are no major symptoms of osteopenia. One may not realize she is suffering from it until the bones become too weak and tend to break. Though osteopenia can be treated with the help of medications, several side effects are seen in many cases. It is, therefore, advisable to maintain stronger bones with the help of diet or physical exercises and keep osteopenia away.

Causes

  • Genetic Factor – The risk of developing osteopenia is high (more than 50%) in patients with a family history of osteoporosis or low bone mass. Such people should consult a doctor when they reach 30 years of age and get their bone density tested.

 

  • Gender – Females are at a higher risk of suffering from bone loss or low bone density than males. It is mainly due to the fact that as a woman nears her menopausal years, hormonal changes take place in the body. This is the reason why early menopause and post-menopausal women are at high risk of bone loss.

 

 

  • Age and race – With age, bones begin to lose minerals along with bone structure and mass. This usually occurs as a person reaches peak bone density at the age of 30 years. Age apart; people belonging to Asian and Caucasian race are at a higher risk of developing osteopenia.

 

  • Diseases – In case a person has a history of anorexia nervosa (eating disorder) or are suffering from cholestasis (a liver condition) or chronic kidney disease, the chances that the bone density is lowered is high. This is because, they cause problems in absorption of vitamin D and other minerals necessary for maintaining bone health.

 

 

  • Medications – Certain medications like anticonvulsant, corticosteroids, chemotherapy and OTC pills like pain relievers and antacids chelate with important minerals calcium causing unavailability of the minerals to the body can cause osteopenia.

 

  • Malnutrition during pregnancy – It is during the last three months of pregnancy that there is transfer of high amounts of calcium and phosphorus to the fetus. Hence, lack of proper nutrition during these days by the mother increases the risk of poor bone health and low bone density in the child.

 

 

  • Faulty metabolism – In some cases, there might be problem in bone metabolism, which in turn affects the absorption and use of vitamins and minerals by the body. Although there might be many causes responsible for this, diagnosis of bone density is the only option to know whether you are suffering from bone loss or not.

 

  • Deficiency of Vitamin D – Lack of vitamin D in the body hinders with absorption of calcium and phosphorus from kidneys and intestines. If these bone minerals are not absorbed, over time there can be decreased bone density leading to osteopenia.

 

  • Lifestyle factors:
    • Lack of exercise and sedentary lifestyle
    • Excess alcohol consumption
    • Excessive smoking
    • Excessive stress
    • Crash dieting and eating disorders
    • Excessive coffee, tea, soda, chocolate or sports and energy drinks
    • Young female athletes with eating disorders and amenorrhea. These women have lower body weight, lower fat percentage, and higher incidence of asthma. This increases the risk of osteopenia.
    • Teenage pregnancy

 

Symptoms

Osteopenia does not cause pain unless a bone is broken (fractured). Interestingly, fractures in patients with osteopenia do not always cause pain. Osteopenia or osteoporosis can be present for many years prior to diagnosis for these reasons. Many bone fractures due to osteopenia or osteoporosis, such as a hip fracture or vertebral fracture (fracture of a bone in the spine), are very painful. However, some fractures, especially vertebral fractures (fractures of the bony building blocks of the spine), can be painless and therefore osteopenia or osteoporosis may go undiagnosed for years.

Treatment

Osteopenia should be prevented or treated in the early stage in order to avoid osteoporosis. The main objective is to make the bones resistant to fractures.

Medication

There are a lot drugs being used to treat osteopenia, some of them being bisphosphonates like alendronate, fosamax, actonel, reclast and boniva, calcitonin, oyster calcium, tamoxifen and fosteum. Bisphosphonates are used on a large scale. They make the bones denser by attaching themselves to the mineral surfaces of the bones. This increases the mineral density of bones. But over a period of years, the bones start to become brittle. The drugs also have various side effects, nasal irritation being the common one. Moreover, these drugs have to be taken for a long period of time, and one becomes dependent upon them. To avoid all this, natural treatment for osteopenia is the safest option. There are numerous ways to treat osteopenia naturally, like making changes in your diet and lifestyle, regular exercises and taking certain supplements.

In addition, several medications can help slow bone loss, reducing the risk of osteoporosis and fractures. These medications include:

  • Forteo (teriparatide), a synthetic form of a hormone that stimulates bone formation
  • Selective estrogen-receptor modulators such as Evista (raloxifene), which have positive estrogen-like effects on the bones
  • Calcitonin, which has been shown to increase bone mineral density

Exercise is important for having strong bones, because bone forms in response to stress. Weight-bearing exercises such as walking, hiking, and dancing are all good choices. Adding exercise with light weights or elastic bands can help the bones in the upper body.

 

Alternative Treatment

 

Reference

http://www.medicinenet.com/osteopenia/page2.htm#what_are_osteopenia_symptoms_and_signs

http://www.ncbi.nlm.nih.gov/pubmed/21234807

http://www.medicinenet.com/osteopenia/article.htm

http://www.webmd.boots.com/osteoporosis/guide/osteopenia-early-signs-of-bone-loss

http://www.rad.washington.edu/academics/academic-sections/msk/teaching-materials/online-musculoskeletal-radiology-book/osteopenia

http://etd.lsu.edu/docs/available/etd-07112005-140541/unrestricted/Mekary_dis.pdf\

http://www.nejm.org/doi/pdf/10.1056/NEJMcp070341

Posted in DEGENERATIVE
February 3, 2017

Osteoarthritis (OA) is the most common form of arthritis. It causes joint pain and stiffness. It usually develops gradually, over time. Several different joints can be affected, but osteoarthritis is most frequently seen in the hands, knees, hips, feet and spine.

Normal joints are hinges at the ends of bones usually covered by cartilage and lubricated inside a closed sack by synovial fluid.

Normally, joints have remarkably little friction and move easily. With degeneration of the joint, the cartilage becomes rough and worn out, causing the joint halves to rub against each other, creating inflammation with pain and the formation of bone spurs. The fluid lubricant may become thin and the joint lining swollen and inflamed.

Osteoarthritis is also known as degenerative joint disease and affects up to 30 million Americans, mostly women and usually those over 45 or 50 years of age. All races in the U.S. appear to be equally affected. This article focuses on osteoarthritis of the spine, particularly on facet joint arthritis.

OA affects people of all races and both sexes. Most often, it occurs in patients age 40 and above. However, it can occur sooner if you have other risk factors (things that raise the risk of getting OA). Risk factors include –

  • Older age
  • Having family members with OA
  • Obesity
  • Previous traumatic Joint injury or repetitive use (overuse) of joints
  • Joint deformity such as unequal leg length, bowlegs or knocked knees

Causes

Genes – Various genetic traits can make a person more likely to develop OA. One possibility is a rare defect in the body’s production of collagen, the protein that makes up cartilage. This abnormality can cause osteoarthritis to occur as early as age 20. Other inherited traits may result in slight defects in the way the bones fit together so that cartilage wears away faster than usual. Researchers have found that a gene called FAAH, previously linked to increased pain sensitivity, is higher in people with knee OA than in people who don’t have the disease.

Weight – Being overweight puts additional pressure on hips and knees. Many years of carrying extra pounds can cause the cartilage that cushions joints to break down faster. Research has shown there is a link between being overweight and having an increased risk of osteoarthritis in the hands. These studies suggest that excess fat tissue produces inflammatory chemicals (cytokines) that can damage the joints.

