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Electroencephalography, or EEG

Monitors brain activity through the skull. EEG is used to help diagnose certain seizure disorders, brain tumors, brain damage from head injuries, inflammation of the brain and/or spinal cord, alcoholism, certain psychiatric disorders, and metabolic and degenerative disorders that affect the brain.

EEGs are also used to evaluate sleep disorders, monitor brain activity when a patient has been fully anesthetized or loses consciousness, and confirm brain death.

This painless, risk-free test can be performed in a doctor’s office or at a hospital or testing facility.

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Nerve Conduction Study (NCS)

A nerve conduction study, also called a nerve conduction velocity (NCV) test, measures the speed of electrical signals through a nerve. The NCV test may be performed to detect nerve damage or destruction and may be used to diagnose specific neurological conditions, including myopathy and myasthenia gravis.

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MRI (Magnetic Resonance Imaging): Head

Magnetic resonance imaging (MRI) uses computer-generated radio waves and a powerful magnetic field to produce detailed images of body structures including tissues, organs, bones, and nerves.  Neurological uses include the diagnosis of brain and spinal cord tumors, eye disease, inflammation, infection, and vascular irregularities that may lead to stroke.  MRI can also detect and monitor degenerative disorders, such as multiple sclerosis, and can document brain injury from trauma.


  • Diagnostic Tests

    Diagnostic tests and procedures are vital tools that help physicians confirm or rule out the presence of a neurological disorder or other medical condition. A century ago, the only way to make a positive diagnosis for many neurological disorders was by performing an autopsy after a patient had died. But decades of basic research into the characteristics of disease, and the development of techniques that allow scientists to see inside the living brain and monitor nervous system activity as it occurs, have given doctors powerful and accurate tools to diagnose disease and to test how well a particular therapy may be working.

    Perhaps the most significant changes in diagnostic imaging over the past 20 years are improvements in spatial resolution (size, intensity, and clarity) of anatomical images and reductions in the time needed to send signals to and receive data from the area being imaged. These advances allow physicians to simultaneously see the structure of the brain and the changes in brain activity as they occur. Scientists continue to improve methods that will provide sharper anatomical images and more detailed functional information.

    Researchers and physicians use a variety of diagnostic imaging techniques and chemical and metabolic analyses to detect, manage, and treat neurological disease. Some procedures are performed in specialized settings, conducted to determine the presence of a particular disorder or abnormality. Many tests that were previously conducted in a hospital are now performed in a physician’s office or at an outpatient testing facility, with little if any risk to the patient. Depending on the type of procedure, results are either immediate or may take several hours to process.

    What are some of the more common screening tests?

    Laboratory screening tests of blood, urine, or other substances are used to help diagnose disease, better understand the disease process, and monitor levels of therapeutic drugs. Certain tests, ordered by the physician as part of a regular check-up, provide general information, while others are used to identify specific health concerns. For example, blood and blood product tests can detect brain and/or spinal cord infection, bone marrow disease, hemorrhage, blood vessel damage, toxins that affect the nervous system, and the presence of antibodies that signal the presence of an autoimmune disease. Blood tests are also used to monitor levels of therapeutic drugs used to treat epilepsy and other neurological disorders. Genetic testing of DNA extracted from white cells in the blood can help diagnose Huntington’s disease and other congenital diseases. Analysis of the fluid that surrounds the brain and spinal cord can detect meningitis, acute and chronic inflammation, rare infections, and some cases of multiple sclerosis. Chemical and metabolic testing of the blood can indicate protein disorders, some forms of muscular dystrophy and other muscle disorders, and diabetes. Urinalysis can reveal abnormal substances in the urine or the presence or absence of certain proteins that cause diseases including the mucopolysaccharidoses.

    Genetic testing or counseling can help parents who have a family history of a neurological disease determine if they are carrying one of the known genes that cause the disorder or find out if their child is affected. Genetic testing can identify many neurological disorders, including spina bifida, in utero (while the child is inside the mother’s womb). Genetic tests include the following:

    Amniocentesis, usually done at 14-16 weeks of pregnancy, tests a sample of the amniotic fluid in the womb for genetic defects (the fluid and the fetus have the same DNA). Under local anesthesia, a thin needle is inserted through the woman’s abdomen and into the womb. About 20 milliliters of fluid (roughly 4 teaspoons) is withdrawn and sent to a lab for evaluation. Test results often take 1-2 weeks.
    Chorionic villus sampling, or CVS, is performed by removing and testing a very small sample of the placenta during early pregnancy. The sample, which contains the same DNA as the fetus, is removed by catheter or fine needle inserted through the cervix or by a fine needle inserted through the abdomen. It is tested for genetic abnormalities and results are usually available within 2 weeks. CVS should not be performed after the tenth week of pregnancy.
    Uterine ultrasound is performed using a surface probe with gel. This noninvasive test can suggest the diagnosis of conditions such as chromosomal disorders (see ultrasound imaging, below).

    What is a neurological examination?

    A neurological examination assesses motor and sensory skills, the functioning of one or more cranial nerves, hearing and speech, vision, coordination and balance, mental status, and changes in mood or behavior, among other abilities. Items including a tuning fork, flashlight, reflex hammer, ophthalmoscope, and needles are used to help diagnose brain tumors, infections such as encephalitis and meningitis, and diseases such as Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis (ALS), and epilepsy. Some tests require the services of a specialist to perform and analyze results.

    X-rays of the patient’s chest and skull are often taken as part of a neurological work-up. X-rays can be used to view any part of the body, such as a joint or major organ system. In a conventional x-ray, also called a radiograph, a technician passes a concentrated burst of low-dose ionized radiation through the body and onto a photographic plate. Since calcium in bones absorbs x-rays more easily than soft tissue or muscle, the bony structure appears white on the film. Any vertebral misalignment or fractures can be seen within minutes. Tissue masses such as injured ligaments or a bulging disc are not visible on conventional x-rays. This fast, noninvasive, painless procedure is usually performed in a doctor’s office or at a clinic.

    Fluoroscopy is a type of x-ray that uses a continuous or pulsed beam of low-dose radiation to produce continuous images of a body part in motion. The fluoroscope (x-ray tube) is focused on the area of interest and pictures are either videotaped or sent to a monitor for viewing. A contrast medium may be used to highlight the images. Fluoroscopy can be used to evaluate the flow of blood through arteries.

    What are some diagnostic tests used to diagnose neurological disorders?

    Based on the result of a neurological exam, physical exam, patient history, x-rays of the patient’s chest and skull, and any previous screening or testing, physicians may order one or more of the following diagnostic tests to determine the specific nature of a suspected neurological disorder or injury. These diagnostics generally involve either nuclear medicine imaging, in which very small amounts of radioactive materials are used to study organ function and structure, or diagnostic imaging, which uses magnets and electrical charges to study human anatomy.

    The following list of available procedures—in alphabetical rather than sequential order—includes some of the more common tests used to help diagnose a neurological condition.

    Angiography is a test used to detect blockages of the arteries or veins. A cerebral angiogram can detect the degree of narrowing or obstruction of an artery or blood vessel in the brain, head, or neck. It is used to diagnose stroke and to determine the location and size of a brain tumor, aneurysm, or vascular malformation. This test is usually performed in a hospital outpatient setting and takes up to 3 hours, followed by a 6- to 8-hour resting period. The patient, wearing a hospital or imaging gown, lies on a table that is wheeled into the imaging area. While the patient is awake, a physician anesthetizes a small area of the leg near the groin and then inserts a catheter into a major artery located there. The catheter is threaded through the body and into an artery in the neck. Once the catheter is in place, the needle is removed and a guide wire is inserted. A small capsule containing a radiopaque dye (one that is highlighted on x-rays) is passed over the guide wire to the site of release. The dye is released and travels through the bloodstream into the head and neck. A series of x-rays is taken and any obstruction is noted. Patients may feel a warm to hot sensation or slight discomfort as the dye is released.

    Biopsy involves the removal and examination of a small piece of tissue from the body. Muscle or nerve biopsies are used to diagnose neuromuscular disorders and may also reveal if a person is a carrier of a defective gene that could be passed on to children. A small sample of muscle or nerve is removed under local anesthetic and studied under a microscope. The sample may be removed either surgically, through a slit made in the skin, or by needle biopsy, in which a thin hollow needle is inserted through the skin and into the muscle. A small piece of muscle or nerve remains in the hollow needle when it is removed from the body. The biopsy is usually performed at an outpatient testing facility. A brain biopsy, used to determine tumor type, requires surgery to remove a small piece of the brain or tumor. Performed in a hospital, this operation is riskier than a muscle biopsy and involves a longer recovery period.

