Tag Archives: Paresthesia

Zanthoxylum

Botanical Name :Zanthoxylum spp
Family: Rutaceae
Subfamily: Toddalioideae
Genus: Zanthoxylum
Kingdom: Plantae
Order: Sapindales

Common NamesPrickly Ash , Szechuan pepper, chuan jiao, Tooth Ache Tree, yellow wood

Habitat:Zanthoxylum is native to northern and central Illinois.It occurs in upland woodlands, bottomland woodlands, savannas, wooded ravines, thinly wooded bluffs, edges of shady seeps, stream banks in wooded areas, thickets, pastures, and fence rows. It probably benefits from occasional wildfires.

Description:
Zanthoxylum  is a shrub is 4-25′ tall, branching abundantly. The bark of trunk and larger branches is gray to brown and fairly smooth, although on old large shrubs it can become shallowly furrowed with a wrinkled appearance. Twigs are brown and glabrous, while young shoots are light green and nearly glabrous to pubescent. Pairs of stout prickles up to 1/3″ long are scattered along the branches, twigs and shoots; these spines are somewhat flattened and curved. Alternate compound leaves about 6-12″ long develop along the twigs and young shoots; they are odd-pinnate with 5-11 leaflets. Individual leaflets are 1½-3¼” long and ½-1½” across; they are lanceolate-oblong to ovate-oblong with margins that are smooth to crenulate (fine rounded teeth). The upper surface of mature leaflets is medium green, minutely glandular, and glabrous, while the lower surface is pale green and short-pubescent to nearly glabrous; in the latter case, fine hairs are restricted to the major veins. Newly emerged leaflets are more hairy than mature leaflets. The lateral leaflets are sessile or nearly so, while the terminal leaflets have slender petiolules (basal stalklets) that are less than ½” long. The light green petioles (basal stalks) and rachises of the compound leaves are hairy while young, but become more glabrous with age; they have scattered small prickles along their undersides.

click to see the pictures……..>…(01).....(1)..…...(2)…….(3)..…..(4)..……...(5)

Prickly Ash is almost always dioecious, producing male (staminate) and female (pistillate) flowers on separate shrubs. These flowers are arranged in small axillary clusters (cymes) along the branches of the preceding year. Individual male flowers are a little less than ¼” across, consisting of 4-5 erect petals and 4-5 stamens; there is no calyx. The petals of male flowers are yellowish green to orange and oblong in shape. Individual female flowers are about ¼” across, consisting of 4-5 erect petals and 2-5 separate pistils; there is no calyx. The petals of female flowers are also yellowish green to orange and oblong in shape. The ovaries of the pistils are glossy green and ovoid in shape; their elongated styles tend to converge at their tips. The blooming period occurs during mid- to late spring before the leaves develop. Afterwards, the female flowers are replaced by berry-like follicles (fruits that open along one-side) about 1/3″ long that are ovoid-globoid in shape with a pitted surface. As the follicles mature, they change from green to red to brown, eventually splitting open to expose shiny black seeds with oily surfaces. Each follicle contains 1-2 seeds. Both the crushed foliage and fruits are highly aromatic, somewhat resembling the fragrance of lemon peels. The root system produces underground runners, from which clonal offsets are produced. This shrub often forms clonal colonies of varying size.

Cultivation: The preference is full or partial sun and moist to dry-mesic conditions. Different types of soil are tolerated, including those that contain loam, clay-loam, and rocky material. This shrub can adapt to light shade, but it may fail to produce flowers and fruit. It has relatively few problems with pests and disease organisms

Medicinal uses:
Paresthesia is the mouth-numbing effect believed to be caused by hydroxyl-alpha-sanshool, an alkylamide found in Zanthoxylum spp.  Anyone who has bitten into a Sichuan pepper can attest to the unique sensation of mild electric shock or “pins and needles” in their mouth.  Researchers have likened this experience to that of “touching their tongue to the terminals of a 9-volt battery”, which is quite different from the burning pain of chilli peppers or the punch of fresh wasabi.

The numbing and analgesic effects of Zanthoxylum have been exploited for centuries as a natural remedy to alleviate acute and chronic pain.  In Nigeria, the roots are used as a chewing stick to give a warm and numbing effect.  This use is believed to be beneficial to the elderly and to those with sore gums and other oral disease conditions.  Zanthoxylum americanum is commonly known as toothache tree in North America and can be found in the eastern US as well as Ontario and Quebec in Canada.

Zanthoxylum spp. have traditionally been administered for a variety of maladies in addition to oral diseases.  In India, the leaf is used against fever, dyspepsia and bronchitis.  In Manipur, India, the seed oil is applied against baldness and bark powder is used to treat toothache (Singh and Singh 2004).  In a 2008 report titled “Indigenous Vegetables of India with a Potential for Improving Livelihoods,” ML Chadha from the ARVDC Regional Center for South Asia reports that Z. hamiltonianum is used as both a vegetable and a remedy; dried, tender leaves are eaten as a vegetable and powdered fruits are consumed to increase the appetite.  The young stems are employed as a toothbrush in cases of toothache and bleeding gums, whereas the roots and bark are used to cure malaria.  Though generally eaten as a vegetable, the leaves of Z. rhetsa are also consumed to kill tapeworms and reduce infection (Chadha 2008).

Scientific studies are validating the traditional medical role of various Zanthoxylum products.  Research has demonstrated the potential of Z. rhetsa leaf extract as a de-worming remedy; it has been found to have a pronounced effect against larval eggs, comparable to a commercial drug (Yadav and Tangpu  2009).  Bark extract from Z. rhetsa has been shown to lessen abdominal contractions and diarrhoea in mice (Rahman 2002).  Other potential pharmaceutical applications include cancer treatment and anti-oxidant, anti-coagulant and anti-bacterial agents.

At the industrial level, Z. armatum has been shown to contain high amounts of linalool (Jain et al. 2001), a compound used commercially as a precursor to vitamin E production and also in soaps, detergents and insecticides.  Clearly, Zanthoxylum spp. have potential beyond traditional uses as spices and folk medicine.

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider

Resources:
http://www.illinoiswildflowers.info/trees/plants/prickly_ash.html
http://en.wikipedia.org/wiki/Zanthoxylum
http://www.anniesremedy.com/herb_detail403.php
http://archive.constantcontact.com/fs035/1102506082274/archive/1104323477745.html

Enhanced by Zemanta

Neuropathy

Definition:
Neuropathy is a general term that refers to diseases or malfunctions of the nerves. Any nerves at any location in the body can be damaged from injury or disease. Neuropathy is often classified according to the types or location of nerves that are affected. It is a disease caused by changes in the nerve cells. These changes may be age related. The degeneration is accelerated and aggravated if the patient suffers from diabetes, hypertension or has an abnormal lipid profile. Neuropathy can affect all three nervous systems — central, peripheral and autonomous.