Injury and overuse – Repetitive movements or injuries to joints (such as a fracture, surgery or ligament tears) can lead to osteoarthritis. Some athletes, for example, repeatedly damage joints, tendons and ligaments, which can speed cartilage breakdown. Certain careers that require standing for long periods of time, repetitive bending, heavy lifting or other movements can also make cartilage wear away more quickly. An imbalance or weakness of the muscles supporting a joint can also lead to altered movement and eventual cartilage breakdown in joints.

OthersSeveral other factors may contribute to osteoarthritis. These factors include bone and joint disorders like rheumatoid arthritis, certain metabolic disorders such as hemochromatosis, which causes the body to absorb too much iron, or acromegaly, which causes the body to make too much growth hormone.

Symptoms

The main symptoms of osteoarthritis are –

Pain – The pain tends to be worse when you move your joint or at the end of the day. If you have severe osteoarthritis, you may feel pain more often.

Stiffness – Your joints may feel stiff after rest, but this usually wears off as you get moving. A grating or grinding sensation (crepitus) – Your joint may creak or crunch as you move.

Swelling – The swelling may be hard (caused by osteophytes) or soft (caused by synovial thickening and extra fluid), and the muscles around your joint may look thin or wasted.

Not being able to use your joint normally – Your joint may not move as freely or as far as normal. Sometimes it may give way because your muscles have weakened or your joint has become less stable. Exercises to strengthen your muscles can help to prevent this.

Treatment

Pain and Anti-inflammatory Medications

Medicines for osteoarthritis are available as pills, syrups, creams or lotions, or they are injected into a joint. They include –

  • Analgesics – These are pain relievers and include acetaminophen, opioids (narcotics) and an atypical opioid called tramadol. They are available over-the-counter or by prescription.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) – These are the most commonly used drugs to ease inflammation and related pain. NSAIDs include aspirin, ibuprofen, naproxen and celecoxib. They are available over-the-counter or by prescription.
  • Corticosteroids – Corticosteroids are powerful anti-inflammatory medicines. They are taken by mouth or injected directly into a joint at a doctor’s office.
  • Hyaluronic acid – Hyaluronic acid occurs naturally in joint fluid, acting as a shock absorber and lubricant. However, the acid appears to break down in people with osteoarthritis. The injections are done in a doctor’s office.

 

Assistive Devices – Assistive devices can help with function and mobility. These include items, such as like scooters, canes, walkers, splints, shoe orthotics or helpful tools, such as jar openers, long-handled shoe horns or steering wheel grips. Many devices can be found at pharmacies and medical supply stores.

Surgery – Joint surgery can repair or replace severely damaged joints, especially hips or knees. A doctor will refer an eligible patient to an orthopaedic surgeon to perform the procedure.

Alternative Treatment

Glucosamine and chondroitin are the building blocks of cartilage. Cartilage is the substance that covers and protects joints. In people with OA, cartilage becomes damaged and degraded with use and time.

Omega 3 fatty acids EPA and DHA can be helpful for inflammatory arthritis including OS.

Vitamin E – Studies suggest that vitamin E can play a key role in treating OS by preventing damage to the cells of the bones and joints.

Selenium – Mild selenium deficiency is common in OS patients. It helps in slowing down the rapid progression of the disease.

SAM-e, pronounced “sammy”, is a naturally occurring compound produced from the amino acid methionine and adenosine triphosphate (ATP), a compound responsible for producing energy within the body. SAM-e is believed to improve joint mobility and relieve pain by raising levels of ATP and stimulating the production of cartilage within the joints. Getting sufficient folic acid in your diet (e.g. dark leafy green vegetables, fortified cereals) may help your body with natural SAM-e production.

Chondroitin sulfate, found naturally in cartilage, is believed to protect articular cartilage from deterioration caused by enzymes that destroy cartilage. It may also help to prevent the formation of microscopic blood clots leading to improvement of circulation to joint tissues.

Flax Seed Oil – Flax seed oil is an anti-inflammatory.

Avocado soybean unsaponifiables (ASUs) – A few preliminary studies suggest that this natural vegetable extract may help reduce the symptoms of OA and maybe even slow progression of the disease. More research is needed to know whether ASUs can actually stop joint damage.

Bromelain – This enzyme that comes from pineapples reduces inflammation. Bromelain increases the risk of bleeding, especially if you also take blood thinners, such as clopidogrel (Plavix), warfarin (Coumadin), or aspirin.

Turmeric – Turmeric is sometimes combined with bromelain, because it makes the effects of bromelain stronger. Turmeric can increase the risk of bleeding, especially for people who take blood thinning medications or NSAIDs.

Cat’s claw – It is useful for OA pain.

Devil’s claw – One study found that more than 50% of people with OA of the knee or hip or low back pain who took devil’s claw reported less pain and better mobility after 8 weeks. Devil’s claw may increase the risk of bleeding, especially if you also take blood thinners

Ginger – One study found that ginger extract blocked COX-2, a chemical in the body that causes pain. Ginger may increase the risk of bleeding, especially if you also take blood thinners such as clopidogrel (Plavix), warfarin (Coumadin), or aspirin.

Capsaicin – Capsaicin is the main component in hot chili peppers (also known as cayenne). Applied to the skin, it is believed to temporarily reduce amounts of “substance P,” a chemical that contributes to inflammation and pain in arthritis.

Acupuncture – Several controlled clinical trials suggest that the ancient Chinese practice of acupuncture works to treat OA pain. It may also help improve joint function. A few clinical studies have found that people with OA experience better pain relief and improvement in function from acupuncture than from NSAIDs, such as aspiroxicam.

Chiropractic – Although there is no evidence that chiropractic care can stop joint damage from OA, some studies indicate that spinal manipulation may:

  • Increase range of motion
  • Restore normal movement of the spine
  • Relax the muscles
  • Improve joint coordination
  • Reduce pain

Balneotherapy (Hydrotherapy or spa therapy)

Ice Massage, Transcutaneous Nerve Stimulation (TENS), and Electroacupuncture

Mechanical Aids (braces, splints)

Reference –

http://www.fbwgynplus.com.au/Portals/0/Documents/presentation.pdf

http://www.ohsu.edu/xd/health/services/women/services/gynecology-and-obstetrics/services/vulvar-health-program/upload/Lichen-Sclerosus.pdf

http://www.niams.nih.gov/health_info/Osteoarthritis/osteoarthritis_ff.asp

http://www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-Conditions/Osteoarthritis

http://www.healthline.com/health/osteoarthritis

http://www.arthritisresearchuk.org/arthritis-information/conditions/osteoarthritis.aspx

http://www.nhs.uk/conditions/osteoarthritis/Pages/Introduction.aspx

http://orthoinfo.aaos.org/topic.cfm?topic=a00227

http://www.spine-health.com/conditions/arthritis/osteoarthritis-spine

https://www.arthritiscare.org.uk/what-is-arthritis/types-of-arthritis/62-osteoarthritis

Posted in DEGENERATIVE
February 3, 2017

Mild Cognitive Impairment is a condition that falls somewhere between normal age-related memory loss and Alzheimer’s disease or a similar impairment. Not everyone with MCI develops dementia. And like dementia, MCI is not an illness, but a cluster of symptoms that describe changes in how the people think or process information. Memory problems are the most common indicators of MCI. A person with MCI may also experience difficulties with judgment, thinking and language beyond what one might expect with normal aging. For unknown reasons, MCI appears to affect men more than women.