    Brain scans are imaging techniques used to diagnose tumors, blood vessel malformations, or hemorrhage in the brain. These scans are used to study organ function or injury or disease to tissue or muscle. Types of brain scans include computed tomography, magnetic resonance imaging, and positron emission tomography (see descriptions, below).

    Cerebrospinal fluid analysis involves the removal of a small amount of the fluid that protects the brain and spinal cord. The fluid is tested to detect any bleeding or brain hemorrhage, diagnose infection to the brain and/or spinal cord, identify some cases of multiple sclerosis and other neurological conditions, and measure intracranial pressure.

    The procedure is usually done in a hospital. The sample of fluid is commonly removed by a procedure known as a lumbar puncture, or spinal tap. The patient is asked to either lie on one side, in a ball position with knees close to the chest, or lean forward while sitting on a table or bed. The doctor will locate a puncture site in the lower back, between two vertebrate, then clean the area and inject a local anesthetic. The patient may feel a slight stinging sensation from this injection. Once the anesthetic has taken effect, the doctor will insert a special needle into the spinal sac and remove a small amount of fluid (usually about three teaspoons) for testing. Most patients will feel a sensation of pressure only as the needle is inserted.

    A common after-effect of a lumbar puncture is headache, which can be lessened by having the patient lie flat. Risk of nerve root injury or infection from the puncture can occur but it is rare. The entire procedure takes about 45 minutes.

    Computed tomography, also known as a CT scan, is a noninvasive, painless process used to produce rapid, clear two-dimensional images of organs, bones, and tissues. Neurological CT scans are used to view the brain and spine. They can detect bone and vascular irregularities, certain brain tumors and cysts, herniated discs, epilepsy, encephalitis, spinal stenosis (narrowing of the spinal canal), a blood clot or intracranial bleeding in patients with stroke, brain damage from head injury, and other disorders. Many neurological disorders share certain characteristics and a CT scan can aid in proper diagnosis by differentiating the area of the brain affected by the disorder.

    Scanning takes about 20 minutes (a CT of the brain or head may take slightly longer) and is usually done at an imaging center or hospital on an outpatient basis. The patient lies on a special table that slides into a narrow chamber. A sound system built into the chamber allows the patient to communicate with the physician or technician. As the patient lies still, x-rays are passed through the body at various angles and are detected by a computerized scanner. The data is processed and displayed as cross-sectional images, or “slices,” of the internal structure of the body or organ. A light sedative may be given to patients who are unable to lie still and pillows may be used to support and stabilize the head and body. Persons who are claustrophobic may have difficulty taking this imaging test.

    Occasionally a contrast dye is injected into the bloodstream to highlight the different tissues in the brain. Patients may feel a warm or cool sensation as the dye circulates through the bloodstream or they may experience a slight metallic taste.

    Although very little radiation is used in CT, pregnant women should avoid the test because of potential harm to the fetus from ionizing radiation.

    Discography is often suggested for patients who are considering lumbar surgery or whose lower back pain has not responded to conventional treatments. This outpatient procedure is usually performed at a testing facility or a hospital. The patient is asked to put on a metal-free hospital gown and lie on an imaging table. The physician numbs the skin with anesthetic and inserts a thin needle, using x-ray guidance, into the spinal disc. Once the needle is in place, a small amount of contrast dye is injected and CT scans are taken. The contrast dye outlines any damaged areas. More than one disc may be imaged at the same time. Patient recovery usually takes about an hour. Pain medicine may be prescribed for any resulting discomfort.

    An intrathecal contrast-enhanced CT scan (also called cisternography) is used to detect problems with the spine and spinal nerve roots. This test is most often performed at an imaging center. The patient is asked to put on a hospital or imaging gown. Following application of a topical anesthetic, the physician removes a small sample of the spinal fluid via lumbar puncture. The sample is mixed with a contrast dye and injected into the spinal sac located at the base of the lower back. The patient is then asked to move to a position that will allow the contrast fluid to travel to the area to be studied. The dye allows the spinal canal and nerve roots to be seen more clearly on a CT scan. The scan may take up to an hour to complete. Following the test, patients may experience some discomfort and/or headache that may be caused by the removal of spinal fluid.

    Electroencephalography, or EEG, monitors brain activity through the skull. EEG is used to help diagnose certain seizure disorders, brain tumors, brain damage from head injuries, inflammation of the brain and/or spinal cord, alcoholism, certain psychiatric disorders, and metabolic and degenerative disorders that affect the brain. EEGs are also used to evaluate sleep disorders, monitor brain activity when a patient has been fully anesthetized or loses consciousness, and confirm brain death.

    This painless, risk-free test can be performed in a doctor’s office or at a hospital or testing facility. Prior to taking an EEG, the person must avoid caffeine intake and prescription drugs that affect the nervous system. A series of cup-like electrodes are attached to the patient’s scalp, either with a special conducting paste or with extremely fine needles. The electrodes (also called leads) are small devices that are attached to wires and carry the electrical energy of the brain to a machine for reading. A very low electrical current is sent through the electrodes and the baseline brain energy is recorded. Patients are then exposed to a variety of external stimuli—including bright or flashing light, noise or certain drugs—or are asked to open and close the eyes, or to change breathing patterns. The electrodes transmit the resulting changes in brain wave patterns. Since movement and nervousness can change brain wave patterns, patients usually recline in a chair or on a bed during the test, which takes up to an hour. Testing for certain disorders requires performing an EEG during sleep, which takes at least 3 hours.

    In order to learn more about brain wave activity, electrodes may be inserted through a surgical opening in the skull and into the brain to reduce signal interference from the skull.

    Electromyography, or EMG, is used to diagnose nerve and muscle dysfunction and spinal cord disease. It records the electrical activity from the brain and/or spinal cord to a peripheral nerve root (found in the arms and legs) that controls muscles during contraction and at rest.

    During an EMG, very fine wire electrodes are inserted into a muscle to assess changes in electrical voltage that occur during movement and when the muscle is at rest. The electrodes are attached through a series of wires to a recording instrument. Testing usually takes place at a testing facility and lasts about an hour but may take longer, depending on the number of muscles and nerves to be tested. Most patients find this test to be somewhat uncomfortable.

    An EMG is usually done in conjunction with a nerve conduction velocity (NCV) test, which measures electrical energy by assessing the nerve’s ability to send a signal. This two-part test is conducted most often in a hospital. A technician tapes two sets of flat electrodes on the skin over the muscles. The first set of electrodes is used to send small pulses of electricity (similar to the sensation of static electricity) to stimulate the nerve that directs a particular muscle. The second set of electrodes transmits the responding electrical signal to a recording machine. The physician then reviews the response to verify any nerve damage or muscle disease. Patients who are preparing to take an EMG or NCV test may be asked to avoid caffeine and not smoke for 2 to 3 hours prior to the test, as well as to avoid aspirin and non-steroidal anti-inflammatory drugs for 24 hours before the EMG. There is no discomfort or risk associated with this test.

    Electronystagmography (ENG) describes a group of tests used to diagnose involuntary eye movement, dizziness, and balance disorders, and to evaluate some brain functions. The test is performed at an imaging center. Small electrodes are taped around the eyes to record eye movements. If infrared photography is used in place of electrodes, the patient wears special goggles that help record the information. Both versions of the test are painless and risk-free.

    Evoked potentials (also called evoked response) measure the electrical signals to the brain generated by hearing, touch, or sight. These tests are used to assess sensory nerve problems and confirm neurological conditions including multiple sclerosis, brain tumor, acoustic neuroma (small tumors of the inner ear), and spinal cord injury. Evoked potentials are also used to test sight and hearing (especially in infants and young children), monitor brain activity among coma patients, and confirm brain death.

    Testing may take place in a doctor’s office or hospital setting. It is painless and risk-free. Two sets of needle electrodes are used to test for nerve damage. One set of electrodes, which will be used to measure the electrophysiological response to stimuli, is attached to the patient’s scalp using conducting paste. The second set of electrodes is attached to the part of the body to be tested. The physician then records the amount of time it takes for the impulse generated by stimuli to reach the brain. Under normal circumstances, the process of signal transmission is instantaneous.

