Neuropathy is a collection of disorders that occurs when nerves of the peripheral nervous system (the part of the nervous system outside of the brain and spinal cord) are damaged. The condition is generally referred to as peripheral neuropathy, and it is most commonly due to damage to nerve axons. Neuropathy usually causes pain and numbness in the hands and feet. It can result from traumatic injuries, infections, metabolic disorders, and exposure to toxins. One of the most common causes of neuropathy is diabetes.
Neuropathy can affect nerves that control muscle movement (motor nerves) and those that detect sensations such as coldness or pain (sensory nerves). In some cases - autonomic neuropathy - it can affect internal organs, such as the heart, blood vessels, bladder, or intestines.
Pain from peripheral neuropathy is often described as a tingling or burning sensation. There is no specific length of time that the pain exists, but symptoms often improve with time - especially if the neuropathy has an underlying condition that can be cured. The condition is often associated with poor nutrition, a number of diseases, and pressure or trauma, but many cases have no known reason (called idiopathic neuropathy).
In the United States, about 20 million people suffer from neuropathy. Over half of diabetes patients also suffer from the condition.
How is neuropathy classified?
Peripheral neuropathy can be broadly classified into the following categories:
Mononeuropathy - involvement of a single nerve. Examples include carpal tunnel syndrome, ulnar nerve palsy, radial nerve palsy, and peroneal nerve palsy.
Multiple mononeuropathy - two or more nerves individually affected.
Polyneuropathy - generalized involvement of peripheral nerves. Examples include diabetic neuropathy and Guillain-Barre syndrome.
Neurophathies may also be categorized based on a functional classification (motor, sensory, autonomic, or mixed) or the type of onset (acute - hours or days, subacute - weeks or months, or chronic - months or years).
The most common form of neuropathy is (symmetrical) peripheral polyneuropathy, which mainly affects the feet and legs on both sides of the body.
What causes neuropathy?
About 30% of neuropathy cases are considered idiopathic, which means they are of unknown cause. Another 30% of neuropathies are due to diabetes. In fact, about 50% of people with diabetes develop some type of neuropathy. The remaining cases of neuropathy, called acquired neuropathies, have several possible causes, including:
Trauma or pressure on nerves, often from a cast or crutch or repetitive motion such as typing on a keyboard
Nutritional problems and vitamin deficiencies, often from a lack of B vitamins
Alcoholism, often through poor dietary habits and vitamin deficiencies
Other diseases and infections, such as kidney disease, liver disease, Lyme disease, HIV/AIDS, or an underactive thyroid (hypothyroidism)
Inherited disorders (hereditary neuropathies), such as Charcot-Marie-Tooth disease and amyloid polyneuropathy
Poison exposure, from toxins such as heavy metals, and certain medications and cancertreatments
Who gets neuropathy?
Risk factors for peripheral neuropathy include several conditions and behaviors. People with diabetes who poorly control their blood sugar levels are very likely to suffer from some neuropathy. Autoimmune diseases such as lupus and rheumatoid arthritis also increase one's chance of developing a neuropathy. People who have received organ transplants, AIDSpatients, and others who have had some type of immune system suppression have a higher risk of neuropathy. In addition, those who abuse alcohol or have vitamin deficiencies (especially B vitamins) are at an increased risk. Neuropathy is also more likely to occur in people with kidney, liver or thyroid disorders.
What are the symptoms of neuropathy?
Neuropathy symptoms depend on several factors, chiefly where the affected nerves are located and which type of nerves are affected (motor, sensory, autonomic). Several types of neuropathy affect all three types of nerves. Some neuropathies suddenly arise while others come on gradually over the course of years.
Motor nerve damage usually leads to symptoms that affect muscles such as muscle weakness, cramps, and spasms. It is not uncommon for this type of neuropathy to lead to a loss of balance and coordination. Patients may find it difficult to walk or run, feel like they have heavy legs, stumble, or tire easily. Damage to arm nerves may make it difficult to do routine tasks like carry bags, open jars, or turn door knobs.
Sensory nerve damage can cause various symptoms, such as an impaired sense of position, tingling, numbness, pinching and pain. Pain from this neuropathy is often described as burning, freezing, or electric-like, and many report a sensation of wearing an invisible "glove" or "stocking". These sensations tend to be worse at night, and can become painful and sever. On the contrary, sensory nerve damage may lead to a lessening or absence of sensation, where nothing at all is felt.
Autonomic nerve damage affects internal organs and involuntary functions and can lead to abnormal blood pressure and heart rate, reduced ability to perspire, constipation, bladder dysfunction, diarrhea, incontinence, sexual dysfunction, and thinning of the skin.