If the central nervous system is affected, memory and cognitive skills decline. Forgetfulness becomes an accepted way of life. Peripheral neuropathy produces the most obvious, incapacitating, and distressing symptoms.

In some, the affected nerves may produce symptoms that are symmetrical (occurring in both limbs) and appear first in the furthest extremity. There may be paraesthesia (tingling, burning or numb sensation), hyperalgesia (abnormally acute pain sensation to innocuous stimuli) or deep aching. The symptoms tend to get worse at night and interfere with sleep.

Neuropathy can also be classified according to the disease causing it. (For example, neuropathy from the effects of diabetes is called diabetic neuropathy.)

You may click to see:
1.Slide show: How your brain works   :
2.Dementia Slideshow Pictures  :
3.Alzheimer’s Disease Slideshow Pictures  :
4.Brain Foods Slideshow Pictures 

Types of Neuropathy::

Peripheral neuropathy: Peripheral neuropathy is when the nerve problem affects the nerves outside of the brain and spinal cord. These nerves are part of the peripheral nervous system. Accordingly, peripheral neuropathy is neuropathy that affects the nerves of the extremities- the toes, feet, legs, fingers, hands, and arms. The term proximal neuropathy has been used to refer to nerve damage that specifically causes pain in the thighs, hips, or buttocks.

Cranial neuropathy: Cranial neuropathy occurs when any of the twelve cranial nerves (nerves that exit from the brain directly) are damaged. Two specific types of cranial neuropathy are optic neuropathy and auditory neuropathy. Optic neuropathy refers to damage or disease of the optic nerve that transmits visual signals from the retina of the eye to the brain. Auditory neuropathy involves the nerve that carries signals from the inner ear to the brain and is responsible for hearing.

Autonomic neuropathy: Autonomic neuropathy is damage to the nerves of the involuntary nervous system, the nerves that control the heart and circulation (including blood pressure), digestion, bowel and bladder function, the sexual response, and perspiration. Nerves in other organs may also be affected.

Focal neuropathy: Focal neuropathy is neuropathy that is restricted to one nerve or group of nerves, or one area of the body. Symptoms of focal neuropathy usually appear suddenly.

Symptoms:
Neuropathy is associated with varied characteristic symptoms. Although some people with neuropathy may not have symptoms, certain symptoms are common. The degree to which an individual is affected by a particular neuropathy varies.

Damage to the sensory nerves is common in peripheral neuropathy. Symptoms often begin in the feet with a gradual onset of loss of feeling, numbness, tingling, or pain and progress toward the center of the body with time. The arms or legs may be involved. The inability to determine joint position may also occur, which can result in clumsiness or falls. Extreme sensitivity to touch can be another symptom of peripheral neuropathy. The sensation of numbness and tingling of the skin is medically known as paresthesia.

The loss of sensory input from the foot means that blisters and sores on the feet may develop rapidly and not be noticed. Because there is a reduced sensation of pain, these sores may become infected and the infection may spread to deeper tissues, including bone. In severe cases, amputation may be necessary.

When damage to the motor nerves (those that control movement) occurs, symptoms include weakness, loss of reflexes, loss of muscle mass, cramping, and/or loss of dexterity.

Autonomic neuropathy, or damage to the nerves that control the function of organs and glands, may manifest with a wide variety of symptoms, including:

•Nausea, vomiting, or abdominal bloating after meals

•Urinary symptoms, such as incontinence, difficulty beginning to urinate, or feeling that the bladder was not completely emptied

•Impotence (erectile dysfunction) in men

•Dizziness or fainting

•Constipation or diarrhea

•Blurred vision

•Heat intolerance or decreased ability to sweat

•Hypoglycemia unawareness: Low blood sugar levels (hypoglycemia) are associated with trembling, sweating, and palpitations. In people with autonomic neuropathy, these characteristic symptoms may not occur, making dangerously low blood sugar levels difficult to recognize.

Causes:
Neuropathy or nerve damage may be caused by a number of different diseases, injuries, infections, and even vitamin deficiency states.
Some of them are :-

•Diabetes: Diabetes is the condition most commonly associated with neuropathy. The characteristic symptoms of peripheral neuropathy often seen in people with diabetes are sometimes referred to as diabetic neuropathy. The risk of having diabetic neuropathy rises with age and duration of diabetes. Neuropathy is most common in people who have had diabetes for decades and is generally more severe in those who have had difficulty controlling their diabetes, or those who are overweight or have elevated blood lipids and high blood pressure.

•Vitamin deficiencies: Deficiencies of the vitamins B12 and folate as well as other B vitamins can cause damage to the nerves.

•Autoimmune neuropathy: Autoimmune diseases such as rheumatoid arthritis, systemic lupus, and Guillain-Barre syndrome can cause neuropathies.

•Infection: Some infections, including HIV/AIDS, Lyme disease, leprosy, and syphilis, can damage nerves.

•Post-herpetic neuralgia: Post-herpetic neuralgia, a complication of shingles (varicella-zoster virus infection) is a form of neuropathy.

•Alcoholic neuropathy: Alcoholism is often associated with peripheral neuropathy. Although the exact reasons for the nerve damage are unclear, it probably arises from a combination of damage to the nerves by alcohol itself along with the poor nutrition and associated vitamin deficiencies that are common in alcoholics.

•Genetic or inherited disorders: Genetic or inherited disorders can affect the nerves and are responsible for some cases of neuropathy. Examples include Friedreich’s ataxia and Charcot-Marie-Tooth disease.

•Amyloidosis: Amyloidosis is a condition in which abnormal protein fibers are deposited in tissues and organs. These protein deposits can lead to varying degrees of organ damage and may be a cause of neuropathy.

•Uremia: Uremia (a high concentration of waste products in the blood due to kidney failure) can lead to neuropathy.

•Toxins and poisons can damage nerves. Examples include, gold compounds, lead, arsenic, mercury, some industrial solvents, nitrous oxide, and organophosphate pesticides.

•Drugs or medication: Certain drugs and medications can cause nerve damage. Examples include cancer therapy drugs such as vincristine (Oncovin, Vincasar), and antibiotics such as metronidazole (Flagyl), and isoniazid (Nydrazid, Laniazid).

•Trauma/Injury: Trauma or injury to nerves, including prolonged pressure on a nerve or group of nerves, is a common cause of neuropathy. Decreased blood flow (ischemia) to the nerves can also lead to long-term damage.