    Auditory evoked potentials (also called brain stem auditory evoked response) are used to assess high-frequency hearing loss, diagnose any damage to the acoustic nerve and auditory pathways in the brainstem, and detect acoustic neuromas. The patient sits in a soundproof room and wears headphones. Clicking sounds are delivered one at a time to one ear while a masking sound is sent to the other ear. Each ear is usually tested twice, and the entire procedure takes about 45 minutes.

    Visual evoked potentials detect loss of vision from optic nerve damage (in particular, damage caused by multiple sclerosis). The patient sits close to a screen and is asked to focus on the center of a shifting checkerboard pattern. Only one eye is tested at a time; the other eye is either kept closed or covered with a patch. Each eye is usually tested twice. Testing takes 30-45 minutes.

    Somatosensory evoked potentials measure response from stimuli to the peripheral nerves and can detect nerve or spinal cord damage or nerve degeneration from multiple sclerosis and other degenerating diseases. Tiny electrical shocks are delivered by electrode to a nerve in an arm or leg. Responses to the shocks, which may be delivered for more than a minute at a time, are recorded. This test usually lasts less than an hour.

    Magnetic resonance imaging (MRI) uses computer-generated radio waves and a powerful magnetic field to produce detailed images of body structures including tissues, organs, bones, and nerves. Neurological uses include the diagnosis of brain and spinal cord tumors, eye disease, inflammation, infection, and vascular irregularities that may lead to stroke. MRI can also detect and monitor degenerative disorders such as multiple sclerosis and can document brain injury from trauma.

    The equipment houses a hollow tube that is surrounded by a very large cylindrical magnet. The patient, who must remain still during the test, lies on a special table that is slid into the tube. The patient will be asked to remove jewelry, eyeglasses, removable dental work, or other items that might interfere with the magnetic imaging. The patient should wear a sweat shirt and sweat pants or other clothing free of metal eyelets or buckles. MRI scanning equipment creates a magnetic field around the body strong enough to temporarily realign water molecules in the tissues. Radio waves are then passed through the body to detect the “relaxation” of the molecules back to a random alignment and trigger a resonance signal at different angles within the body. A computer processes this resonance into either a three-dimensional picture or a two-dimensional “slice” of the tissue being scanned, and differentiates between bone, soft tissues and fluid-filled spaces by their water content and structural properties. A contrast dye may be used to enhance visibility of certain areas or tissues. The patient may hear grating or knocking noises when the magnetic field is turned on and off. (Patients may wear special earphones to block out the sounds.) Unlike CT scanning, MRI does not use ionizing radiation to produce images. Depending on the part(s) of the body to be scanned, MRI can take up to an hour to complete. The test is painless and risk-free, although persons who are obese or claustrophobic may find it somewhat uncomfortable. (Some centers also use open MRI machines that do not completely surround the person being tested and are less confining. However, open MRI does not currently provide the same picture quality as standard MRI and some tests may not be available using this equipment). Due to the incredibly strong magnetic field generated by an MRI, patients with implanted medical devices such as a pacemaker should avoid the test.

    Functional MRI (fMRI) uses the blood’s magnetic properties to produce real-time images of blood flow to particular areas of the brain. An fMRI can pinpoint areas of the brain that become active and note how long they stay active. It can also tell if brain activity within a region occurs simultaneously or sequentially. This imaging process is used to assess brain damage from head injury or degenerative disorders such as Alzheimer’s disease and to identify and monitor other neurological disorders, including multiple sclerosis, stroke, and brain tumors.

    Myelography involves the injection of a water- or oil-based contrast dye into the spinal canal to enhance x-ray imaging of the spine. Myelograms are used to diagnose spinal nerve injury, herniated discs, fractures, back or leg pain, and spinal tumors.

    The procedure takes about 30 minutes and is usually performed in a hospital. Following an injection of anesthesia to a site between two vertebrae in the lower back, a small amount of the cerebrospinal fluid is removed by spinal tap (see cerebrospinal fluid analysis, above) and the contrast dye is injected into the spinal canal. After a series of x-rays is taken, most or all of the contrast dye is removed by aspiration. Patients may experience some pain during the spinal tap and when the dye is injected and removed. Patients may also experience headache following the spinal tap. The risk of fluid leakage or allergic reaction to the dye is slight.

    Positron emission tomography (PET) scans provide two- and three-dimensional pictures of brain activity by measuring radioactive isotopes that are injected into the bloodstream. PET scans of the brain are used to detect or highlight tumors and diseased tissue, measure cellular and/or tissue metabolism, show blood flow, evaluate patients who have seizure disorders that do not respond to medical therapy and patients with certain memory disorders, and determine brain changes following injury or drug abuse, among other uses. PET may be ordered as a follow-up to a CT or MRI scan to give the physician a greater understanding of specific areas of the brain that may be involved with certain problems. Scans are conducted in a hospital or at a testing facility, on an outpatient basis. A low-level radioactive isotope, which binds to chemicals that flow to the brain, is injected into the bloodstream and can be traced as the brain performs different functions. The patient lies still while overhead sensors detect gamma rays in the body’s tissues. A computer processes the information and displays it on a video monitor or on film. Using different compounds, more than one brain function can be traced simultaneously. PET is painless and relatively risk-free. Length of test time depends on the part of the body to be scanned. PET scans are performed by skilled technicians at highly sophisticated medical facilities.

    A polysomnogram measures brain and body activity during sleep. It is performed over one or more nights at a sleep center. Electrodes are pasted or taped to the patient’s scalp, eyelids, and/or chin. Throughout the night and during the various wake/sleep cycles, the electrodes record brain waves, eye movement, breathing, leg and skeletal muscle activity, blood pressure, and heart rate. The patient may be videotaped to note any movement during sleep. Results are then used to identify any characteristic patterns of sleep disorders, including restless legs syndrome, periodic limb movement disorder, insomnia, and breathing disorders such as obstructive sleep apnea. Polysomnograms are noninvasive, painless, and risk-free.

    Single photon emission computed tomography (SPECT), a nuclear imaging test involving blood flow to tissue, is used to evaluate certain brain functions. The test may be ordered as a follow-up to an MRI to diagnose tumors, infections, degenerative spinal disease, and stress fractures. As with a PET scan, a radioactive isotope, which binds to chemicals that flow to the brain, is injected intravenously into the body. Areas of increased blood flow will collect more of the isotope. As the patient lies on a table, a gamma camera rotates around the head and records where the radioisotope has traveled. That information is converted by computer into cross-sectional slices that are stacked to produce a detailed three-dimensional image of blood flow and activity within the brain. The test is performed at either an imaging center or a hospital.

    Thermography uses infrared sensing devices to measure small temperature changes between the two sides of the body or within a specific organ. Also known as digital infrared thermal imaging, thermography may be used to detect vascular disease of the head and neck, soft tissue injury, various neuromusculoskeletal disorders, and the presence or absence of nerve root compression. It is performed at an imaging center, using infrared light recorders to take thousands of pictures of the body from a distance of 5 to 8 feet. The information is converted into electrical signals which results in a computer-generated two-dimensional picture of abnormally cold or hot areas indicated by color or shades of black and white. Thermography does not use radiation and is safe, risk-free, and noninvasive.

    Ultrasound imaging, also called ultrasound scanning or sonography, uses high-frequency sound waves to obtain images inside the body. Neurosonography (ultrasound of the brain and spinal column) analyzes blood flow in the brain and can diagnose stroke, brain tumors, hydrocephalus (build-up of cerebrospinal fluid in the brain), and vascular problems. It can also identify or rule out inflammatory processes causing pain. It is more effective than an x-ray in displaying soft tissue masses and can show tears in ligaments, muscles, tendons, and other soft tissue masses in the back. Transcranial Doppler ultrasound is used to view arteries and blood vessels in the neck and determine blood flow and risk of stroke.

    During ultrasound, the patient lies on an imaging table and removes clothing around the area of the body to be scanned. A jelly-like lubricant is applied and a transducer, which both sends and receives high-frequency sound waves, is passed over the body. The sound wave echoes are recorded and displayed as a computer-generated real-time visual image of the structure or tissue being examined. Ultrasound is painless, noninvasive, and risk-free. The test is performed on an outpatient basis and takes between 15 and 30 minutes to complete.