Family members and friends who notice these problems might not express concern because the early symptoms can mimic normal, age-related changes. People suffering from MCI often recognize they are having trouble but are still able to carry on most of their usual activities and live independently.

The diagnosis of MCI relies on the fact that the individual is able to perform all their usual activities successfully, without more assistance from others than they previously needed.

Types

Amnestic vs. Non-Amnestic MCI – In amnestic MCI, memory is significantly impaired. Other cognitive functions are spared. Alzheimer’s disease is believed to cause amnestic MCI. In non-amnestic MCI, memory remains intact, but one (single domain) or more (multiple domain) other cognitive abilities (e.g., language, visual-spatial skills, executive functioning) are significantly impaired.

Single Domain vs. Multiple Domain MCI – In single domain MCI, only memory or one other domain of cognition is impaired. In multiple domain MCI, memory plus one or more other cognitive abilities are affected.

Causes

Current evidence indicates that MCI often, but not always, arises from a lesser degree of the same types of brain changes seen in Alzheimer’s disease or other forms of dementia. Some of these changes have been identified in autopsy studies of people with MCI. These changes include –

  • Abnormal clumps of beta-amyloid protein (plaques) and microscopic protein clumps characteristic of Alzheimer’s disease (tangles)
  • Lewy bodies, which are microscopic clumps of another protein associated with Parkinson’s disease, dementia with Lewy bodies and some cases of Alzheimer’s disease
  • Small strokes or reduced blood flow through brain blood vessels

Brain-imaging studies show that the following changes may be associated with MCI –

  • Shrinkage of the hippocampus, a brain region important for memory
  • Plaques throughout the brain
  • Enlargement of the brain’s fluid-filled spaces (ventricles)
  • Reduced use of glucose, the sugar that’s the primary source of energy for cells, in key brain regions

Brain imaging and medical research have shown that some people with MCI also have the plaques, neurofibrillary tangles and shrinkage in the memory center of the brain that is observed in those with Alzheimer’s disease (AD).

Other problems (which may be reversible) can contribute to memory loss, including: medication interactions (from both presciption and over-the-counter drugs), infections, vitamin shortages, malnutrition, thyroid and other metabolic disturbances, depression and drug/alcohol abuse.

It’s important to note that some people with MCI never get worse, and do not develop Alzheimer’s. Current studies find that approximately half of the people diagnosed with MCI will experience continued progression of the symptoms leading to a diagnosis of Alzheimer’s disease or a similar dementia.

Risk Factors

The causes of MCI may not be clear, but it appears some of the same risks for Alzheimer’s disease are risks for MCI. Those risks include:

  • Being 65 or older
  • Having a family history of MCI, Alzheimer’s disease, or another form of dementia
  • Having certain medical conditions, such as high blood pressure, diabetes, stroke, high cholesterol, or heart disease
  • Substance abuse, alcohol abuse
  • Lack of exercise

There are many factors that may influence cognitive decline –

  • Cerebrovascular events.
  • Hyperparathyroidism, hypoparathyroidism.
  • Hypoperfusion – eg, heart failure.
  • Head trauma, including recurrent trauma of having been a boxer.
  • Deficiencies of folate, vitamin B12 and vitamin B6 are associated with neurological and psychological dysfunction, and are potential factors for cognitive impairment and the development of dementia in the elderly
  • Open heart surgery with cardiopulmonary bypass.
  • Medication use, especially sedatives.
  • Hepatic impairment.
  • Sleep disorders – eg, obstructive sleep apnoea.
  • Psychological stress.
  • Drug or alcohol abuse.
  • Toxins, infections, metabolic (eg, hypoglycaemia) and structural causes.

Symptoms

The term MCI describes a set of symptoms, rather than a specific disease. A person with MCI has mild problems with one or more of the following –

  • Memory – for example, forgetting recent events or repeating the same question
  • reasoning, planning or problem-solving – for example, struggling with thinking things through
  • Attention – for example, being very easily distracted
  • Language – for example, taking much longer than usual to find the right word for something
  • Visual depth perception – for example, struggling to interpret an object in three dimensions, judge distances or navigate stairs.

These symptoms will have been noticed by the individual, or by those who know them. For a person with MCI, these changes may cause them to experience minor problems or need a little help with more demanding daily tasks (eg paying bills, managing medication, driving). However, MCI does not cause major problems with everyday living. If there is a significant impact on everyday activities, this may suggest dementia.

Most healthy people experience a gradual decline in mental abilities as part of ageing. In someone with MCI, however, the decline in mental abilities is greater than in normal ageing. For example, it’s common in normal ageing to have to pause to remember directions or to forget words occasionally, but it’s not normal to become lost in familiar places or to forget the names of close family members.

If the person with MCI has seen a doctor and taken tests of mental abilities, their problems will also be shown by a low test score or by falling test scores over time. This decline in mental abilities is often caused by an underlying illness.

Treatment

No medications are currently approved by the U.S. Food and Drug Administration (FDA) to treat mild cognitive impairment. Drugs approved to treat symptoms of Alzheimer’s disease have not shown any lasting benefit in delaying or preventing progression of MCI to dementia.

The following coping strategies may be helpful for those with MCI. Some studies suggest that these strategies may help slow decline in thinking skills, although more research is needed to confirm their effect.

  • Exercise on a regular basis to benefit the heart and blood vessels, including those that nourish the brain.
  • Control cardiovascular risk factors to protect the heart and blood vessels, including those that support brain function.
  • Participate in mentally stimulating and socially engaging activities, which may help sustain brain function.

Treating other conditions that can affect mental function

Other common conditions besides MCI can make people feel forgetful or less mentally sharp than usual. Treating these conditions can help improve your memory and overall mental function. Conditions that can affect memory include –

  • High blood pressure – People with MCI tend to be more likely to have problems with the blood vessels inside their brains. High blood pressure can worsen these problems and cause memory difficulties.
  • Depression – When people are depressed, they often feel forgetful and mentally “foggy.” Depression is common in people with MCI. Treating depression may help improve memory, while making it easier to cope with the changes in the life.
  • Sleep apnea– In this condition, the breathing repeatedly stops and starts while people are asleep, making it difficult to get a good night’s rest. Sleep apnea can make people feel excessively tired during the day, forgetful and unable to concentrate. Treatment can improve these symptoms and restore alertness.

Alternative Treatment

Curcumin is the compound that gives turmeric, the popular curry spice, its vibrant yellow color and has been shown to protect against neurodegeneration and mild cognitive impairment.

Resveratrol – Another anti-inflammatory powerhouse is resveratrol, the compound found in the skins of grapes and also found in Japanese knotweed. In addition to combatting inflammation and acting as a potent antioxidant, resveratrol has also been shown to increase blood flow to the brain, stimulate brain growth and synaptic connections, inhibit plaque formation in the brain, and reduce the damage caused by strokes, inflammation, and seizures.

Vitamins (particularly vitamin E), play a significant role in slowing the progression from mild cognitive impairment to Alzheimer’s disease.

Phospholipids are fats that make up the membranes of cells. Phosphatidylserine is a phospholipid that determines how well cell membranes communicate with each other. Low phosphatidylserine levels are associated with memory loss and depression. Studies have shown phosphatidylserine can significantly improve cognitive function, including in people with mild cognitive impairment and Alzheimer’s disease.