•Tumors: Benign or malignant tumors of the nerves or nearby structures may damage the nerves directly, by invading the nerves, or cause neuropathy due to pressure on the nerves.

•Idiopathic: Idiopathic neuropathy is neuropathy for which no cause has been established. The term idiopathic is used in medicine to denote the fact that no cause is known.

Diagnosis:
The diagnosis of neuropathy and its cause involve a thorough medical history and physical examination to help your health care professional determine the cause and severity of neuropathy. A neurological examination, testing the reflexes and function of sensory and motor nerves, is an important component of the initial examination.

Although there are no blood tests that are specific for determining whether of not neuropathy is present, when neuropathy is suspected, blood tests are often used to check for the presence of diseases and conditions (for example, diabetes or vitamin deficiencies) that may be responsible for nerve damage.

Imaging studies such as X-rays, CT scans, and MRI scans may be performed to look for sources of pressure on or damage to nerves.

Exams and Tests:

Specific tests of nerve function include:

•Electromyography (EMG) is a test that measures the function of the nerves. For this test a very thin needle is inserted through the skin into the muscle. The needle contains an electrode that measures the electrical activity of the muscle.

•A nerve conduction velocity test (NCV) measures the speed at which signals travel through the nerves. This test is often done with the EMG. In the NCV test, patches containing surface electrodes are placed on the skin over nerves at various locations. Each patch gives off a very mild electrical impulse, which stimulates the nerve. The electrical activity of the nerves is measured and the speed of the electrical impulses between electrodes (reflecting the speed of the nerve signals) is calculated.

•In some cases, a nerve biopsy may be recommended. A biopsy is the surgical removal of a small piece of tissue for examination under a microscope. A pathologist, a physician specially trained in tissue diagnosis, examines the specimen and can help establish the cause of the neuropathy. The procedure is performed using a local anesthetic. The sural nerve (in the ankle), or the superficial radial nerve (wrist) are the sites most often used for biopsy.

Treatment:
The treatment of neuropathy involves measures to control the symptoms as well as treatment measures that address the underlying cause of neuropathy, if appropriate. Medical treatments for diabetes, autoimmune diseases, infections, kidney disease, and vitamin deficiencies are varied and are directed at the specific underlying condition. In many cases, treatment of the underlying disease can reduce or eliminate the symptoms of neuropathy. Some cases, especially those involving compression or entrapment of nerves by tumors or other conditions, can be relieved by surgery.

Many adjuvant medications have been tried, such as mega doses of vitamins, iron, zinc, calcium, alpha lipoic acid, acetyl-L carnitine. Increasing doses of painkillers like tramadol are also used. Sometimes they are combined with anti histamines like diphendydramnine (Benadryl) and pain modifying drugs. Combinations with anti epileptics such as gabapentin and anti depressants like amitriptyline reduce the intensity of symptoms. None of these treatments has been 100 per cent successful. The pain is still present in 80 per cent of the patients 5-10 years later.

Control of blood glucose (sugar) levels is important in the treatment of diabetic neuropathy to help prevent further damage to nerves.

Clinical trials are underway to help find new and more effective treatments for neuropathy. For example, treatments that involve electrical nerve stimulation or magnetic nerve stimulation are being studied.

Self care at home:
Special and careful care of the feet is important in people with neuropathy to reduce the chance of developing sores and infections. The nerves to the feet are the nerves most commonly affected by neuropathy. Proper foot care includes:

•wash the feet with warm water each day and thoroughly dry feet after washing (especially between the toes);

•never go barefoot or wear improperly-fitting, damaged, or too-tight footwear;

•inspect the feet daily, looking for cuts, blisters, or other problems;

•cut and file toenails when needed;

•thick, seamless socks can help prevent irritation of the feet;

•call your health care practitioner if you have any problems with your feet;

•massaging the feet can improve circulation; and

•smoking cessation can further improve blood circulation, since smoking damages circulation to the extremities and may worsen foot problems.

.The intensity of the pain can be reduced by soaking the legs up to the knees in warm salted water for 10 minutes, half-an-hour before bed. Application of pain relieving ointments that contain capsaicin also provides relief. The ointment should be applied every 3-4 hours. Do not rub the ointment in too vigorously as it will damage the skin.

Prevention:

Neuropathy is preventable only to the extent that the underlying condition or cause is preventable. For those with diabetes, studies have conclusively shown that long-term control of blood glucose levels is critically important in preventing the development of neuropathy and other complications of diabetes. Neuropathy that arises due to poor nutrition or alcohol abuse may be preventable if these causes can be eliminated. Genetic or inherited causes of neuropathy are not preventable.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.emedicinehealth.com/neuropathy/article_em.htm
http://www.telegraphindia.com/1130211/jsp/knowhow/story_16546702.jsp

Enhanced by Zemanta

Raynaud’s disease


Definition:-

Raynaud’s disease is a condition that causes some areas of your body — such as your fingers, toes, tip of your nose and your ears — to feel numb and cool in response to cold temperatures or stress. In Raynaud’s disease, smaller arteries that supply blood to your skin narrow, limiting blood circulation to affected areas.

Click to see the pictures of  Raynaud’s  diseas

Raynaud’s disease (also known as “Primary Raynaud’s phenomenon” where the phenomenon is idiopathic, and Raynaud’s syndrome (secondary Raynaud’s), where it is caused by some other instigating factor. Measurement of hand-temperature gradients is one tool used to distinguish between the primary and secondary forms.

It is possible for the primary form to progress to the secondary form.

Symptoms:-
Raynaud’s disease is more than simply having cold hands and cold feet, and it’s not the same as frostbite. Signs and symptoms of Raynaud’s depend on the frequency, duration and severity of the blood vessel spasms that underlie the disorder.

The list of signs and symptoms mentioned in various sources for Raynaud’s phenomenon includes the 51 symptoms listed below:

•Symptoms usually affect fingers, toes, nose, lips or earlobes
•Skin color changes
•Skin whiteness then blueness then redness
•Cold sensitivity
•Pallor (whiteness)
•Cyanosis (blueness)
•Redness (rubor)
•Finger symptoms
*Finger color changes
*Finger pallor
*Finger tingling
*Finger redness
*Finger numbness
*Finger sensitivity
*Finger pain

•Toe symptoms

*Toe color changes
*Toe numbness
*Toe redness
*Toe pallor
*Toe sensitivity
*Toe pain

•Nose symptoms
*Nose color changes
*Nose numbness
*Nose redness
*Nose pallor
*Nose sensitivity
*Nose pain

•Earlobe symptoms
*Earlobe color changes
*Earlobe numbness
*Earlobe redness
*Earlobe pallor
*Earlobe pain
•Lip symptoms

*Lip color changes
*Lip numbness
*Lip redness
*Lip pallor
*Lip sensitivity
*Lip pain

•Episodic attacks – lasting minutes or hours
•Small blood vessel constriction (vasospastic attacks)
•Symmetric symptoms – usually both hands or both feet rather than just one
•Both hands and both feet – primary Raynaud’s affects all 4; secondary Raynaud’s typically affects either hands or feet but not both.