  • Alzheimer's Disease (Dementia)

    Dementia describes a brain disorder that seriously impairs a person’s ability to carry out normal, daily activities.

    Alzheimer’s disease (AD) is most common form of dementia among older people.

    Alzheimer’s disease involves the parts of the brain that control thought, memory, and language. Great advances are being made in the diagnosis and treatment of Alzheimer’s, but there is presently no cure.

    Other forms of dementia include:

    • Frontotemporal dementia (FTD), also called “Pick’s disease”
    • Vascular dementia, associated with strokes
    • Lewy body dementia
  • Stroke: Risks and Prevention

    Some people are at a higher risk for stroke than others. There are “unmodifiable risk factors” that a person cannot change, such as their age, gender, race/ethnicity, and family history of stroke. However, there are “modifiable risk factors” for stroke that can be changed, such as body weight, high blood pressure and cigarette smoking.

    It is possible to dramatically reduce these risks through healthier lifestyle choices or medications, such as blood pressure-lowering medications. In fact, since 1950, there has been about a 60% decline in the mortality rate from stroke and a smaller but significant decline in the age-adjusted annual incidence of stroke – the number of people who have a stroke each year, adjusted to account for the increasing age of the population.

    Many experts attribute these trends to increasing awareness and control of stroke risk factors.

    Stroke Prevention – Reducing Risk Factors

    The most important modividal risk factors for stroke are hypertension, heart disease, diabetes, and cigarette smoking. Others include heavy alcohol consumption, high blood cholesterol levels, and  illicit drug use. People with more than one risk factor have what is called “amplification of risk.” This means that the multiple risk factors compound their destructive effects and create an overall risk greater than the simple cumulative effect of the individual risk factors.

    Hypertension

    • Hypertension increases the risk of having a stroke 2-4 times before age 80. After the age of 80, the increased risk from hypertension declines and other risk factors become more important.
    • Hypertension promotes atherosclerosis and causes mechanical damage to the walls of blood vessels.
    • Blood pressure medications, such as thiazide diuretics and angiotensin-converting enzyme (ACE) inhibitors, can reduce the risk of stroke by 30 to 40 percent.
    • Early treatment is essential. among older people with normal blood pressure, prior mid-life hypertension increases stroke risk up to 92%.
    • Guidelines from the Centers for Disease Control and Prevention recommend a target blood pressure of less than 140/90 mm Hg.

    Cigarette smoking

    • Smoking causes about a two-fold increase in the risk of ischemic stroke and up to a four-fold increase in the risk of hemorrhagic stroke.
    • Smoking promotes atherosclerosis and aneurysm formation, and stimulates blood clotting factors.
    • Stroke risk decreases significantly two years after quitting smoking and is at the level of nonsmokers by five years.

    Diabetes

    • In terms of stroke and cardiovascular disease risk, having diabetes is the equivalent of aging 15 years.
    • In diabetes, glucose is not efficiently taken up by the body’s cells and accumulates in the blood instead, where it can damage the vascular system.
    • Hypertension is common among diabetics and accounts for much of their increased stroke risk.
    • Blood pressure medications, dietary changes, and weight loss can lower stroke risk.
    • Controlling blood sugar appears to reduce the risk of recurrent stroke.

    Physical inactivity and obesity

    • Waist-to-hip ratio equal to or above the median (mid-value for the population) increases the risk of ischemic stroke three-fold.
    • Obesity is associated with hypertension, diabetes, and heart disease.
    • While no clinical studies have tested the effects of exercise or weight loss on stroke risk, both tend to reduce hypertension and boost cardiovascular health.

    Atrial fibrillation (AF)

    • Atrial fibrillation affects fewer than 1% of people under age 60, but is more prevalent in older people. It is responsible for one in four strokes after age 80, and is associated with high mortality and disability.
    • AF refers to irregular contraction of the atrium – the chamber where blood enters the heart. aF can lead to blood stagnation and increased clotting.
    • Warfarin, a blood-thinning medication, can reduce the risk of stroke in people with aF. People under age 60 with aF and no other stroke risk factors may benefit from aspirin. Importantly, pacemakers have no effect on the risk of stroke associated with AF.

    Cholesterol imbalance

    • High-density lipoprotein (HDL) cholesterol is generally considered protective against ischemic stroke. Low-density lipoprotein (LDL) cholesterol, when present in excess, is considered harmful.
    • LDL and HDL are needed to carry cholesterol (a fatty substance) through the blood (made up mostly of water), and deliver it to cells. because LDL delivers cholesterol to cells throughout the body, excess LDL can cause cholesterol to build up in blood vessels, leading to atherosclerosis. HDL sends cholesterol to the liver to be eliminated.
    • Clinical trials have shown that cholesterol-lowering drugs known as statins reduce the risk of stroke. However, some studies point to only a weak association between stroke and cholesterol, and there is speculation that statins reduce stroke risk by acting through some unknown mechanism.
  • Parkinson’s Disease

    Parkinson’s disease (PD) belongs to a group of conditions called movement disorders.

    Parkinson’s disease is chronic and progressive, meaning its symptoms grow worse over time.

    Parkinson’s disease occurs when nerve cells (neurons) in an area of the brain known as the substantia nigra, die or become impaired. Normally, these neurons produce an important brain chemical known as dopamine. Loss of dopamine results in abnormal nerve firing patterns within the brain that cause impaired movement. Studies have shown that most Parkinson’s patients have lost 60 to 80% or more of the dopamine-producing cells in by the time symptoms appear.

    Although some cases of Parkinson’s disease appear to be hereditary, and a few can be traced to specific genetic mutations, most cases are sporadic, meaning that it does not seem to run in families. Learn more about the cause of Parkinson’s disease.
    What are the symptoms of Parkinson’s disease?

    Early symptoms of Parkinson’s are subtle and develop gradually. As they become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks. Not everyone with one or more of these symptoms has Parkinson’s disease, as these symptoms can also appear in other diseases.

    Parkinson’s disease symptoms often begin on one side of the body. However, as it progresses, the disease eventually affects both sides. Even after the disease involves both sides of the body, the symptoms are often less severe on one side than on the other.

    The four main symptoms of Parkinson’s disease are:

    Tremor, or trembling in hands, arms, legs, jaw, or head
    Rigidity, or stiffness of the limbs and trunk
    Bradykinesia, or slowness of movement
    Postural instability, or impaired balance

    Other symptoms that may be experienced in people with Parkinson’s disease include:

    Depression. Fortunately, depression usually can be successfully treated with antidepressant medications.
    Emotional changes. Some people with Parkinson’s disease become fearful and insecure.
    Difficulty with swallowing and chewing.
    Speech changes.
    Urinary problems or constipation.
    Skin problems. It is common for the skin on the face to become very oily, particularly on the forehead and at the sides of the nose. The scalp may become oily too, resulting in dandruff.
    Sleep problems, including difficulty staying asleep at night, restless sleep, nightmares and emotional dreams, and drowsiness or sudden sleep onset during the day.
    Dementia or other cognitive problems. Some, but not all, people with Parkinson’s disease may develop memory problems and slow thinking.
    Orthostatic hypotension. Orthostatic hypotension is a sudden drop in blood pressure when a person stands up from a lying-down position that can lead to dizziness, lightheadedness, and, in extreme cases, loss of balance or fainting.
    Muscle cramps and dystonia.
    Pain. Many people with Parkinson’s disease develop aching muscles and joints because of the rigidity and abnormal postures often associated with the disease. Treatment with levodopa and other dopaminergic drugs often alleviates these pains to some extent.
    Fatigue and loss of energy.

    How is Parkinson’s disease diagnosed?

    Parkinson’s disease can be difficult to diagnose accurately because other conditions may produce symptoms of Parkinson’s disease and there are currently no blood or laboratory tests that can diagnose Parkinson’s disease. Therefore the diagnosis is based on medical history and a neurological examination.

    Early signs and symptoms of Parkinson’s disease may sometimes be dismissed as the effects of normal aging. The physician may need to observe the person for some time until it is apparent that the symptoms are consistently present. Doctors may sometimes request brain scans or laboratory tests in order to rule out other diseases. However, CT and MRI brain scans of people with Parkinson’s disease usually appear normal. Since many other diseases have similar features but require different treatments, making a precise diagnosis as soon as possible is essential so that patients can receive the proper treatment.
    How does Parksinson’s disease evolve?