Magnesium-L-threonate – A deficiency in magnesium has been linked with memory impairment, slow recovery after a brain injury, and accelerated aging of brain cells. While magnesium citrate, glycinate, or malate are often recommended, researchers say they don’t cross the blood-brain barrier and therefore, are not effective. However, a newer, synthetic form of magnesium called magnesium-L-threonate has been shown to cross the blood-brain barrier, enhance memory and prevent impairment, thus lowering the risk of mild cognitive impairment.

 

Reference –

http://www.mldfoundation.org/

http://emedicine.medscape.com/article/951840-treatment

http://www.nejm.org/doi/full/10.1056/NEJM197109302851407

http://www.healthline.com/health/metachromatic-leukodystrophy#Outlook6

http://www.webmd.com/brain/leukodystrophy-metachromatic

http://www.brains4brain.eu/developing-treatment-options-for-metachromatic-leukodystrophy-mld/

http://www.cdc.gov/aging/pdf/cognitive_impairment/cogimp_poilicy_final.pdf

http://www.alzheimer.ca/en/About-dementia/Treatment-options

http://healthland.time.com/2013/04/15/mental-exercises-are-most-successful-at-preventing-cognitive-decline/

http://www.alz.org/dementia/mild-cognitive-impairment-mci.asp#treatment

Posted in DEGENERATIVE
February 3, 2017

Lewy Body Dimentia (LBD) is a progressive degenerative disease or syndrome of the brain. It shares symptoms,and sometimes overlaps, with several diseases, especially Alzheimer’s and Parkinson’s.

Lewy bodies were first described in the early 20th century by Dr Friedrich Lewy, who was studying the brains of people with Parkinson’s disease, a condition recognised by a combination of a shaking tremor, slowness of limb movements, and a shuffling walk.

Lewy bodies are, in fact, microscopic clumps of a protein called alpha-synuclein which may, under certain and as yet not understood circumstances, accumulate within nerve cells in the brain. When some critical brainstem and midbrain structures including the substantia nigra are involved, there is a loss of the neurotransmitter dopamine and Parkinson’s disease is the result.

LBD can take two forms: dementia with Lewy bodies or Parkinson’s disease dementia. The difference between them lies mainly in how the disease starts. In dementia with Lewy bodies, the person may have a memory disorder that looks like Alzheimer’s but later develop movement and other distinctive problems, such as hallucinations. In Parkinson’s disease dementia, the person may initially have a movement disorder that looks like Parkinson’s but later also develop dementia symptoms. Over time, though, both diagnoses will appear the same. Most people with LBD develop a similar spectrum of problems that include variations in attention and alertness, recurrent visual hallucinations, shuffling gait, tremors, and blank expression, along with various sleep disorders.

Other names for Lewy body dementia include –

  • Diffuse Lewy body disease
  • Cortical Lewy body disease
  • Lewy body disease
  • Senile Dementia of Lewy Type
  • Dementia with Lewy bodies
  • Lewy body variant of Alzheimer’s disease

While Lewy Body Dementia can bear a striking resemblance to Alzheimer’s disease or Parkinson’s disease, treatment can be very different, making early recognition of the signs and symptoms key to managing the condition.

 

 

Causes

Lewy body dementia is caused by degeneration or deterioration of brain tissue. Lewy body dementia may be genetic, but it is not always clear why someone develops Lewy body dementia. Lewy bodies in the brain affect substances called neurotransmitters. A neurotransmitter is a chemical that helps to transmit signals from one nerve cell to another.

One type of neurotransmitter is dopamine, which helps transmit signals that cause muscle movement. Lewy bodies interfere with the production of dopamine. A lack of dopamine causes movement problems, such as those seen in Parkinson disease.

Acetylcholine is another type of neurotransmitter found in the parts of the brain responsible for memory, thinking, and processing information. When Lewy bodies build up in these areas, they use up the acetylcholine, causing symptoms of dementia.

Risk Factors

DLB accounts for around 4 per cent of all recorded dementia, but there is good evidence that the condition is under-diagnosed. Based on studies of brain tissue after death, scientists think DLB may represent as much as 10 per cent of all dementia.

DLB appears to affect men and women about equally. As with Alzheimer’s disease and vascular dementia, DLB becomes more common over the age of 65. However, in certain cases people under 65 develop DLB.

Other Factos

  • Diseases and health conditions—Certain diseases and health conditions, particularly Parkinson’s disease and REM sleep behavior disorder, are linked to a higher risk of LBD.
  • Genetics—While having a family member with LBD may increase a person’s risk, LBD is not normally considered a genetic disease. A small percentage of families with dementia with Lewy bodies has a genetic association, such as a variant of the GBA gene, but in most cases, the cause is unknown. At this time, no genetic test can accurately predict whether someone will develop LBD. Future genetic research may reveal more information about causes and risk.
  • Lifestyle—No specific lifestyle factor has been proven to increase one’s risk for LBD. However, some studies suggest that a healthy lifestyle—including regular exercise, mental stimulation, and a healthy diet—might reduce the chance of developing age-associated dementias.

 

Symptoms

Lewy body dementia has 3 features that distinguish it from other forms of dementia –

  • Fluctuating effects on mental functioning, particularly alertness and attention, which may resemble delirium
  • Recurrent visual hallucinations
  • Parkinson-like movement symptoms, such as rigidity and lack of spontaneous movement

In Lewy body dementia, memory problems often occur later in the progression of the disease.

Lewy body dementia can be confused with other forms of dementia, but it also has unique features, such as hallucinations and delirium.

The primary sign of Lewy body dementia is a progressive decline in cognitive functions, such as memory, thinking, and problem-solving. The decline in cognitive function is enough to affect the ability to work and perform normal daily activities. Although memory may be affected, it isn’t usually as impaired as in someone with Alzheimer disease.

Lewy body dementia is generally diagnosed when at least 2 of the following features are also present with dementia –

  • Fluctuations in attention and alertness – These fluctuations may last for hours or days. Signs of these fluctuations include staring into space, lethargy, drowsiness, and disorganized speech. These fluctuations have been referred to as “pseudo delirium” because they are a lot like delirium.
  • Visual hallucinations – These hallucinations recur and are very detailed. While the hallucinations may be upsetting to someone observing them, they generally don’t bother the person having them. Many people with Lewy body dementia have detailed visual hallucinations.
  • Movement symptoms consistent with Parkinson disease (PD) – Such movement symptoms include slow movement, shuffling gait, rigidity, and falls. Tremors may also be present, but not as pronounced as in a person with PD with dementia.

Additional signs and symptoms seen in Lewy body dementia include –

  • Depression
  • Sleep disorder that affects REM sleep, causing vivid dreams with body movement
  • Dizziness, feeling lightheaded, fainting, or falling
  • Urinary incontinence

The symptoms of Lewy body dementia may resemble other conditions. Always see a health care provider for a diagnosis.

Complications

Lewy body dementia is progressive. Signs and symptoms worsen, causing –

  • Severe dementia
  • Death, on average about eight years after onset of the condition

Treatment

Medications

  • Cholinesterase inhibitors – These Alzheimer’s disease medications, such as rivastigmine (Exelon), work by increasing the levels of chemical messengers believed to be important for memory, thought and judgment (neurotransmitters) in the brain.
  • Parkinson’s disease medications – These medications — such as carbidopa-levodopa (Sinemet) can help reduce parkinsonian symptoms, such as rigid muscles and slow movement — in some people with Lewy body dementia. However, these medications may also cause increased confusion, hallucinations and delusions.
  • Antipsychotic medications – These medications, such as quetiapine (Seroquel), olanzapine (Zyprexa) and others, may somewhat improve delusions and hallucinations. However, some people with Lewy body dementia have a dangerous sensitivity to some of these drugs. Reactions, which are sometimes irreversible, can include severe parkinsonian symptoms and confusion.
  • Medications to treat symptoms – The doctor may prescribe medications to treat other symptoms associated with Lewy body dementia, such as sleep or movement problems.