•Other areas affected – hands and feet most common but others are possible
*Nose symptoms
*Lips symptoms
*Ear lobes symptoms

Causes:-
Doctors don’t completely understand the cause of Raynaud’s attacks, but blood vessels in the hands and feet appear to overreact to cold temperatures or stress:

*Cold temperatures. When your body is exposed to cold temperatures, your extremities lose heat. Your body slows down blood supply to your fingers and toes to preserve your body’s core temperature. Your body specifically reduces blood flow by narrowing the small arteries under the skin of your extremities. In people with Raynaud’s, this normal response is exaggerated.
*Stress. Stress causes a similar reaction to cold in the body, and likewise the body’s response may be exaggerated in people with Raynaud’s.


Blood vessels in spasm
:
With Raynaud’s, arteries to your fingers and toes go into what’s called vasospasm. This narrows your vessels dramatically and temporarily limits blood supply. Over time, these same small arteries may also thicken slightly, further limiting blood flow. The result is that affected skin turns a pale and dusky color due to the lack of blood flow to the area. Once the spasms go away and blood returns to the area, the tissue may turn red before returning to a normal color.

Cold temperatures are most likely to trigger an attack. Exposure to cold can be as simple as putting your hands under a faucet of running cold water, taking something out of the freezer or exposure to cold air. For some people, exposure to cold temperatures isn’t necessary. Emotional stress alone can cause an episode of Raynaud’s.

Raynaud’s may be partly an inherited disorder.

In extreme cases, the secondary form can progress to necrosis or gangrene of the fingertips.

Raynaud’s phenomenon is an exaggeration of vasomotor responses to cold or emotional stress. More specifically, it is a hyperactivation of the sympathetic system causing extreme vasoconstriction of the peripheral blood vessels, leading to tissue hypoxia. Chronic, recurrent cases of Raynaud phenomenon can result in atrophy of the skin, subcutaneous tissues, and muscle. In rare cases it can cause ulceration and ischemic gangrene.

It is important to distinguish Raynaud’s disease from syndrome. In order to diagnose these two forms of Raynaud’s, a doctor may look for signs of arthritis or vasculitis, and may conduct a number of laboratory tests.

Primary Raynaud’s (disease):
Raynaud’s disease, or “Primary Raynaud’s”, is diagnosed if the symptoms are idiopathic, that is, they occur by themselves and not in association with other diseases. Some refer to Primary Raynaud’s disease as “being allergic to coldness”. It often develops in young women in their teens and early adulthood. Primary Raynaud’s is thought to be at least partly hereditary, although specific genes have not yet been identified.

Smoking worsens frequency and intensity of attacks, and there is a hormonal component. Caffeine also worsens the attacks. Sufferers are more likely to have migraine and angina than controls.

Secondary Raynaud’s (syndrome)
:
Raynaud’s syndrome, or “Secondary Raynaud’s”, occurs secondary to a wide variety of other conditions. Secondary Raynaud’s has a number of associations:

Connective tissue disorders:
*scleroderma
*systemic lupus erythematosus
*rheumatoid arthritis
*Sjögren’s syndrome
*dermatomyositis
*polymyositis
*mixed connective tissue disease

*cold agglutinin disease

*Ehlers-Danlos Syndrome

Eating disorders
*anorexia nervosa

Obstructive disorders :
*atherosclerosis
*Buerger’s disease
*Takayasu’s arteritis
*subclavian aneurysms
*thoracic outlet syndrome


Drugs
:
*Beta-blockers
*cytotoxic drugs – particularly chemotherapeutics and most especially *bleomycin
*ciclosporin
*ergotamine
*sulfasalazine
*anthrax vaccines whose primary ingredient is the Anthrax Protective Antigen


Occupation
:
*jobs involving vibration, particularly drilling
*exposure to vinyl chloride, mercury
*exposure to the cold (e.g. by working packing frozen food)


Others
:
*hypothyroidism
*cryoglobulinemia
*malignancy
*reflex sympathetic dystrophy
*carpal tunnel syndrome
*Magnesium Deficiency
*Erythromelalgia, (the opposite of Raynaud’s, with hot and warm extremities) often co-exists in patients with Raynaud’s)
It is important to realize that Raynaud’s can herald these diseases by periods of more than 20 years in some cases, making it effectively their first presenting symptom. This can be the case in the CREST syndrome, of which Raynaud’s is a part.

Patients with Secondary Raynaud’s can also have symptoms related to their underlying diseases. Raynaud’s phenomenon is the initial symptom that presents for 70% of patients with scleroderma, a skin and joint disease.

Raynaud’s phenomenon which is limited to one hand (or to one foot) is referred to as Unilateral Raynaud’s. This is an uncommon form, and it is always secondary to local or regional vascular disease. It commonly progresses within several years to affect other limbs as the vascular disease progresses.

Risk factors:-
Risk factors for primary Raynaud’s include:

*Your gender.
Primary Raynaud’s affects women more than men.
*Your age. Although anyone can develop the condition, primary Raynaud’s often begins between the ages of 15 and 30.
*Where you live. The disorder is also more common in people who live in colder climates.
*Your family history. Additionally, a family history appears to increase your risk of primary Raynaud’s. About one-third of people with primary Raynaud’s have a first-degree relative — a parent, sibling or child — with the disorder.

Risk factors for secondary Raynaud’s include:


*Associated diseases.
These include conditions such as scleroderma and lupus.

*Certain occupations. People in occupations that cause repetitive trauma, such as workers who operate tools that vibrate, also may be more vulnerable to secondary Raynaud’s.

*Exposure to certain substances.
Smoking, medications that affect the blood vessels and exposure to chemicals such as vinyl chloride are associated with an increased risk of Raynaud’s.
Complications:
If Raynaud’s is severe — which is rare — blood circulation to your fingers or toes could permanently diminish, causing deformities of your fingers or toes.

If an artery to an affected area becomes blocked completely, sores (skin ulcers) or dead tissue (gangrene) may develop. Ulcers and gangrene can be difficult to treat.