    Parkinson’s Disease gets worse with time. The average life expectancy of a Parkinson’s dsease patient is generally the same as for people who do not have the disease. However, in the late stages of the disease, Parkinson’s dsease may cause complications such as choking, pneumonia, and falls that can lead to death. Fortunately, there are many treatment options available for people with Parkinson’s dsease.

    The progression of symptoms in Parkinson’s dsease may take 20 years or more. In some people, however, the disease progresses more quickly. There is no way to predict what course the disease will take for an individual person. One commonly used system for describing how the symptoms of Parkinson’s dsease progress is called the Hoehn and Yahr scale.

    Staging of Parkinson’s Disease

    Stage 1 – Symptoms on one side of the body only.
    Stage 2- Symptoms on both sides of the body. No impairment of balance.
    Stage 3 – Balance impairment. Mild to moderate disease. Physically independent.
    Stage 4 – Severe disability, but still able to walk or stand unassisted.
    Stage 5 – Wheelchair-bound or bedridden unless assisted.

    Another commonly used scale is the Unified Parkinson’s Disease Rating Scale (UPDRS). This much more complicated scale has multiple ratings that measure mental functioning, behavior, and mood; activities of daily living; and motor function. Both the Hoehn and Yahr scale and the UPDRS are used to measure how individuals are faring and how much treatments are helping them.

    With appropriate treatment, most people with Parkinson’s dsease can live productive lives for many years after diagnosis.
    How is Parkinson’s disease treated?

    There is presently no cure for Parkinson’s disease. However, medications and other treatment options can provide dramatic relief from the symptoms.

    Parkinson’s disease medications fall into three categories.

    Medications that work directly or indirectly to increase the level of dopamine in the brain. The most commonly prescribed medications for Parkinson’s disease are substances, such as levodopa (L-dopa), that cross from the blood to the brain and are then changed into dopamine. Other drugs mimic dopamine or prevent or slow its breakdown.
    Medications that affect other neurotransmitters in the body in order to ease some of the symptoms of the disease. For example, anticholinergic drugs interfere with production or uptake of the neurotransmitter acetylcholine to help to reduce tremors and muscle stiffness, which can result from having more acetylcholine than dopamine.
    Medications that help control the non-motor symptoms of the disease, such as depression and sleep.

    The following Parkinson disease medications increase levels of dopamine in the brain (category 1).

    Levodopa. The cornerstone of therapy for Parkinson’s disease is the drug levodopa (also called L-dopa). Although it can reduce the symptoms of Parkinson’s disease, it does not replace lost nerve cells and it does not stop the disease from progressing.

    Dopamine agonists, such as bromocriptine, apomorphine, pramipexole (Mirapex), and ropinirole (Requip). These medications mimic the role of dopamine in the brain. They can be given alone or in conjunction with levodopa. They may be used in the early stages of the disease, or later on in order to lengthen the duration of response to levodopa in patients who experience wearing off or on-off effects. They are generally less effective than levodopa in controlling rigidity and bradykinesia.

    MAO-B inhibitors, such as selegiline (Elepryl) and Azilect (rasagiline). These drugs inhibit the enzyme monoamine oxidase B, or MAO-B, which breaks down dopamine in the brain. These medications can delay the need for levodopa therapy by up to a year or more. When selegiline is given with levodopa, it appears to enhance and prolong the response to levodopa and thus may reduce wearing-off fluctuations.

    COMT inhibitors, such as entacapone (Comtan) and tolcapone (Tasmar). These medications prolong the effects of levodopa by preventing the breakdown of dopamine. COMT inhibitors can decrease the duration of “off” periods, and they usually make it possible to reduce the person’s dose of levodopa.

    Amantadine. An antiviral drug, amantadine, can help reduce symptoms of Parkinson’s disease and levodopa-induced dyskinesia. It is often used alone in the early stages of the disease. It also may be used with an anticholinergic drug or levodopa. After several months, amantadine’s effectiveness wears off in up to half of the patients taking it.

    Anticholinergics, such as trihexyphenidyl, benztropine, and ethopropazine. Anticholinergics decrease the activity of the neurotransmitter acetylcholine and help to reduce tremors and muscle rigidity. Only about half the patients who receive anticholinergics are helped by it, usually for a brief period and with only a 30 percent improvement.

    Your doctor will prescribe one or more medications for Parkinson’s disease depending on several factors, including

    Type of symptoms
    Severity of symptoms
    Response to past treatments
    Other medication conditions

    Since no two people will react the same way to a medication, it may take time and patience to find the appropriate medications and dosages to provide maximal benefit. Even then, symptoms may not be completely alleviated.

    Neurosurgical procedures are also available for the treatment of severe cases of Parkinson’s disease that fail to respond to medical treatment, particularly tremor. (see Brain Surgery for Parkinson’s Disease). However, since these procedures cause permanent destruction of brain tissue, they have largely been replaced by Deep brain stimulation (DBS) for the treatment of Parkinson’s disease.
    Complementary and supportive therapies

    Diet. At this time there are no specific vitamins, minerals, or other nutrients that have any proven therapeutic value in Parkinson’s disease. Some early reports have suggested that dietary supplements might be protective in Parkinson’s disease. In addition, a phase II clinical trial of a supplement called coenzyme Q10 suggested that large doses of this substance might slow disease progression in patients with early-stage Parkinson’s disease. While there is currently no proof that any specific dietary factor is beneficial, a normal, healthy diet can promote overall well-being for Parkinson’s disease patients just as it would for anyone else. Eating a fiber-rich diet and drinking plenty of fluids also can help alleviate constipation. A high protein diet, however, may limit levodopa’s effectiveness.

    Exercise. Exercise can help people with Parkinson’s disease improve their mobility and flexibility. Some doctors prescribe physical therapy or muscle-strengthening exercises to tone muscles and to put underused and rigid muscles through a full range of motion. Exercises will not stop disease progression, but they may improve body strength so that the person is less disabled.

    Exercises also improve balance, helping people minimize gait problems, and can strengthen certain muscles so that people can speak and swallow better. Exercise can also improve the emotional well-being of people with Parkinson’s disease, and it may improve the brain’s dopamine synthesis or increase levels of beneficial compounds called neurotrophic factors in the brain. Although structured exercise programs help many patients, more general physical activity, such as walking, gardening, swimming, calisthenics, and using exercise machines, also is beneficial. People with Parkinson’s disease should always check with their doctors before beginning a new exercise program.

    Other complementary therapies that are used by some individuals with Parkinson’s disease include massage therapy, yoga, tai chi, hypnosis, acupuncture, and the Alexander technique, which optimizes posture and muscle activity. There have been limited studies suggesting mild benefits with some of these therapies, but they do not slow Parkinson’s disease and there is no convincing evidence that they are beneficial.

  • Neuropathy

    Peripheral neuropathy is damage to nerves of the peripheral nervous system, which may be caused either by diseases of or trauma to the nerve or the side-effects of systemic illness.[1]

    The four cardinal patterns of peripheral neuropathy are polyneuropathy, mononeuropathy, mononeuritis multiplex and autonomic neuropathy. The most common form is (symmetrical) peripheral polyneuropathy, which mainly affects the feet and legs. The form of neuropathy may be further broken down by cause, or the size of predominant fiber involvement, i.e., large fiber or small fiber peripheral neuropathy. Frequently the cause of a neuropathy cannot be identified and it is designated idiopathic.

    Neuropathy may be associated with varying combinations of weakness, autonomic changes, and sensory changes. Loss of muscle bulk or fasciculations, a particular fine twitching of muscle, may be seen. Sensory symptoms encompass loss of sensation and “positive” phenomena including pain. Symptoms depend on the type of nerves affected (motor, sensory, or autonomic) and where the nerves are located in the body. One or more types of nerves may be affected. Common symptoms associated with damage to the motor nerve are muscle weakness, cramps, and spasms. Loss of balance and coordination may also occur. Damage to the sensory nerve can produce tingling, numbness, and a burning pain.[2] Pain associated with this nerve is described in various ways such as the following: burning, freezing, or electric-like, extreme sensitivity to touch. The autonomic nerve damage causes problems with involuntary functions leading to symptoms such as abnormal blood pressure and heart rate, reduced ability to perspire, constipation, bladder dysfunction (e.g., incontinence), and sexual dysfunction.[3]
    Contents

    Classification

    Peripheral neuropathy may be classified according to the number of nerves affected or the type of nerve cell affected (motor, sensory, autonomic), or the process affecting the nerves (e.g. inflammation in neuritis).
    Mononeuropathy
    See also: Compression neuropathy and Ulnar neuropathy

    Mononeuropathy is a type of neuropathy that only affects a single nerve.[4] It is diagnostically useful to distinguish them from polyneuropathies, because the limitation in scope makes it more likely that the cause is a localized trauma or infection.