Complementary Treatment

  • Physical therapists can help with movement problems through cardiovascular, strengthening, and flexibility exercises, as well as gait training and general physical fitness programs.
  • Speech therapists may help with low voice volume, voice projection, and swallowing difficulties.
  • Occupational therapists help identify ways to more easily carry out everyday activities, such as eating and bathing, to promote independence.
  • Music or expressive arts therapists may provide meaningful activities that can reduce anxiety and improve well-being.
  • Mental health counselors can help people with LBD and their families learn how to manage difficult emotions and behaviors and plan for the future.
  • Aromatherapy is largely used in cases of dementia. These effects from the smells influence the outcomes in treatments.
  • Recreational Therapy – These programs include things such as exercise and movement groups, pet therapy, cognitive fitness which includes things such as playing trivia and word type games.
  • Exercise – Exercising may increase your muscle strength, flexibility and balance. Exercise can also improve your well-being and reduce depression or anxiety.
  • Massage – Massage therapy can reduce muscle tension and promote relaxation. These services, however, are rarely covered by health insurance.
  • Acupuncture – During an acupuncture session, a trained practitioner inserts tiny needles into many specific points on the body, which may reduce the pain.
  • Tai chi – An ancient form of Chinese exercise, tai chi employs slow, flowing motions that may improve flexibility, balance and muscle strength. Tai chi may also prevent falls. Several forms of tai chi are tailored for people of any age or physical condition.
  • Yoga – In yoga, gentle stretching movements and poses may increase theflexibility and balance.
  • Alexander technique – This technique — which focuses on muscle posture, balance and thinking about how you use muscles — may reduce muscle tension and pain.
  • Meditation – In meditation, body quietly reflects and focuses on mind, on an idea or image. Meditation may reduce stress and pain and improve the sense of well-being.

Alternative Treatment

Chiropractic – Upper cervical chiropractic care has been noted in some cases to have success on the outcome of Parkinson’s disease. It had shown improvements in such areas of spinal pain, posture, improvement in fluid walking, facial expression and reduced tremors. Since treatments of this disease are used for those of Alzheimer’s and Parkinson’s it could help improve symptoms. However, there have been no scientific studies done on this concept.

Vitamin E – Vitamin E can fight damage in the brain caused by free radicals, and has been suggested to lower the risk of LBD. But taking vitamin E alone did not seem to have the same effect. More studies are needed to know whether there is any real benefit. Vitamin E supplements can increase the risk of bleeding, especially if you also take blood thinners, such as warfarin (Coumadin), clopidogrel (Plavix), or aspirin. Selenium is an antioxidant that works with vitamin E. It also helps to increase circulation and tissue oxygenation, thereby limiting damage to nerve cells.

Gamma-aminobutyric acid (GABA) is an amino acid that acts as a neurotransmitter. It helps both to strengthen and relax the nervous system.

Acidophilus and bifidobacteria are friendly bacteria that ensure a healthy gastrointestinal tract. Probiotics are especially helpful for preventing constipation, which is often a problem for people with Parkinson’s disease.

Alpha-lipoic acid is an antioxidant that also helps to “recharge” other antioxidants in the body.

Calcium and magnesium are imperative for maintaining a healthy nervous system.

Coenzyme Q10 is an oxygenating antioxidant that helps prevent free-radical damage and important for cell renewal.

Evening primrose oil and flaxseed oil contain valuable essential fatty acids (EFAs), which are often deficient in people with LBD.

Green-foods supplements supply chlorophyll and important trace minerals.

Marine alginate concentrate and N-acetylcysteine may help in the process of chelating (binding to) heavy metals in the body so that they can be excreted.

Nicotinamide adenine dinucleotide hydrogren (NADH) is an enzyme that helps to improve neurotransmitter function.

Phosphatidylserine is a type of lipid important for normal brain function and the effective transmission of nerve impulses. Low levels of phosphatidylserine are associated with LBD.

Soy Lecithin is rich in phosphatidylcholine. Choline is a vital building block for acetylcholine.

Pine-bark and grape-seed extracts fight free-radical damage and have anti-inflammatory properties. Many people consider Parkinson’s disease to be a consequence of degeneration of nerve cells due to free-radical damage.

The B vitamins are very important for brain and nerve function.

Vitamin C and the bioflavonoids are powerful antioxidants that fight free radicals.

Creatine – Some studies suggest that taking creatine, an amino acid that helps supply energy to muscles, may help slow progression of Parkinson’s among people who are in the early stages, and who do not need medication to control symptoms.

 

 

Reference –

http://www.mayoclinic.org/diseases-conditions/lewy-body-dementia/basics/causes/con-20025038

https://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=113

http://www.hopkinsmedicine.org/healthlibrary/conditions/nervous_system_disorders/dementia_with_lewy_bodies_dlb_134,76/

http://www.medicalnewstoday.com/articles/302230.php

http://memory.ucsf.edu/education/diseases/dlb

http://www.nhs.uk/Conditions/dementia-with-lewy-bodies/Pages/Introduction.aspx

http://health.usnews.com/health-news/patient-advice/articles/2015/09/22/living-with-lewy-body-dementia

http://www.independent.co.uk/life-style/health-and-families/features/robin-williams-death-lewy-bodies-dementia-causes-symptoms-parkinsons-disease-brain-alzheimers-a6726801.html

https://www.caregiver.org/dementia-lewy-bodies

http://www.alzheimer.ca/en/About-dementia/Dementias/Lewy-Body-Dementia

https://fightdementia.org.au/about-dementia/types-of-dementia/lewy-body-disease

http://www.alz.org/dementia/dementia-with-lewy-bodies-symptoms.asp

http://www.naturalhealthadvisory.com/daily/cognitive-decline-and-memory-issues/what-is-lewy-body-dementia/

http://www.acupuncturetoday.com/mpacms/at/article.php?id=28184

Posted in DEGENERATIVE
February 3, 2017

Krabbe disease is also known by many other names, these include Globoid cell leukodystrophy, Galactosylcerebrosidase deficiency and Galactosylceramidase deficiency. It is a very rare condition that is caused by a genetic defect that affects the nervous system.

Those affected by Krabbe typically appear healthy until onset, or when an individual experiences symptoms, of the disease. Onset can vary from the first few weeks or months of life (Early Infantile Onset) into adulthood (Adult Onset).

Those who suffer from Krabbe Disease have a deficiency of an important enzyme called Galactosylceramidase (GALC).

Krabbe Disease is both a Leukodystrophy and Lysosomal Storage Disorder (LSD). Leukodystrophies are characterized as degenerative diseases of the white matter of the brain. LSDs occur when a part of the cell, called the lysosome, does not function properly. In a healthy individual, enzymes break down material in the lysosomes, however, if the body does not produce enough of a specific enzyme (ex: GALC), material builds up and becomes toxic.