How is neuropathy diagnosed?
a nerve conduction test
Peripheral neuropathy is often not easy to diagnose. It is not a single disease, but a symptom with often several potential causes. The standard diagnostic process begins with a full medical history with physical and neurological exams that will examine tendon reflexes, muscle strength and tone, the ability to feel sensations, and posture and coordination. Blood tests are also common in order for doctors to measure levels of vitamin B-12. Other common tests include urinalysis, thyroid function tests, and a nerve conduction study that includes electromyography (to measure electrical discharges produced in muscles). Physicians may also recommend a nerve biopsy, where a small portion of nerve is removed and examined under a microscope.
How is neuropathy treated?
There are a variety of treatments available for peripheral neuropathy. They range from traditional pills and creams to special diets and therapies that stimulate the nervous system. Antidepressants, especially tricyclics and selective serotonin-norepinephrine re-uptake inhibitors (SNRI's), are a favored treatment for neuropathies. They will relieve neuropathic pain in non-depressed persons. Another class of medicines commonly prescribed for neuropathy is that of anticonvulsants. These medicines block calcium channels on neurons to limit pain. Opioid narcotic treatments for neuropathy are used as well to treat the condition, but are less favored because of the risk of dependency. However, opioids have been the most consistently effective in reducing pain.
For some types of neuropathy, such as post-herpes neuralgia, physicians recommend treatment with a topical anesthetic such as lidocaine. Topical applications of capsaicin (the chemical that makes peppers hot) has also been used to treat neuropathic pain.
Alternative therapies for peripheral neuropathy include cannabinoids (an class of chemicals found in marijuana), Botulinum Toxin Type A (better known as Botox), NMDA antagonists (such as ketamine), dietary supplements (such as alpha lipoic and benfotiamine), chiropractic massages, yoga, meditation, cognitive therapy, and accupuncture.
A final class of therapies for neuropathy are called neuromodulators. These include both implantable and non-implantable technologies (electrical and chemical) such as spinal cord stimulators, implanted spinal pumps, electrodes that stimulate the motor cortex of the brain, and methods called deep brain stimulation.
How can neuropathy be managed and prevented?
There are several ways to manage neuropathy and prevent its symptoms. Good foot health is important, especially for diabetics. Patients should check feet for blisters, cuts, or calluses and avoid tight fitting shoes and socks. Doctors can recommend an exercise plan that will reduce neuropathy pain and control blood sugar levels. Patients should also quit smoking and eat healthful meals. Massages of hands and feet may also aid neuropathy management by stimulating nerves and temporarily relieving pain. Finally, it is advised to avoid prolonged pressure on knees or elbows in order to prevent new nerve damage.
What is neuropathy? - Video
What Is Neuropathy? Written by Peter Crosta M.A. Original article date: 29 April 2009 Article updated: 20 February 2012
If you have a sinus infection, taking a course of amoxicillin, an antibiotic medication, does not help you recover faster or reduce symptoms any more effectively than taking an inactive placebo, according to a new study by Washington University School of Medicine in St. Louis, Missouri, USA, that is published in the 15 February issue of JAMA.
First author Dr Jane M Garbutt is a research associate professor of medicine at the School of Medicine. She told the media that she and her colleagues believe antibiotics are overused in primary care, and referred to efforts by the Centers for Disease Control and Prevention (CDC) to encourage more judicious use of the drugs.
"We hope this study provides scientific evidence that doctors can use with patients to explain that an antibiotic is not likely to help an acute sinus infection," said Garbutt.
Senior author Dr Jay F Piccirillo, professor of otolaryngology at the School, said:
"Our results show that antibiotics aren't necessary for a basic sinus infection - most people get better on their own."
Sinusitis means inflammation of a sinus, one of the small, air-filled spaces inside the forehead and cheekbones. The sinuses make mucus which normally drains through small tubes into the nose. Most incidences of sinusitis are due to infection and mainly affect the ones in the cheekbones.
Sinusitis is very common in the US, where 1 in 5 prescriptions for antibiotics are for treating the condition.
One reason for the CDC's campaign to encourage more judicious use of antibiotics is the increasing number of bacteria species that are developing resistance to antibiotics, so the purpose of the study was to see if this very common use of such drugs is being effective. And the results show it isn't.
Instead of straight away giving out antibiotics like amoxicillin, the one investigated in this study, the researchers suggest doctors and patients should just treat the symptoms, such as pain,fever, cough and congestion, and monitor the situation to see if further treatment is necessary.
For their study, Garbutt and colleagues examined data on 166 adults with acute sinus infection whose symptoms matched the criteria recommended by a CDC expert panel. The patients were recruited through primary care outlets in St Louis.
To be included in the study, the symptoms had to be moderate, severe, or very severe: specifically they had to include pain or tenderness in the face and sinuses, and nasal discharge lasting between 7 and 28 days.