    The most common cause of mononeuropathy is by physical compression of the nerve, known as compression neuropathy. Carpal tunnel syndrome and axillary nerve palsy are examples of this. The “pins-and-needles” sensation of one’s “foot falling asleep” (paresthesia) is caused by a compression mononeuropathy,[citation needed] albeit a temporary one which can be resolved merely by moving around and adjusting to a more appropriate position. Direct injury to a nerve, interruption of its blood supply (ischemia), or inflammation can also cause mononeuropathy.
    Mononeuritis multiplex

    Mononeuritis multiplex is simultaneous or sequential involvement of individual noncontiguous nerve trunks, either partially or completely, evolving over days to years and typically presents with acute or subacute loss of sensory and motor function of individual nerves. The pattern of involvement is asymmetric; however, as the disease progresses deficit(s) becomes more confluent and symmetrical, making it difficult to differentiate from polyneuropathy. Therefore, attention to the pattern of early symptoms is important.

    Mononeuritis multiplex may also cause pain, which is characterized as deep, aching pain that is worse at night, is frequently in the lower back, hip, or leg. In people with diabetes mellitus, mononeuritis multiplex is typically encountered as acute, unilateral, severe thigh pain followed by anterior muscle weakness and loss of knee reflex.

    Electrodiagnostic studies will show multifocal sensory motor axonal neuropathy.

    It is caused by, or associated with, several medical conditions:

    diabetes mellitus
    vasculitides: polyarteritis nodosa, Wegener’s granulomatosis, and Churg–Strauss syndrome
    immune-mediated diseases like rheumatoid arthritis, lupus erythematosus (SLE), and sarcoidosis
    infections: leprosy, lyme disease, HIV
    amyloidosis
    cryoglobulinemia
    chemical agents, including trichloroethylene and dapsone
    rarely, the sting of certain jellyfish, such as the sea nettle

    Polyneuropathy
    Main article: Polyneuropathy

    Polyneuropathy is a pattern of nerve damage which is quite different from mononeuropathy, and often more serious and affecting more areas of the body. The term “peripheral neuropathy” is sometimes used loosely to refer to polyneuropathy.[5] In cases of polyneuropathy, many nerve cells in various parts of the body are affected, without regard to the nerve through which they pass; not all nerve cells are affected in any particular case. In distal axonopathy, one common pattern is that the cell bodies of neurons remain intact, but the axons are affected in proportion to their length. Diabetic neuropathy is the most common cause of this pattern. In demyelinating polyneuropathies, the myelin sheath around axons is damaged, which affects the ability of the axons to conduct electrical impulses. The third and least common pattern affects the cell bodies of neurones directly. This usually picks out either the motor neurones (known as motor neurone disease) or the sensory neurones (known as sensory neuronopathy or dorsal root ganglionopathy).

    The effect of this is to cause symptoms in more than one part of the body, often on left and right sides symmetrically. As for any neuropathy, the chief symptoms include weakness or clumsiness of movement (motor); unusual or unpleasant sensations such as tingling or burning; reduction in the ability to feel texture, temperature, etc.; and impaired balance when standing or walking (sensory). In many polyneuropathies, these symptoms occur first and most severely in the feet. Autonomic symptoms may also occur, such as dizziness on standing up, erectile dysfunction and difficulty controlling urination.

    Polyneuropathies are usually caused by processes that affect the body as a whole. Diabetes and impaired glucose tolerance are the most common causes. Other causes relate to the particular type of polyneuropathy, and there are many different causes of each type, including inflammatory diseases such as lyme disease, vitamin deficiencies, blood disorders, and toxins (including alcohol and certain prescribed drugs). Most types of polyneuropathy progress fairly slowly, over months or years, but rapidly progressive polyneuropathy also occurs. It is important to recognize that glucose levels in the blood can spike to nerve-damaging levels after eating even though fasting blood sugar levels and average blood glucose levels can still remain below normal levels (currently typically considered below 100 for fasting blood plasma and 6.0 for HGBA1c, the test commonly used to measure average blood glucose levels over an extended period). Studies have shown that many of the cases of peripheral small fiber neuropathy with typical symptoms of tingling, pain and loss of sensation in the feet and hands are due to glucose intolerance before a diagnosis of diabetes or pre-diabetes. Such damage is often reversible, particularly in the early stages, with diet, exercise and weight loss.

    The treatment of polyneuropathies is aimed firstly at eliminating or controlling the cause, secondly at maintaining muscle strength and physical function, and thirdly at controlling symptoms such as neuropathic pain.
    Autonomic neuropathy

    Autonomic neuropathy is a form of polyneuropathy which affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system) affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person’s conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen and pelvis outside spinal cord, however they have connections with the spinal cord and ultimately the brain. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most but not all cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.

    Autonomic neuropathy is one cause of malfunction of the autonomic nervous system, but not the only one; some conditions affecting the brain or spinal cord can also cause autonomic dysfunction, such as multiple system atrophy, and therefore cause similar symptoms to autonomic neuropathy.

    The signs and symptoms of autonomic neuropathy include the following:

    Urinary bladder conditions: bladder incontinence or urine retention
    Gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, gastroparesis, diarrhea, constipation
    Cardiovascular system: disturbances of heart rate (tachycardia, bradycardia), orthostatic hypotension, inadequate increase of heart rate on exertion
    Other areas: hypoglycemia unawareness, genital impotence, sweat disturbances

    Neuritis

    Neuritis is a general term for inflammation of a nerve[6] or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved, but may include pain, paresthesia (pins & needles), paresis (weakness), hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes. Causes include:

    Physical injury

    One common cause of neuritis and subsequent inflammation of the nerves to the toes is the wearing of high-heeled shoes or ill-fitting shoes that bind the toes painfully. This can cause temporary numbness and pain in the affected toes for several days.

    Infection
    Herpes simplex
    Shingles
    Leprosy
    Guillain-Barre syndrome
    Lyme Disease

    Chemical injury
    Radiation

    Underlying conditions causing localized neuritis (affecting a single nerve):
    Diphtheria
    Localized injury
    Diabetes

    Underlying conditions causing polyneuritis (affecting multiple nerves):
    Beriberi (vitamin B1 deficiency)
    Vitamin B12 deficiency
    Vitamin B6 excess[7]
    Metabolic diseases
    Diabetes
    Herpes zoster
    Hypothyroidism
    Porphyria
    Infections, bacterial and/or viral
    Autoimmune disease, especially Multiple Sclerosis
    Cancer
    Alcoholism
    Wartenbergs migratory sensory neuropathy

    Types of neuritis include:

    Polyneuritis or multiple neuritis (not to be confused with multiple sclerosis)
    Brachial neuritis
    Optic neuritis
    Vestibular neuritis
    Cranial neuritis, often representing as Bell’s Palsy
    Arsenic neuritis

    Signs and symptoms

    Those with diseases or dysfunctions of their nerves can present with problems in any of the normal nerve functions.

    In terms of sensory function, there are commonly loss of function (negative) symptoms, which include numbness, tremor, and gait abnormality.

    Gain of function (positive) symptoms include tingling, pain, itching, crawling, and pins and needles. Pain can become intense enough to require use of opioid (narcotic) drugs (i.e., morphine, oxycodone).

    Skin can become so hypersensitive that patients are prohibited from having anything touch certain parts of their body, especially the feet. People with this degree of sensitivity cannot have a bedsheet touch their feet or wear socks or shoes, and eventually become housebound.

    Motor symptoms include loss of function (negative) symptoms of weakness, tiredness, heaviness, and gait abnormalities; and gain of function (positive) symptoms of cramps, tremor, and muscle twitch (fasciculations).

    There is also pain in the muscles (myalgia), cramps, etc., and there may also be autonomic dysfunction.