Krabbe disease is divided into four subtypes based on when the disease begins:

  • Type 1 – Infantile: begins at age 3 – 6 months
  • Type 2 – Late infantile: begins at age 6 months – 3 years
  • Type 3 – Juvenile: begins at age 3 – 8 years
  • Type 4 – Adult onset: begins any time after 8 years of age

 

Krabbe Disease affects both the central and peripheral nervous systems, which are responsible for all of the body’s voluntary and involuntary movements. The central nervous system is made up of the nerves within the brain and spinal cord and is the primary control center of the body. The peripheral nervous system’s primary function is to carry information from the brain and spinal cord throughout the body to the limbs and organs.

Causes

Krabbe disease is an autosomal recessive disease caused by mutations in the GALC gene. An individual who inherits one copy of a GALC mutation is a “carrier” and is not expected to have related health problems. An individual who inherits two disease-causing mutations in this gene, one from each parent, is expected to be affected with Krabbe disease.

 

If both members of a couple are carriers, the risk for an affected child is 25% in each pregnancy; therefore, it is especially important that the reproductive partner of a carrier be offered testing.

A defect in the GALC gene causes Krabbe disease. Persons with this gene defect do not make enough of a substance called galactocerebroside beta-galactosidase (galactosylceramidase). The body needs this substance to make myelin, the material that surrounds and protects nerve fibers. Without it, myelin breaks down, brain cells die, and nerves in the brain and other body areas do not work properly.

This condition is very rare. It is most common among people of Scandinavian descent.

Risk Factors

Krabbe disease can occur in individuals of all races and ethnicities, but it occurs most commonly among Muslim Arabs and Druze communities in Israel. The incidence is estimated to be 1 in 100,000 in the United States and Europe, with a calculated carrier frequency of 1 in 158.3

Having a relative who is a carrier or who is affected can increase an individual’s risk of being a carrier. Consultation with a genetics health professional may be helpful in determining carrier risk and appropriate testing.

Symptoms

The majority of cases of Krabbe Disease appear within the first year of life. The patients rapidly regress to a condition with little to no brain function, and generally die by age 2, though some have lived longer. Death generally occurs as a result of a respiratory infection or brain fever. Symptoms that might be encountered in the infantile form of Krabbe Disease include –

  • Developmental delay
  • Seizures
  • Limb stiffness
  • Optic atrophy: wasting of a muscle of the eye, resulting in vision diffculties
  • Neurosensoral deafness
  • Extreme irritability
  • Spasticity – presence of spasms
  • Ataxia – loss of the ability to control muscular movement
  • Progressive psychomotor decline: progressive decline in the coordination of movement

Although the majority of Krabbe Disease patients show symptoms within the first year of life, there have been cases diagnosed at all ages, through late adulthood. In general, the earlier the diagnosis, the more rapid the progression of the disease. Those who first show symptoms at ages 2-14 will regress and become severely incapacitated, and generally die 2-7 years following diagnosis. Some patients who have been diagnosed in the adolescent and adult years have symptoms that remain confined to weakness without any intellectual deterioration, while others may become bedridden and deteriorate both mentally and physically.

Complications

This disease damages the central nervous system. It can cause –

  • Blindness
  • Deafness
  • Severe problems with muscle tone

The disease is usually life-threatening.

Treatment

Bone marrow transplantation and umbilical cord blood stem cell transplant are the ecognized treatments and have been found to preserve cognitive functions in some cases.

Anticonvulsant medications to manage seizures

Drugs to ease muscle spasticity and irritability

Physical therapy to minimize deterioration of muscle tone

Nutritional support, such as the use of a tube to deliver fluids and nutrients directly into the stomach (gastric tube)

 

Reference –

http://www.perkinelmer.com/industries/healthcare/newborntestingservices/clinician-information/krabbe-disease.xhtml

http://www.babysfirsttest.org/newborn-screening/conditions/krabbe

http://ulf.org/krabbe-disease

http://www.tloaf.org/krabbe.html

http://www.omim.org/entry/245200

https://rarediseases.info.nih.gov/gard/6844/krabbe-disease/resources/1

https://umm.edu/health/medical/ency/articles/krabbe-disease

http://www.wadsworth.org/newborn-screening/krabbe-disease

http://www.wadsworth.org/newborn-screening/krabbe-disease

Posted in DEGENERATIVE
February 3, 2017

Definition and Symptoms:

Dementia is a collection of symptoms that effects one’s memory, thinking, and social skills to the extent in which daily functioning is interrupted. Dementia is more severe than the normal aging process which can slow one’s memory and cognition. Symptoms include memory loss, difficulty with communication such as finding words, difficulty completing complex tasks, difficulty with planning and organizing, difficulty with coordination and motor function, disorientation, personality changes, and inability to reason, paranoia, agitation, and hallucinations.

Causes and Complications:

Dementia involves damage to the nerve cells of the brain. Because different areas of the brain can be involved, patients may exhibit different signs and symptoms based on the area of the brain affected. Some dementia can be caused by reaction to medication or infection and are reversible with treatment. Other forms of dementia are progressive and worsen over time.

Preparing for your appointment:

Prior to your appointment with a doctor at the Center for Occupational and Environmental Medicine it is important for you to review the new patient information sent to you by our new patient coordinator. This packet includes specific information about preparing for you visit as well as an in depth medical history form. Please take some time to fill out the form to the best of your ability. This form will take some time, and may require reaching out to family members for additional medical history. Please also complete all registration forms prior to arriving at the center for your appointment. If you have completed any recent blood work or laboratory tests please bring copies with you to your appointment. Your clinician and doctor will review this information as part of your medical history. Plan on being with us at the center for a full day on the first day of your appointment. Some of your recommendations may include allergy testing, and this process will take some time.

Diagnostic tools:

  • Heavy Metal Hair Analysis
  • Blood work:

CBC, CMP, RBC Mg, homocysteine, Vitamin D 3 level, serum B12, MMA level, Cardiac CRP, fasting insulin, lipid panel, HgB AIC

  • Optimal Nutritional Evaluation
  • Toxic Urine Elements
  • Comprehensive Digestive Stool Analysis
  • Chlorinated Pesticide Panel or Toxic Effect CORE

 

Treatment:

  • Anti-inflammatory diet
  • Yeast Eradication- Diflucan and Nystatin (?)
  • Train your brain using cross words, learning a musical instrument or new language, or site such as luminosity.com
  • Reduce Stress
  • Increase physical exercise
  • Optimize sleep

 

Products and Services:

Nutritional Supplements:

  • Vitamin D 3 5000 IU daily
  • Vitamin K 2 (MK7)
  • PQQ Caps
  • Ubiquinol
  • CDP Choline
  • Carlson’s Fish Oil
  • Annatto Tocotrieols
  • Thera B
  • Vitaspectrum
  • Melatonin
  • N-Acetyl-Cysteine
  • Phosphatidyl Serine
  • Chlorophyllin
  • Liposomal Glutathione
  • Ultra Hepatrope
  • Therbiotic Complete
  • Think Clear

 

Allergy Extracts/Signal Therapy:

  • Neutralize to favorite foods and Mediators
  • Memory Drops
  • NGF

IV Therapy:

  • Myers Cocktail (double B12)
Posted in DEGENERATIVE
February 3, 2017

Corticobasal degeneration (CBD) is a rare and gradually progressive neurodegenerative disorder where brain cells become damaged over time and certain sections of the brain start to shrink. It is a form of atypical parkinsonism (a parkinsonism-plus syndrome), which means that it shares some features with Parkinson’s disease such as stiffness (rigidity), tremor, slowness of movement (bradykinesia) and instability. Several regions of the brain degenerate in CBD. The cortex, or outer layer of the brain, is severely affected, especially the fronto-parietal regions, located near the center-top of the head. Other, deeper brain regions are also affected, including parts of the basal ganglia, hence the name corticobasal degeneration.