Patients with chronic sinusitis, or serious complications from the condition were not included. Serious complications include things like ear or chest infection.
The participants were randomly assigned either to receive a 10-day course of amoxicillin, or a 10-day course of placebo. Both groups also received medications for relieving symptoms such as pain, cough, fever and congestion.
The researchers assessed the participants' symptoms at various points in the trial: at the start (day 0), and then on days 3, 7, 10 and 28. At each assessment, the participants filled in a questionnaire called the Sinonasal Outcome Test-16 (SNOT-16) which assesses a number of quality of life measures related to the condition.
The researchers also noted relapse and recurrence of symptoms and days absent from work.
The results showed that on day 3 there was no difference between the treatment and placebo group on any of the measures. On day 7, there was a small improvement in the treatment group, as assessed from the questionnaire responses.
But Garbutt said this small difference was unlikely to represent a noticeable relief in symptoms.
"Even though it was a statistically significant change, it's likely not a change that a patient would notice," said Garbutt.
The small improvement had disappeared by day 10, by which time 8 out 10 of participants in both groups reported their symptoms had either gone altogether or were very much improved.
The results showed there was no difference between the groups in the amount of symptom relief medications they chose to use.
While the study shows that antibiotics don't work for acute sinusitis, it does not answer the question of what does work for this "nasty disease" as Garbutt describes it:
"People have significant symptoms. They feel miserable and miss time from work. If an antibiotic is not going to be of any benefit, then what is? That's a question we haven't answered yet. But we are working on it," she said.
Fructose does not make you gain more weight than other types of carbohydrates, Canadian researchers reported in theAnnals of Internal Medicine. They found that a little extra fructose added to foods did not trigger weight gain, as long as the participants reduced the equivalent total calories from other carbs. In other words, fructose calories are no more fattening than the same number of calories in other carbohydrate foods.
The authors explained that fructose's contribution to excess bodyweight in Western societies is often mentioned, but no studies have clearly shown a connection. John L. Sievenpiper, MD, PhD., and team set out to determine what effect fructose might have on people's weight in controlled eating trials.
They gathered data on 41 controlled feeding trials which had lasted for at least seven days. 31 of them, involving 637 participants, compared the effect of free fructose and non-fructose carbohydrates in isocaloric trials. Isocaloric means with similar total calories. 10 studies, involving 119 participants were hypercaloric trials (high calories). They excluded trials that evaluated high-fructose corn syrup (42% to 55% free fructose).
They found that in the isocaloric trials, fructose made no overall difference to body weight, when compared to non-fructose carbohydrates. However, high calorie fructose diets did lead to increases in body weight.
Put simply: when people ate foods with fructose, and their meals had the same number of calories as people's with non-fructose carbohydrate, there was no significant different is body weight. However, high calorie fructose diets did make people put on weight.
The authors stressed that several of the trials available were not of very good quality. They suggested that in the fructose hypercaloric trials, weight gain may have simply been due to too many calories, rather than fructose itself.
In an Abstract in the same journal, the researchers concluded:
"Fructose does not seem to cause weight gain when it is substituted for other carbohydrates in diets providing similar calories.
Free fructose at high doses that provided excess calories modestly increased body weight, an effect that may be due to the extra calories rather than the fructose."
What is fructose?
Fructose is also called fruit sugar or levulose. It is found in many plants. Fructose, along with glucose and galactose, is one of three dietary monosaccharides - they are absorbed into the bloodstream during digestion. A monosaccharide is the smallest possible unit of sugar.
Pure fructose, in its dry form, is an odorless sweet, white, crystalline solid - it is the most water-soluble sugar. Fructose is found in honey, berries, the majority of root vegetables, and vine fruits. Commercial fructose typically comes from sugar beets, sugar cane, and corn. Fructose, in various forms, is commonly added to foods and drinks to make them taste better.
The Tongue Drive System is getting less conspicuous and more capable. Tongue Drive is a wireless device that enables people with high-level spinal cord injuries to operate a computer and maneuver an electrically powered wheelchair simply by moving their tongues.
The newest prototype of the system allows users to wear an inconspicuous dental retainer embedded with sensors to control the system. The sensors track the location of a tiny magnet attached to the tongues of users. In earlier versions of the Tongue Drive System, the sensors that track the movement of the magnet on the tongue were mounted on a headset worn by the user.
"By moving the sensors inside the mouth, we have created a Tongue Drive System with increased mechanical stability and comfort that is nearly unnoticeable," said Maysam Ghovanloo, an associate professor in the School of Electrical and Computer Engineering at the Georgia Institute of Technology.
The new intraoral Tongue Drive System was presented and demonstrated on Feb. 20, 2012 at the IEEE International Solid-State Circuits Conference in San Francisco. Development of the system is supported by the National Institutes of Health, National Science Foundation, and Christopher and Dana Reeve Foundation.