Diagnosis:-
Examinations & Tests:
To diagnose Raynaud’s, your doctor will ask detailed questions about your symptoms and medical history and conduct a physical examination. Your doctor may also run tests to rule out other medical problems that may cause similar signs and symptoms, such as a pinched nerve.

Your doctor may perform a simple test called a cold-stimulation test during your office visit. This test may involve placing your hands in cool water or exposing you to cold air, to trigger an episode of Raynaud’s.

A careful medical history will often reveal whether the condition is primary or secondary. Once this has been established, an examination is largely to identify or exclude possible secondary causes.

Digital artery pressure: pressures are measured in the arteries of the fingers before and after the hands have been cooled. A decrease of at least 15 mmHg is diagnostic (positive).

Doppler ultrasound: to assess blood flow.

Full blood count: this can reveal a normocytic anaemia suggesting the anaemia of chronic disease or renal failure.

Blood test for urea and electrolytes:
this can reveal renal impairment.
Thyroid function tests: this can reveal hypothyroidism.
An autoantibody screen, tests for rheumatoid factor, Erythrocyte sedimentation rate and C-reactive protein, which may reveal specific causative illnesses or a generalised inflammatory process.
Nail fold vasculature: this can be examined under the microscope

Sorting out primary vs. secondary Raynaud’s
:
To distinguish between primary and secondary Raynaud’s, your doctor may perform an in-office test called nail fold capillaroscopy. During the test, the doctor examines your nail fold — the skin at the base of your fingernail — under a microscope. Tiny blood vessels (capillaries) near the nail fold that are enlarged or deformed may indicate an underlying disease. However, some secondary diseases can’t be detected by this test.

If your doctor suspects that another condition, such as an autoimmune or connective tissue disease, underlies Raynaud’s, he or she may order blood tests, such as:

*Antinuclear antibodies test. A positive test for the presence of these antibodies — produced by your immune system — indicates a stimulated immune system and is common in people who have connective tissue diseases or other autoimmune disorders.

*Erythrocyte sedimentation rate. This blood test determines the rate at which red blood cells settle to the bottom of a tube in the space of an hour. A faster than normal rate may signal an underlying inflammatory or autoimmune disease. Autoimmune diseases are commonly associated with secondary Raynaud’s.
There’s no single blood test to diagnose Raynaud’s. Your doctor may order other tests, such as those that rule out diseases of the arteries, to help pinpoint a disease or condition that may be associated with Raynaud’s.

Modern Treatments and drugs:-

Treatment options are dependent on the type of Raynaud’s present. Raynaud’s syndrome is treated primarily by addressing the underlying cause, but includes all options for Raynaud’s disease as well. Treatment of primary Raynaud’s focuses on avoiding triggers.

General care:
*Avoid environmental triggers, e.g. cold, vibration, etc. Emotional stress is another recognized trigger; although the various sources of stress can not all be avoided, it is possible to learn healthier, more effective ways of dealing with them, which will reduce stress and its damaging physical effects overall.

*Keep your hands, feet and head warm—especially your fingers, toes, ears and nose—by wearing mittens, insulated footwear, a ski mask; by using hand and foot warmers, etc.

*Quit smoking.

*Avoid caffeine and other stimulants and vasoconstrictors that have not been prescribed to you by your doctor. Read product labels; caffeine is found not only in coffee and tea, stay-awake pills, many soft drinks and candies, but also in some cosmetics, soaps and shampoos(reference needed).

  • Exercise. Your doctor may encourage you to exercise regularly, particularly if you have primary Raynaud’s. Exercise can increase circulation, among other health benefits.
  • Control stress. Because stress may trigger an attack, learning to recognize and avoid stressful situations may help control the number of attacks.

*Make sure all your doctors know about all the medicines you take and about all the OTC remedies you use, especially hormones and drugs that regulate hormones, such as hormonal contraception, so that these professionals can make an assessment of your chemical regimen and make any changes that may be indicated. Contraception which is low in estrogen is preferable, and the progesterone only pill is often prescribed for women with Raynaud’s.

*If you are diabetic, follow your diabetes treatment plan.

Emergency measures:
*If white finger (Raynaud’s) occurs unexpectedly and a source of warm water is available, allow tepid to slightly warm water to run over the affected digits while you gently massage the area. Continue this process until the white area returns to its normal, healthy color.

*If triggered by exposure in a cold environment, and no warm water is available, place the affected digits in a warm body cavity – arm pit, crotch, or even in the mouth. Keep the affected area warm at least until the whiteness returns to its normal, healthy color. Get out of the cold as soon as possible.

Drug therapy
:
*Treatment for Raynaud’s phenomenon may include prescription medicines that dilate blood vessels, such as calcium channel blockers (nifedipine) or diltiazem.  It has the usual common side effects of headache, flushing, and ankle edema; but these are not typically of sufficient severity to require cessation of treatment.

*There is some evidence that Angiotensin II receptor antagonists (often Losartan) reduce frequency and severity of attacks,and possibly better than nifedipine.

*Alpha-1 adrenergic blockers such as prazosin can be used to control Raynaud’s vasospasms under supervision of a health care provider.

*In a study published in the November 8, 2005 issue of Circulation, sildenafil (Viagra) improved both microcirculation and symptoms in patients with secondary Raynaud’s phenomenon resistant to vasodilatory therapy. The authors, led by Dr Roland Fries (Gotthard-Schettler-Klinik, Bad Schönborn, Germany), report: “In the present study, capillary blood flow was severely impaired and sometimes hardly detectable in patients with Raynaud’s phenomenon. Sildenafil led to a more than 400% increase of flow velocity.”

*Fluoxetine, a selective serotonin reuptake inhibitor, and other antidepressant medications may reduce the frequency and severity of episodes if caused mainly by psychological stress.

Surgical Intervention
:
*In severe cases, a sympathectomy   procedure can be performed. Here, the nerves that signal the blood vessels of the fingertips to constrict are surgically cut. Microvascular surgery of the affected areas is another possible therapy. Infusions of prostaglandins, e.g. prostacyclin, may be tried, with amputation in exceptionally severe cases.

*A more recent treatment for severe Raynaud’s is the use of Botox. The 2009 article studied 19 patients ranging in age from 15 to 72 years with severe Raynaud’s phenomenon of which 16 patients (84%) reported pain reduction at rest. 13 patients reported immediate pain relief, 3 more had gradual pain reduction over 1-2 months. All 13 patients with chronic finger ulcers healed within 60 days. Only 21% of the patients required repeated injections. A 2007 article describes similar improvement in a series of 11 patients. All patients had significant relief of pain.