The disease, also known as corticobasal ganglionic degeneration, leads to the loss of brain tissue in the cortex, or outer layer of the brain, especially the area in the upper, front section of the brain. The brain tissue of patients with CBD show cell changes that also appear in patients with two other disorders — frontotemporal dementia and progressive supranuclear palsy. These changes involve a brain protein called tau and may provide researchers with some initial clues regarding the causes of corticobasal degeneration. Currently, there are no known causes, such as toxins or infections.

As the cortex is responsible for higher level cognitive functioning like thinking and understanding, and the basal ganglia helps people to perform smooth movements, CBD may affect both the physical and cognitive functioning of people with the disease.

CBD is rare, affecting an estimated 2000-3000 people in United States, of whom only 500-750 are diagnosed. It usually progresses slowly over the course of 6 to 8 years. Death is generally caused by pneumonia or other complications of severe debility such as sepsis or pulmonary embolism.

Causes

CBD occurs when brain cells in certain parts of the brain are damaged as a result of a build-up of a protein called tau. The surface of the brain (cortex) is affected, as well as a deep part of the brain called the basal ganglia. Tau occurs naturally in the brain and is usually broken down before it reaches high levels. In people with CBD, it isn’t broken down properly and forms harmful clumps in brain cells.

CBD has been linked to changes in certain genes, but these genetic links are weak and the risk to other family members is very low.

However, corticobasal degeneration does not run in families, meaning that environmental factors such as exposure to certain infections or toxins may play a role. All in all, it is not known why some people develop corticobasal degeneration while others don’t.

Risk Factors

  • Race – No racial predilection is known.
  • Sex – In several studies, CBDG was reported to be more common in women.
  • Age – Typically, CBGD presents between the ages of 50 and 80 years.

Symptoms

Symptoms of CBD usually begin after age 60. The initial symptoms of CBD are often stiffness, shakiness, jerkiness, slowness, and clumsiness, in either the upper or lower extremities. Other initial symptoms may include dysphasia (difficulty with speech generation), dysarthria (difficulty with articulation), difficulty controlling the muscles of the face and mouth, or walking and balance difficulties. Symptoms usually begin on one side of the body, and spread gradually to the other. Some patients (probably more than commonly recognized in the past) may have memory or behavioral problems as the earliest or presenting symptoms.

Symptoms begin, on average, when an individual is in the early 60’s, but may start as early as in the 40’s. These include:

  • Stiffness, shakiness, jerkiness, slowness, and clumsiness in either the upper or lower extremities
  • Difficulty with speech generation (dysphasia)
  • Difficulty with articulation (aphasia)
  • Difficulty controlling the muscles of the face and mouth (dysarthria)
  • Walking and balance difficulty
  • Asymmetric onset of symptoms (occuring on one side of the body first then gradually moving to the other side)

 

  • Memory or behavior problems

Symptoms of advanced CBD include –

  • Parkinsonism (rigidity, slow movements, postural instability)
  • Tremor
  • Myoclonus (sudden, brief jerky movements)
  • Dystonia, including blepharospasm
  • Speech difficulty
  • Mild-to-moderate cognitive impairment (memory loss, difficulty planning or executing unrehearsed movements, dementia)
  • Sensory loss
  • “Alien hand/limb” phenomenon (difficulty controlling the movements of a limb, which seems to undertake movements on its own, sometimes combined with a feeling that the limb is not one’s own)

Corticobasal degeneration usually progresses slowly over the course of 6–8 years. Movement symptoms tend to progress slowly from one side of the body to the other or from leg to arm on the same side of the body.

Treatment

  • Physical therapy – Physical therapy aims to help an individual regain strength, flexibility, coordination, and balance of movement through exercise and practice. Physical therapy also supports adaptation to changing ability levels, such as teaching a person how to get around using a wheelchair.
  • Occupational therapy – Occupational therapy focuses on supporting and adapting an individual’s ability to complete “activities of daily living” (ADLs), such as dressing, feeding, bathing, grooming, toileting, doing chores, and completing errands.
  • Speech-language and swallow therapy – A speech-language therapist is a professional who works with both communication disorders and swallowing impairment (dysphagia). Speech-language and swallowing therapy focus on supporting speech, language, cognitive-linguistic, communicative, reading, writing, and swallowing abilities, and providing adaptive strategies as needed.
  • Parkinson’s medications – Medications typically used for Parkinson’s disease, such as levodopa, may help to relieve some of the physical symptoms of corticobasal degeneration in some people.
  • Alzheimer’s medications – Medications aimed at relieving some of the symptoms of Alzheimer’s disease, such as memantine, may help some individuals see improvement in cognitive or physical symptoms.
  • Muscle relaxants / seizure medications – Stiffness and spasms may be partly relieved in some people with the use of muscle relaxants, such as baclofen, or seizure medications, such as clonazepam.
  • Antidepressants – Individuals who experience depression or anxiety may benefit from antidepressant medications.

Alternative Treatment

Reference –

https://stanfordhealthcare.org/medical-conditions/brain-and-nerves/corticobasal-degeneration.html

http://www.ajnr.org/content/30/10/1884.full

http://healthcare.utah.edu/neurosciences/neurology/movement-disorders/corticobasal-degeneration.php

https://neurosciences.ucsd.edu/centers/movement-disorders/movement-disorders/Pages/cbd.aspx

https://www.patientslikeme.com/conditions/1366-corticobasal-degeneration

http://www.thelancet.com/pdfs/journals/laneur/PIIS1474442204009366.pdf

http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Lng=GB&Expert=278

Posted in DEGENERATIVE
February 3, 2017

Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) is a rare neurological disorder characterized by gradually increasing sensory loss and weakness associated with loss of reflexes. It is an inflammatory disease of the peripheral nerves wherein the body’s immune system attacks its own nerves.

During infancy the body’s immune system learns to differentiate between self and non-self, i.e. normally the body learns not to attack itself and knows to attack any foreign objects like viruses or bacteria that has entered and needs to be destroyed. In an autoimmune disease, the recognition of self and non self is lost, and body attacks itself. In CIPD, myelin is attacked, resulting in demyelination. Myelin is an important part of the peripheral nervous system, which wraps around the nerve axon (the long, wire-like part of a nerve cell) just like insulation around an electrical wire. The nerves extend from the spinal cord to the rest of the body, stimulating muscle contraction and transmitting sensory information back to the nervous system from receptors in the skin and joints. This insulation (myelin) allows electrical impulses to efficiently travel along the nerve axon. When myelin is damaged or removed, these electrical impulses are slowed or lost, and messages transmitted from the brain are disrupted and may never make it to their final destination. If this occurs acutely then the illness is called Guillain-Barre and if it becomes chronic then it is called Chronic Inflammatory Demyelinating Polyneuropathy or CIDP.

CIDP is usually classified by these three types:

  • Progressive :The disease continues to worsen over time
  • Recurrent : Episodes of symptoms that stop and start
  • Monophasic : One bout of the disease that lasts one to three years and doesn’t recur

CIPD is a rare disorder that may affect any age group and the onset of the disorder may begin during any decade of life. It affects males twice as often as females and the average onset age is 50 years. At any one time, between 5,000 and 10,000 people in the United States are affected by it. CIDP, by definition has ongoing symptoms for over 8 weeks and usually does not improve unless ongoing treatment is given.