The new dental appliance contains magnetic field sensors mounted on its four corners that detect movement of a tiny magnet attached to the tongue. It also includes a rechargeable lithium-ion battery and an induction coil to charge the battery. The circuitry fits in the space available on the retainer, which sits against the roof of the mouth and is covered with an insulating, water-resistant material and vacuum-molded inside standard dental acrylic.
"One of the problems we encountered with the earlier headset was that it could shift on a user's head and the system would need to be recalibrated," explained Ghovanloo. "Because the dental appliance is worn inside the mouth and molded from dental impressions to fit tightly around an individual's teeth with clasps, it is protected from these types of disturbances."
When in use, the output signals from the sensors are wirelessly transmitted to an iPod or iPhone. Software installed on the iPod interprets the user's tongue commands by determining the relative position of the magnet with respect to the array of sensors in real-time. This information is used to control the movements of a cursor on the computer screen or to substitute for the joystick function in a powered wheelchair.
Ghovanloo and his team have also created a universal interface for the intraoral Tongue Drive System that attaches directly to a standard electric wheelchair. The interface boasts multiple functions: it not only holds the iPod, but also wirelessly receives the sensor data and delivers it to the iPod, connects the iPod to the wheelchair, charges the iPod, and includes a container where the dental retainer can be placed at night for charging.
In preliminary tests, the intraoral device exhibited an increased signal-to-noise ratio, even when a smaller magnet was placed on the tongue. That improved sensitivity could allow additional commands to be programmed into the system. The existing Tongue Drive System that uses a headset interprets commands from seven different tongue movements.
The ability to train the system with additional commands - as many commands as an individual can comfortably remember - and having all of the commands available to the user at the same time are significant advantages over the common sip-n-puff device that acts as a simple switch controlled by sucking or blowing through a straw.
The researchers plan to begin testing the usability of the intraoral Tongue Drive System by able-bodied individuals soon and then move onto clinical trials to test its usability by people with high-level spinal cord injuries.
In recent months, Ghovanloo and his team have recruited 11 individuals with high-level spinal cord injuries to test the headset version of the system at the Atlanta-based Shepherd Center and the Rehabilitation Institute of Chicago. Trial participants received a clinical tongue piercing and tongue stud that contained a tiny magnet embedded in the upper ball. They repeated two test sessions per week during a six-week period that assessed their ability to use the Tongue Drive System to operate a computer and navigate an electric wheelchair through an obstacle course.
"During the trials, users have been able to learn to use the system, move the computer cursor quicker and with more accuracy, and maneuver through the obstacle course faster and with fewer collisions," said Ghovanloo. "We expect even better results in the future when trial participants begin to use the intraoral Tongue Drive System on a daily basis."
Yale scientists have discovered the molecular pathway by which maternally inherited deafness appears to occur: Mitochondrial DNA mutations trigger a signaling cascade, resulting in programmed cell death. The study is in Cell.
Mitochondria are cellular structures that function as "cellular power plants" because they generate most of the cell's supply of energy. They contain DNA inherited from one's mother. Mitochondria determine whether a cell lives or dies via the process of programmed cell death, or apoptosis.
The Yale scientists focused on a specific mitochondrial DNA mutation that causes maternally inherited deafness. The mutation occurs in a gene that codes for RNA in mitochondrial ribosomes, which generate proteins required for cellular respiration. The team found that cell lines containing this mutation are prone to cell death not directly due to the mutation, but rather because it enhanced a normal chemical modification of the RNA called methylation, which regulates ribosome assembly.
"Our lab had previously discovered that overexpression of the enzyme responsible for this methylation could cause cell death, even in cells without the deafness mutation," said corresponding author Gerald S. Shadel, professor of pathology and genetics at Yale School of Medicine. "But when the researchers overexpressed the enzyme in mice to mimic the effects of the mutation," he said, "we were astonished to discover that the animals progressively lost their hearing, reflecting how such disease would develop due to a known pathogenic human mitochondrial DNA mutation. This new mouse model will be instrumental in understanding genetic and environmental factors known to impact mitochondrial disease pathology.
The researchers found that reactive oxygen molecules produced by diseased mitochondria are what trigger events leading to a cell death-inducing gene expression program. By genetically depleting the protein ultimately responsible for activating this programmed cell death response, they were able to restore normal hearing to the mice.
The study not only sheds light on inherited deafness in humans, but possibly also age-related hearing loss and other human diseases. First author Nuno Raimundo, a postdoctoral associate in pathology, said, "Mitochondrial diseases are complicated because different tissues are affected in often unpredictable ways. Defining the molecular mechanism underlying death of only a specific subset of cells in the inner ear is a major step toward unraveling this complexity."