Sometimes in cases of severe Raynaud’s, approaches other than medications may be a treatment option:

*Nerve surgery
. Nerves called sympathetic nerves in your hands and feet control the opening and narrowing of blood vessels in your skin. Sometimes it’s necessary in cases of severe Raynaud’s to cut these nerves to interrupt their exaggerated response. Through small incisions in the affected hands or feet, a doctor strips away these tiny nerves around the blood vessels. The surgery, called sympathectomy, may reduce the frequency and duration of attacks, but it’s not always successful.
*Chemical injection. Doctors can inject chemicals to block sympathetic nerves in affected hands or feet. You may need to have the procedure repeated if symptoms return or persist.
*Amputation. Sometimes, doctors need to remove tissue damaged from a lack of blood supply. This may include amputating a finger or toe affected by Raynaud’s in which the blood supply has been completely blocked and the tissue has developed gangrene. But this is rare.


Alternative and Experimental (Research) Approaches
:-
Lifestyle changes and supplements that encourage better circulation may be effective alternatives for managing Raynaud’s. If  one is interested, may talk to the doctor about:

*Biofeedback. Biofeedback — using your mind to control body temperature — may help decrease the severity and frequency of attacks. Biofeedback includes guided imagery to increase the temperature of hands and feet, deep breathing and other relaxation exercises. Your doctor may be able to suggest a therapist who can help you learn biofeedback techniques. Books and tapes also are available on the subject.

*Niacin. Niacin, also known as vitamin B-3, causes blood vessels to dilate, increasing blood flow to skin. Niacin supplements may be useful in treating Raynaud’s, although niacin supplements may have side effects.
*The extract of the Ginkgo biloba leaves (Egb 761, 80 mg) may reduce frequency of attacks.

*Two separate gels combined on the fingertip (somewhat like two-part epoxy, they cannot be combined before use because they will react) increased blood flow in the fingertips by about three times. One gel contained 5% sodium nitrite and the other contained 5% ascorbic acid. The milliliter of combined gel covered an area of ~3 cm². The gel was wiped off after a few seconds.

*Piracetam, a nootropic drug, can be useful as a long-term treatment for vasospastic disorders.

*Arginine, which increase nitrous oxide acts as a vasodilator

*Milder cases of Raynaud’s can often be addressed by biofeedback[23] or other techniques to help control involuntary body functions like skin temperature.

*Fish oil supplements which contain long-chain omega-3 fatty acids may help to control symptoms of primary Raynaud’s. There are few studies in the medical literature dealing with this subject. However, in one 1989 controlled, double-blinded study of 32 patients, consumption of roughly 6.5 grams of long chain omega-3 fatty acids in the form of fish oil significantly increased the time to onset or entirely prevented symptoms in response to cold in patients with primary Raynaud’s. Lower doses of fish oil such as may be commonly available from commercial vendors have not been studied and may not be as effective.

Coping with the stress and nuisance of Raynaud’s takes patience and effort. Work with your doctor to manage your condition and maintain a positive attitude. The majority of people with Raynaud’s respond to treatment..

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.


Rersources:
http://en.wikipedia.org/wiki/Raynaud’s_phenomenon
http://www.mayoclinic.com/health/raynauds-disease/DS00433/DSECTION=lifestyle-and-home-remedies
http://www.wrongdiagnosis.com/r/raynauds_phenomenon/symptoms.htm
http://www.myfootshop.com/detail.asp?Condition=Raynauds%20Disease.

Enhanced by Zemanta

Hypoglycemia

Definition:
Hypoglycemia is the clinical syndrome that results from low blood sugar. The symptoms of hypoglycemia can vary from person to person, as can the severity. Classically, hypoglycemia is diagnosed by a low blood sugar with symptoms that resolve when the sugar level returns to the normal range….CLICK & SEE

Risk Factor:
While patients who do not have any metabolic problems can complain of symptoms suggestive of low blood sugar, true hypoglycemia usually occurs in patients being treated for diabetes (type 1 and type 2). Patients with pre-diabetes who have insulin resistance can also have low sugars on occasion if their high circulating insulin levels are further challenged by a prolonged period of fasting. There are other rare causes for hypoglycemia, such as insulin producing tumors (insulinomas) and certain medications. These uncommon causes of hypoglycemia will not be discussed in this article, which will primarily focus on the hypoglycemia occurring with diabetes mellitus and its treatment.

Despite our advances in the treatment of diabetes, hypoglycemic episodes are often the limiting factor in achieving optimal blood sugar control. In large scale studies looking at tight control in both type 1 and type 2 diabetes, low blood sugars occurred more often in the patients who were managed most intensively. This is important for patients and physicians to recognize, especially as the goal for treating patients with diabetes become tighter blood sugar control.

Low Blood sugar is Also Bad:
The body needs fuel to work. One of its major fuel sources is sugars, which the body gets from what is consumed as either simple sugar or complex carbohydrates. For emergency situations (like prolonged fasting), the body stores a stash of sugar in the liver as glycogen. If this store is needed, the body goes through a biochemical process called gluco-neo-genesis (meaning to “make new sugar”) and converts these stores of glycogen to sugar. This backup process emphasizes that the fuel source of sugar is important (important enough for human beings to have developed an evolutionary system of storage to avoid a sugar drought).

Of all the organs in the body, the brain depends on sugar (which we are now going to refer to as glucose) almost exclusively. Rarely, if absolutely necessary, the brain will use ketones as a fuel source, but this is not preferred. The brain cannot make its own glucose and is 100% dependent on the rest of the body for its supply. If for some reason, the glucose level in the blood falls (or if the brain’s requirements increase and demands are not met) there can be effects on the function of the brain.

Our Body’s Natural Protection
:
When the circulating level of blood glucose falls, the brain actually senses the drop. The brain then sends out messages that trigger a series of events, including changes in hormone and nervous system responses that are aimed at increasing blood glucose levels. Insulin secretion decreases and hormones that promote higher blood glucose levels, such as glucagon, cortisol, growth hormone and epinephrine, all increase. As mentioned above, there is a store in the liver of glycogen that can be converted to glucose rapidly.

In addition to the biochemical processes that occur, the body starts to consciously alert the affected person that is needs food by causing the signs and symptoms of hypoglycemia discussed below.

Signs and symptoms:
Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.