Causes

Chronic inflammatory poly neuropathy is one cause of damage to nerves outside the brain or spinal cord (peripheral neuropathy). Polyneuropathy means several nerves are involved. It usually affects both sides of the body equally.

 

Chronic inflammatory demyelinating polyneuropathy (CIDP) is the most common chronic neuropathy caused by an abnormal immune response. CIDP occurs when the immune system attacks the myelin cover of the nerves. The cause of chronic inflammatory polyneuropathy is an abnormal immune response. The specific triggers vary. In many cases, the cause cannot be identified.

It may occur with other conditions, such as:

  • Idiopathic Neuropathy

Sometimes CIDP seems to happen for no particular reason. Doctors call this disorder “idiopathic”, which means “of unknown cause.” Typically, idiopathic CIDP occurs in people over 60 years old; progresses slowly (or doesn’t progress at all after the initial onset); and it can be very disruptive to someone’s normal life and lifestyle.

 

  • Diabetes

Diabetic neuropathy, or nerve damage caused by diabetes, is one of the most common known causes of neuropathy. It is one of many complications associated with diabetes, with nearly 60 percent of diabetics having some form of nerve damage. It is a progressive disease that can involve loss of sensation, as well as pain and weakness, in the feet and sometimes in the hands.

 

  • Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) involves chronic inflammation of all or part of your digestive tract.

 

  • Toxic Chemicals

Toxins, poisons and chemicals can cause peripheral neuropathy, which may cause CIDP. This can happen through drug or chemical abuse or through exposure to industrial chemicals in the workplace or in the environment. Common causes include: exposure to lead, mercury, arsenic and thalium.

 

It may occur with following diseases as well: HIV, Chronic hepatitis, Systemic lupus erythematosus, Lymphoma, Paraneoplastic syndrome, Thyrotoxicosis, Side effects of medicines to treat cancer or HIV, Vasculitis.

 

Symptoms

 

The symptoms of Chronic Inflammatory Demyelinating Polyneuropathy include numbness, tingling, burning and weakness, generally occurring in the feet first and they gradually ascend to involve other parts of the body. One of the first signs that could develop is a foot drop, where patients develop weakness in their ankles and as a result tend to trip over their feet, or they could develop numbness and tingling in the feet and toes which gradually spreads to the other parts of the body.

 

The symptoms of CIDP are as follows:

  • Loss of strength and sensation on the limbs
  • Muscle weakness
  • Numbness, pins and needles sensation
  • Poor Balance on Body
  • Trembling of the hands when reaching anything

 

At times, related physical symptoms also include:

  • Signs of cranial nerve (CN) involvement
  • Gait abnormalities
  • Motor deficits
  • Diminished or absent deep tendon reflexes
  • Sensory deficits
  • Impaired coordination

Treatment

Improvement in functional status and maintenance of long term remission are the main goals of treatment of CIDP. Early intervention is necessary to avoid the permanent weakness, sensory loss, pain and imbalance that are commonly caused by axonal loss. Corticosteroids, IVIg and plasmapherisis are the three conventional therapies that remain as a standard treatment for CIDP.

  • Corticosteroids – Similar to naturally occurring anti-inflammatory hormones made by the body, and can be used as an initial treatment. Corticosteroids often improve strength, are conveniently taken by mouth, and are inexpensive. Side effects however can limit long-term use. These include osteoporosis (thinning of bones), cataracts, diabetes, hypertension (raised blood pressure), obesity and myopathy (muscle weakness).
  • Immunosuppressive drugs – Clinical experience suggests that immunosuppressive drugs help. These include azathioprine, cyclophosphamide and cyclosporin. Azathioprine is the most widely used in the treatment of CIDP. The use of these drugs carries the theoretical side effect of increased risk of developing cancer, but in practice this increased risk is very small.
  • Intravenous Immune Globulins (IVIG) – The only drug that has FDA, Canadian, and European approval for treatment of CIDP. IVIG contains naturally occurring antibodies obtained from healthy volunteers. IVIG is given through a vein over the course of several hours. Newer preparations of higher concentrations that can be given under the skin (subcutaneous) are currently being tested in controlled trials in CIDP patients. The most common side effects are headache, nausea, chills, flushing, myalgia, hypotension, hypertension, chest discomfort, and fatigue. Infrequent adverse reactions include thromboembolic events, skin reactions, aseptic meningitis, renal tubular necrosis, and severe anaphylactic reaction.
  • Plasma Exchange (PE) – A process by which some of the patient’s blood is removed and the blood cells returned without the liquid plasma portion of the patient’s blood. It may work by removing harmful antibodies contained in the plasma.
  • Physiotherapy – Physiotherapy has an important role to play in the assessment and management of CIDP. It helps to maximize a patient’s physical potential, particularly where weakness is the main problem.

The aims of physiotherapy are to –

  • maximise muscle strength and minimise muscle wastage by exercise using strengthening techniques;
  • minimise the development of contractures (or stiffness) around joints; a physiotherapist can advise on passive stretching techniques to help maintain full range movement at joints;
  • facilitate mobility and function; sometimes, if muscles are very weak, function can be improved by the use of splints and
  • provide a physical assessment which may help in planning future management.

Alternative Treatment

Alternative medicine involves treatment of underlying conditions can help control neuropathy pain. Alternative medicine may also play a role in reducing the symptoms of peripheral neuropathy.

Acids

Studies suggest that supplementing essential acids called ALA (alpha-Lipoic acid) and GLA (gamma linolenic acid) and omega-3 fatty acids may all have a beneficial effect on diabetic peripheral neuropathy, which may be an underlying cause. Over the course of long-term treatment a reduction in symptoms and better blood flow is seen in the patients.

L-Carnitine

L-carnitine is a substance that the body makes and stores in various organs, including the liver and the brain. It helps to regain regular sensation in their limbs when they increase their consumption of a type of carnitine called acetyl-L-carnitine. Red meat, peanut butter and dairy products are good dietary sources of the nutrient, but supplements are also widely available at health food stores and pharmacies.

Vitamins and Minerals

Studies show that vitamin deficiencies may result in peripheral neuropathy conditions in some people. Replenishing vitamins B1, B12 and E may lead to a decrease in symptoms. Recommended dosages are 300mg daily of vitamin E.

Traditional Chinese Medicine

Acupuncture, a form of traditional Chinese medicine, may be an effective way to manage CIPD. Some herbal supplement taken orally may reduce the pain that is consistent with neuropathy. Topical creams containing capsaicin, an anti-inflammatory substance found in chili peppers, can reduce the burning sensation in some people who experience this painful symptom. Tai chi and yoga help align the body and mind, encourage relaxation and may distract people from the pain, even if the measure is temporary.

Herbal Supplements

Several herbal remedies may be alternatives to explore when treating peripheral neuropathy. Some herbal supplement taken orally may reduce the pain that is consistent with neuropathy. Topical creams containing capsaicin, an anti-inflammatory substance found in chili peppers, can reduce the burning sensation in some people who experience this painful symptom.

Treatment does not only mean doctors and physicians making single efforts for the patient, the patient should also be actively interested in getting cured. It always is a team effort…..

Posted in DEGENERATIVE