    During physical examination, specifically a neurological examination, those with generalized peripheral neuropathies most commonly have distal sensory or motor and sensory loss, though those with a pathology (problem) of the nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies like Guillain–Barré syndrome; or may show focal sensory disturbance or weakness, such as in mononeuropathies. Ankle jerk reflex is classically absent in peripheral neuropathy.

  • Migraine / Headache

    What are migraine headaches?

    Migraine headaches are a common type of vascular headache experienced by about 12% of people.

    Woman with Migraine Headache (fromyourdoctor)Migraine headaches involve recurrent attacks of moderate to severe pain that is throbbing or pulsing and often strikes one side of the head, though both sides may ache. Other common symptoms are increased sensitivity to light, noise, and odors; and nausea and vomiting. Routine physical activity, movement, or even coughing or sneezing can worsen the headache pain.

    Migraines occur most frequently in the morning, especially upon waking. Some people have migraines at predictable times, such as before menstruation or on weekends following a stressful week of work. Many people feel exhausted or weak following a migraine but are usually symptom-free between attacks.
    What happens during a migraine?

    An untreated migraine attack usually lasts from 4 to 72 hours. This may unfold in four phases that can overlap.

    Premonitory symptoms occur up to 24 hours prior to developing a migraine. These include food cravings, unexplained mood changes (depression or euphoria), uncontrollable yawning, fluid retention, or increased urination.
    Aura. Some people will see flashing or bright lights or what looks like heat waves immediately prior to or during the migraine, while others may experience muscle weakness or the sensation of being touched or grabbed.
    Headache. A migraine usually starts gradually and builds in intensity. It is possible to have migraine without a headache.
    Postdrome (following the headache). Individuals are often exhausted or confused following a migraine. The postdrome period may last up to a day before people feel healthy.

    What is a “Common” or “Classic” Migraine?

    Most people with migraine headaches will experience either a “classic migraine” or “common migraine”.

    “Common migraine” is also called “migraine without aura”. As its name implies, this is the most frequent form of migraine. Symptoms include headache pain that occurs without warning and is usually felt on one side of the head, along with nausea, confusion, blurred vision, mood changes, fatigue, and increased sensitivity to light, sound, or noise.

    “Classic migraine” is also called a “migraine with aura”. It includes visual disturbances (flashing lights, zigzag lines) and other neurological symptoms that appear about 10 to 60 minutes before the actual headache and usually last no more than an hour. Individuals may temporarily lose part or all of their vision. The aura may occur without headache pain, which can strike at any time.

    Other classic symptoms include trouble speaking; an abnormal sensation, numbness, or muscle weakness on one side of the body; a tingling sensation in the hands or face, and confusion. Nausea, loss of appetite, and increased sensitivity to light, sound, or noise may precede the headache.

    Both common and classic migraines can strike as often as several times a week, or as rarely as once every few years. Both types can occur at any time.
    What are other types of migraines?

    Other types of migraine headaches include:

    Benign exertional headache is brought on by running, lifting, coughing, sneezing, or bending. The headache begins at the onset of activity, and pain rarely lasts more than several minutes.
    Abdominal migraine mostly affects young children and involves moderate to severe pain in the middle of the abdomen lasting 1 to 72 hours, with little or no headache. Additional symptoms include nausea, vomiting, and loss of appetite. Many children who develop abdominal migraine will have migraine headaches later in life.
    Basilar-type migraine mainly affects children and adolescents. It occurs most often in teenage girls and may be associated with their menstrual cycle. Symptoms include partial or total loss of vision or double vision, dizziness and loss of balance, poor muscle coordination, slurred speech, a ringing in the ears, and fainting. The throbbing pain may come on suddenly and is felt on both sides at the back of the head.
    Hemiplegic migraine is a rare but severe form of migraine that causes temporary paralysis-sometimes lasting several days-on one side of the body prior to or during a headache. Symptoms such as vertigo, a pricking or stabbing sensation, and problems seeing, speaking, or swallowing may begin prior to the headache pain and usually stop shortly thereafter. When it runs in families the disorder is called Familial Hemiplegic Migraine (FHM).
    Menstrual migraine affects women around the time of their period, although most women with menstrually-related migraine also have migraines at other times of the month. Symptoms may include migraine without aura (which is much more common during menses than migraine with aura), pulsing pain on one side of the head, nausea, vomiting, and increased sensitivity to sound and light.
    Migraine without headache is characterized by visual problems or other aura symptoms, nausea, vomiting, and constipation, but without head pain. Headache specialists have suggested that fever, dizziness, and/or unexplained pain in a particular part of the body could also be possible types of headache-free migraine.
    Ophthalmoplegic migraine an uncommon form of migraine with head pain, along with a droopy eyelid, large pupil, and double vision that may last for weeks, long after the pain is gone.
    Retinal migraine is a condition characterized by attacks of visual loss or disturbances in one eye. These attacks, like the more common visual auras, are usually associated with migraine headaches.
    Status migrainosus is a rare and severe type of acute migraine in which disabling pain and nausea can last 72 hours or longer. The pain and nausea may be so intense that sufferers need to be hospitalized.

    Who Gets Migraine Headaches?

    Migraine symptoms can begin in infancy, but are usually first experienced between the ages of 5 and 35. Although migraines affect both men and women, adult women are three times more likely to suffer migraine headaches than men.

    Most people who suffer migraine headaches have a family history of headaches. This suggests that there is some genetic trait that may be inherited.

    Migraine in women often relates to changes in hormones. Women may have “menstrual migraines” around the time of their menstrual period. These may disappear during pregnancy, while other women develop migraines for the first time when they become pregnant. Some are first affected after menopause.

    Women with migraine who take birth control pills may experience changes in the frequency and severity of migraine attacks, while women who do not suffer from headaches may develop migraines as a side effect of oral contraceptives.

    Migraine headaches also more frequently in people who have other medical conditions, such as eepression, anxiety, bipolar disorder, sleep disorders, and epilepsy.
    What causes migraine headaches?

    The precise cause of migraine headaches in unclear, but there is general agreement that blood flow changes in the brain are a key factor.

    People who get migraine headaches have a nervous system that overreacts to a trigger such as stress by causing a spasm of the arteries at the base of the brain. This spasm closes down or constricts several arteries supplying blood to the brain. As these arteries constrict, the flow of blood to the brain is reduced. At the same time, platelets in the blood clump together and release a chemical called serotonin that further constricts the arteries.

    This reduced blood flow decreases the brain’s supply of oxygen and results in distorted vision or speech, and the general symptoms of an aura.

    Then, other arteries within the brain react to the reduce oxygen supply and open wider (dilate) The dilation of these arteries triggers the release of pain-producing substances called prostaglandins from various tissues and blood cells. Chemicals which cause inflammation and swelling, and substances which increase sensitivity to pain, are also released. The circulation of these chemicals and the dilation of the scalp arteries stimulate the pain receptors in the arteries (there are no pain receptors in the brain tissue). A throbbing pain in the head results.
    What triggers a migraine?

    There are a variety of factors that can trigger a migraine attack in someone who is susceptible to developing migraine headaches. These triggers vary from person to person and include sudden changes in weather or environment, too much or not enough sleep, strong odors or fumes, emotion, stress, overexertion, loud or sudden noises, motion sickness, low blood sugar, skipped meals, tobacco, depression, anxiety, head trauma, hangover, some medications, hormonal changes, and bright or flashing lights.

    Medication overuse or missed doses of medications may also cause headaches.

    About one-half of migraine sufferers report that foods or certain ingredients can trigger their migraines. These include aspartame, caffeine (or caffeine withdrawal), wine and other types of alcohol, chocolate, aged cheeses, monosodium glutamate, some fruits and nuts, fermented or pickled goods, yeast, and cured or processed meats. Seemingly harmless foods as yogurt, nuts, and lima beans can result in a painful migraine headache. However, some scientists believe that these foods and several others contain chemical substances, such as tyramine, which constrict arteries – the first step of the migraine process.

    Keeping a diet journal can help you identify foods that may trigger your migraines.
    What are the treatment options for migraine?

    Migraine treatment options include:

    Migraine headache medications
    Stress reduction and biofeedback training
    Elimination of certain foods
    Regular exercise, such as swimming or vigorous walking, can also reduce the frequency and severity of migraine headaches.

    During a migraine headache, temporary relief can sometimes be obtained by applying cold packs to the head or by pressing on the bulging artery found in front of the ear on the painful side of the head.