Adrenergic manifestations

*Shakiness, anxiety, nervousness, tremor

*Palpitations, tachycardia

*Sweating, feeling of warmth

*Pallor, coldness, clamminess

*Dilated pupils (mydriasis)

Feeling of numbness “pins and needles” (parasthaesia) in the fingers

Glucagon manifestations:

*Hunger, borborygmus

*Nausea, vomiting, abdominal discomfort

*Headache

Neuroglycopenic manifestations:

*Abnormal mentation, impaired judgement

*Nonspecific dysphoria, anxiety, moodiness, depression, crying

*Negativism, irritability, belligerence, combativeness, rage

*Personality change, emotional lability

*Fatigue, weakness, apathy, lethargy, daydreaming, sleep

*Confusion, amnesia, dizziness, delirium

*Staring, “glassy” look, blurred vision, double vision

*Automatic behavior, also known as automatism

*Difficulty speaking, slurred speech

*Ataxia, incoordination, sometimes mistaken for “drunkenness”

*Focal or general motor deficit, paralysis, hemiparesis

*Paresthesia, headache

*Stupor, coma, abnormal breathing

*Generalized or focal seizures

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms, if symptoms even occur. Specific manifestations may vary by age and by severity of the hypoglycemia. In young children, vomiting can sometimes accompany morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person may be similar from episode to episode, but are not necessarily so and may be influenced by the speed at which glucose levels are dropping, and previous incidence.

In newborns, hypoglycemia can produce irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating, hypothermia, somnolence, hypotonia, refusal to feed, and seizures or “spells”. Hypoglycemia can resemble asphyxia, hypocalcemia, sepsis, or heart failure.

In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed hypoglycemia unawareness and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.

Nearly always, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.

Causes:-
Hundreds of conditions can cause hypoglycemia. Common causes by age are listed below. While many aspects of the medical history and physical examination may be informative, the two best guides to the cause of unexplained hypoglycemia are usually

1.The circumstances

2.A critical sample of blood obtained at the time of hypoglycemia, before it is reversed.

There are several ways to classify hypoglycemia. The following is a list of the more common causes and factors which may contribute to hypoglycemia grouped by age, followed by some causes that are relatively age-independent. See causes of hypoglycemia for a more complete list grouped by etiology.

Hypoglycemia in newborn infants:-

Hypoglycemia is a common problem in critically ill or extremely low birthweight infants. If not due to maternal hyperglycemia, in most cases it is multifactorial, transient and easily supported. In a minority of cases hypoglycemia turns out to be due to significant hyperinsulinism, hypopituitarism or an inborn error of metabolism and presents more of a management challenge.

*Transient neonatal hypoglycemia

*Prematurity, intrauterine growth retardation, perinatal asphyxia

*Maternal hyperglycemia due to diabetes or iatrogenic glucose administration

*Sepsis

*Prolonged fasting (e.g., due to inadequate breast milk or condition interfering with feeding)

*Congenital hypopituitarism

*Congenital hyperinsulinism, several types, both transient and persistent

*Inborn errors of carbohydrate metabolism such as glycogen storage disease

Hypoglycemia in young children:-

Single episodes of hypoglycemia may occur due to gastroenteritis or fasting, but recurrent episodes nearly always indicate either an inborn error of metabolism, congenital hypopituitarism, or congenital hyperinsulinism. A list of common causes:

*Prolonged fasting

*Diarrheal illness in young children, especially rotavirus gastroenteritis

*Idiopathic ketotic hypoglycemia

*Isolated growth hormone deficiency, hypopituitarism

*Insulin excess

*Hyperinsulinism due to several congenital disorders of insulin secretion

*Insulin injected for type 1 diabetes

*Hyperinsulin Hyperammonia syndrome (HIHA)due toGlutamate dehydrogenase 1gene.Can cause mental retardation and epilepsy in severe cases.

*Gastric dumping syndrome (after gastrointestinal surgery)

*Other congenital metabolic diseases; some of the common include

*Maple syrup urine disease and other organic acidurias

*Type 1 glycogen storage disease

*Type III glycogen storage disease. Can cause less severe hypoglycemia than type I

*Disorders of fatty acid oxidation

*Medium chain acylCoA dehydrogenase deficiency (MCAD)

*Familial Leucine sensitive hypoglycemia

*Accidental ingestions

*Sulfonylureas, propranolol and others

*Ethanol (mouthwash, “leftover morning-after-the-party drinks”)

Hypoglycemia in older children and young adults:-

By far, the most common cause of severe hypoglycemia in this age range is insulin injected for type 1 diabetes. Circumstances should provide clues fairly quickly for the new diseases causing severe hypoglycemia. All of the congenital metabolic defects, congenital forms of hyperinsulinism, and congenital hypopituitarism are likely to have already been diagnosed or are unlikely to start causing new hypoglycemia at this age. Body mass is large enough to make starvation hypoglycemia and idiopathic ketotic hypoglycemia quite uncommon. Recurrent mild hypoglycemia may fit a reactive hypoglycemia pattern, but this is also the peak age for idiopathic postprandial syndrome, and recurrent “spells” in this age group can be traced to orthostatic hypotension or hyperventilation as often as demonstrable hypoglycemia.

*Insulin-induced hypoglycemia

*Insulin injected for type 1 diabetes

*Factitious insulin injection (Munchausen syndrome)

*Insulin-secreting pancreatic tumor

*Reactive hypoglycemia and idiopathic postprandial syndrome

*Addison’s disease

*Sepsis

Hypoglycemia in older adults:-

The incidence of hypoglycemia due to complex drug interactions, especially involving oral hypoglycemic agents and insulin for diabetes rises with age. Though much rarer, the incidence of insulin-producing tumors also rises with advancing age. Most tumors causing hypoglycemia by mechanisms other than insulin excess occur in adults.

*Insulin-induced hypoglycemia

*Insulin injected for diabetes

*Factitious insulin injection (Munchausen syndrome)

*Excessive effects of oral diabetes drugs, beta-blockers, or drug interactions

*Insulin-secreting pancreatic tumor

*Alimentary (rapid jejunal emptying with exaggerated insulin response)

*After gastrectomy dumping syndrome or bowel bypass surgery or resection

*Reactive hypoglycemia and idiopathic postprandial syndrome

*Tumor hypoglycemia, Doege-Potter syndrome

*Acquired adrenal insufficiency

*Acquired hypopituitarism

*Immunopathologic hypoglycemia

Treatment:-
Management of hypoglycemia involves immediately raising the blood sugar to normal, determining the cause, and taking measures to hopefully prevent future episodes.

Reversing acute hypoglycemia:-
The blood glucose can be raised to normal within minutes by taking (or receiving) 10-20 grams of carbohydrate. It can be taken as food or drink if the person is conscious and able to swallow. This amount of carbohydrate is contained in about 3-4 ounces (100-120 ml) of orange, apple, or grape juice although fruit juices contain a higher proportion of fructose which is more slowly metabolized than pure dextrose, alternatively, about 4-5 ounces (120-150 ml) of regular (non-diet) soda may also work, as will about one slice of bread, about 4 crackers, or about 1 serving of most starchy foods. Starch is quickly digested to glucose (unless the person is taking acarbose), but adding fat or protein retards digestion. Symptoms should begin to improve within 5 minutes, though full recovery may take 10-20 minutes. Overfeeding does not speed recovery and if the person has diabetes will simply produce hyperglycemia afterwards.

If a person is suffering such severe effects of hypoglycemia that they cannot (due to combativeness) or should not (due to seizures or unconsciousness) be given anything by mouth, medical personnel such as EMTs and Paramedics, or in-hospital personnel can establish an IV and give intravenous Dextrose, concentrations varying depending on age (Infants are given 2cc/kg Dextrose 10%, Children Dextrose 25%, and Adults Dextrose 50%). Care must be taken in giving these solutions because they can be very necrotic if the IV is infiltrated. If an IV cannot be established, the patient can be given 1 to 2 milligrams of Glucagon in an intramuscular injection. More treatment information can be found in the article diabetic hypoglycemia.

One situation where starch may be less effective than glucose or sucrose is when a person is taking acarbose. Since acarbose and other alpha-glucosidase inhibitors prevents starch and other sugars from being broken down into monosaccharides that can be absorbed by the body, patients taking these medications should consume monosaccharide-containing foods such as glucose tablets, honey, or juice to reverse hypoglycemia.

Prevention:
The most effective means of preventing further episodes of hypoglycemia depends on the cause.

The risk of further episodes of diabetic hypoglycemia can often (but not always) be reduced by lowering the dose of insulin or other medications, or by more meticulous attention to blood sugar balance during unusual hours, higher levels of exercise, or alcohol intake.

Many of the inborn errors of metabolism require avoidance or shortening of fasting intervals, or extra carbohydrates. For the more severe disorders, such as type 1 glycogen storage disease, this may be supplied in the form of cornstarch every few hours or by continuous gastric infusion.

Several treatments are used for hyperinsulinemic hypoglycemia, depending on the exact form and severity. Some forms of congenital hyperinsulinism respond to diazoxide or octreotide. Surgical removal of the overactive part of the pancreas is curative with minimal risk when hyperinsulinism is focal or due to a benign insulin-producing tumor of the pancreas. When congenital hyperinsulinism is diffuse and refractory to medications, near-total pancreatectomy may be the treatment of last resort, but in this condition is less consistently effective and fraught with more complications.

Hypoglycemia due to hormone deficiencies such as hypopituitarism or adrenal insufficiency usually ceases when the appropriate hormone is replaced.

Hypoglycemia due to dumping syndrome and other post-surgical conditions is best dealt with by altering diet. Including fat and protein with carbohydrates may slow digestion and reduce early insulin secretion. Some forms of this respond to treatment with a glucosidase inhibitor, which slows starch digestion.

Reactive hypoglycemia with demonstrably low blood glucose levels is most often a predictable nuisance which can be avoided by consuming fat and protein with carbohydrates, by adding morning or afternoon snacks, and reducing alcohol intake.

Idiopathic postprandial syndrome without demonstrably low glucose levels at the time of symptoms can be more of a management challenge. Many people find improvement by changing eating patterns (smaller meals, avoiding excessive sugar, mixed meals rather than carbohydrates by themselves), reducing intake of stimulants such as caffeine, or by making lifestyle changes to reduce stress.

Herbal medication for Hypoglycemia:-
THE following HERBS as stated below can help to ease low blood sugar with symptoms that include lightheadedness, headache, irritability, depression, anxiety, cravings for sweets, confusion, night sweats, weakness in the legs and arms, swollen feet, insatiable hunger, eye pain, nervous tics, mental disturbances, insomnia, aggressiveness, hair-trigger temper.

Cinnamon bark extract, coral calcium with trace minerals, L-carnitine, bilberry extract, Mexican wild yam, dandelion root, milk thistle extract.

Quik Tip
: Cinnamon bark decreases insulin resistance and improves blood-sugar profiles better than most prescription drugs, USDA studies confirm.

Hypoglycemia as “folk” medicine:-
Hypoglycemia is also a term of contemporary folk medicine which refers to a recurrent state of symptoms of altered mood and subjective cognitive efficiency, sometimes accompanied by adrenergic symptoms, but not necessarily by measured low blood glucose. Symptoms are primarily those of altered mood, behavior, and mental efficiency. This condition is usually treated by dietary changes which range from simple to elaborate. Advising people on management of this condition is a significant “sub-industry” of alternative medicine. More information about this form of “hypoglycemia”, with far more elaborate dietary recommendations, is available on the internet and in health food stores. Most of these websites and books describe a conflation of reactive hypoglycemia and idiopathic postprandial syndrome but do not recognize a distinction. The value of most of their recommendations is – from a scientific perspective – unproved.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.medicinenet.com/hypoglycemia/article.htm
http://en.wikipedia.org/wiki/Hypoglycemia
http://www.herbnews.org/hypoglycemiadone.htm

Enhanced by Zemanta

Why Do Parts of Our Body ‘Fall Asleep’?

The weird “separate” sensations we experience when a particular limb “falls asleep” are the result of nerves under pressure.

CLICK & SEE

For example, if an arm has fallen asleep, it is most likely that the person had slept on the arm. The sleeping position squeezed and exerted pressure on the nerves, which were as a result unable to carry messages to the brain as well as other parts of the body. And if the position also squeezed the blood vessels, it would mean that oxygen carried by them did not reach the nerves.

When one removes the pressure on the nerves and on the blood vessels, in this case by a change in the position, the nerve fibres awaken in order of their thickness and of the thickness of their myelin sheaths (protective covering). Hence, the thickest and most protected ones awaken last. This gradual awakening process causes the different sensations we experience as the affected body part returns to normalcy.

The first sensation we experience is a tingling sensation, followed by a burning sensation, as the fibres that control pain and temperature now function and are again able to transmit these messages to the brain. Not until later, does the numbness we feel disappear, simply because the fibres that control touch and position are thicker fibres with thicker myelin sheaths.

Similar fibres, known as motor neurons, travel in the same nerves, but take direct orders from the brain to the spinal cord to the muscles, and awaken shortly after those controlling touch and position. For this reason, after the numbness disappears, we regain our ability to move the affected body part, and life is finally back to normal.

Sources: The Telegraph (Kolkata, India)