    Migraine Medications

    For infrequent migraine, drugs can be taken at the first sign of a headache in order to stop it or to at least ease the pain. People who get occasional mild migraine may benefit by taking aspirin or acetaminophen at the start of an attack. Aspirin raises a person’s tolerance to pain and also discourages clumping of blood platelets. Small amounts of caffeine may be useful if taken in the early stages of migraine.

    For most people who suffer from moderate to severe migraines, stronger medications are usually necessary to effectively treat an acute headache.

    Triptans are one of the most commonly prescribed medications for the treatment of migraine headaches. Triptans ease moderate to severe migraine pain and are available as tablets, nasal sprays, and injections. Some brands of triptans include Imitrex® (sumatriptan), Maxalt® (rizatriptan), Treximet® (sumatriptan and naproxen), and Zomig (zolmitriptan).

    For optimal benefit, a triptan should be taken during the early stages of an attack. If a migraine has been in progress for about an hour after the drug is taken, a repeat dose can be given.

    People are advised not to take triptans if they have angina pectoris, basilar migraine, severe hypertension, or vascular, or liver disease.

    Ergotamines (Cafergot®) bind to serotonin receptors on nerve cells and decrease the transmission of pain messages along nerve fibers. They are most effective during the early stages of migraine and are available as nasal sprays and injections.

    Taking headache relief drugs more than three times a week may lead to medication overuse headache (previously called rebound headache), in which the initial headache is relieved temporarily but reappears as the drug wears off. Taking more of the drug to treat the new headache leads to progressively shorter periods of pain relief and results in a pattern of recurrent chronic headache. Headache pain ranges from moderate to severe and may occur with nausea or irritability. It may take weeks for these headaches to end once the drug is stopped.

    For headaches that occur three or more times a month, preventive treatment may be recommended. Medications used to prevent classic and common migraine include methysergide maleate, propranolol, amitriptyline, valproic acid, and verapamil.

    Many antimigraine drugs can have adverse side effects. But like most medicines they are relatively safe when used carefully and under a physician’s supervision. To avoid long-term side effects of preventive medications, reduce the dosage of these drugs and then stop taking them as soon as possible.

  • Seizures / Epilepsy

    Generalized seizures are a type of seizure that involve the entire brain and which can lead to a loss of consciousness, falls, or massive muscle spasms.

    These are different from “focal” seizures that involve just one part of the brain.

    Not all seizures can be easily defined as either generalized or focal. Some people have seizures that begin as focal seizures but then spread to the entire brain. Other people may have both types of seizures but with no clear pattern.

    There are many kinds of generalized seizures. Some common types include:

    In absence seizures, the person may appear to be staring into space and/or have jerking or twitching muscles. These seizures are sometimes referred to as petit mal seizures, which is an older term.
    Tonic seizures cause stiffening of muscles of the body, generally those in the back, legs, and arms.
    Clonic seizures cause repeated jerking movements of muscles on both sides of the body.
    Myoclonic seizures cause jerks or twitches of the upper body, arms, or legs.
    Atonic seizures cause a loss of normal muscle tone. The affected person will fall down or may drop his or her head involuntarily.
    Tonic-clonic seizures cause a mixture of symptoms, including stiffening of the body and repeated jerks of the arms and/or legs as well as loss of consciousness. Tonic-clonic seizures are sometimes referred to by an older term: grand mal seizures.

  • Multiple Sclerosis

    Multiple sclerosis (MS) is a chronic, often disabling disease that attacks the central nervous system (CNS). It is a life-long chronic disease that usually afflicts young adults.

    Multiple Sclerosis Myelin Neuron DamageMultiple sclerosis causes inflammation in random areas of the brain, spinal cord and optic nerves. The inflammation destroys the myelin sheath that covers the nerve cell fibers. The loss of the myelin leads to a slowing down or complete blockage of nerve signals. The areas of inflammation are called plaques and can be seen as lesions on an MRI of the brain and/or spinal cord. A worsening of inflammation is called an “attack” or “exacerbation”.

    The diagnosis of multiple sclerosis can sometimes be made soon after the initial onset of symptoms. However, some cases requires months or years for the symptoms to evolve sufficiently for the diagnosis to be clear. Approximately 300,000 people in the U.S. have been diagnosed with multiple sclerosis and about 200 people are newly diagnosed each week.

    There is no single test that can definitively diagnose MS, so a variety of tests are performed to collect information and rule out other causes of neurological symptoms. Commonly performed tests include and and MRI of the brain, visual evoked potentials or spinal fluid analysis.

    The course of multiple sclerosis is unpredictable and can vary from person to person. The vast majority of people with MS are mildly affected, but severe cases can render a person unable to write, speak, or walk as connections between the brain and other parts of the body are disrupted.

    Fortunately, a variety of multiple sclerosis treatments are available that can reduce the number of MS attacks and slow disease progression for many people.
    Who gets multiple sclerosis?

    Most people experience their first symptoms of multiple sclerosis between the ages of 20 and 40. Although there have been cases of multiple sclerosis in young children and elderly adults, symptoms rarely begin before age 15 or after age 60. Whites are more than twice as likely as other races to develop multiple sclerosis and women are twice as likely as men to develop MS. However, among patients who develop the symptoms of multiple sclerosis at a later age, the gender ratio is more balanced.
    What causes multiple sclerosis?

    The exact cause of multiple sclerosis remains unknown.

    Multiple sclerosis is an autoimmune disease, one in which the body, through its immune system, launches a defensive attack against its own tissues. In the case of multiple sclerosis, it is the myelin sheath that surround nerve cells that comes under assault. Such assaults may be associated with a combination of genetic risk and some external trigger, such as viral infection.
    What is the course of multiple sclerosis?

    Multiple sclerosis symptoms tend to evolve according to four different courses. Each of these may be described as mild, moderate or severe.

    Relapsing-Remitting Multiple Sclerosis (RRMS) is the most common “type” of MS, affecting 85% of people with multiple sclerosis. Multiple sclerosis symptoms appear as an “attack” with a sudden worsening of symptoms. These attacks (also called “flare-ups” or “exacerbations”) are followed by a complete or partial remission of symptoms. There may be be periods of stability between these attacks that last months or years during which time there is no disease progression.
    Primary-Progressive Multiple Sclerosis (PPMS) affects about 10% of people with MS. It defines a type of multiple sclerosis that results in slowly worsening function from the time of disease onset with no distinct relapses nor remissions. The rate of progression for those with PPMS can change over time, with occasional periods of stability and temporary minor improvements.
    Secondary-Progressive Multiple Sclerosis (SPMS) describes a type of MS that may develop in those with relapsing-remitting MS in which MS symptoms worsen more steadily. Before the advent of interferons and other multiple sclerosis treatments, about one-half of people with RRMS developed SPMS within 10 years.
    Progressive-Relapsing Multiple Sclerosis (PRMS) is relatively uncommon. People with PRMS experience a steady worsening of symptoms from the onset of symptoms with additional attacks that lead to declines in neurological functioning. There may or may not be some recovery following these attacks, but the disease continues to progress without full remissions.

    PPMS, SPMS and PRMS are sometimes lumped together as described as “chronic progressive multiple sclerosis” to distinguish them from relapsing-remitting MS.

    20% of people with multiple sclerosis have a benign form of the disease in which symptoms show little or no progression after the initial attack. These individuals remain fully functional.

    A few patients experience “malignant MS”, defined as a swift and relentless decline resulting in significant disability or even death shortly after disease onset. However, multiple sclerosis is very rarely fatal and most people with multiple have a fairly normal life expectancy.
    What are the symptoms of multiple sclerosis?

    Multiple sclerosis symptoms may be mild or severe, of long duration or short, and may appear in various combinations, depending on the part of the nervous system affected. Complete or partial remission of symptoms, especially in the early stages of the disease, occurs in approximately 70% of those with multiple sclerosis.

    Muscle weakness
    MS-related fatigue
    Cognitive impairment
    Spasticity
    Altered sensation of temperature and pain.
    Pain (moderate to severe)
    Ataxia
    Tremor
    Speech disturbances
    Visual disturbances
    Bladder dysfunction
    Bowel dysfunction
    Sexual dysfunction
    Depression
    Euphoria

    Multiple Sclerosis Treatment

    There is presently no cure for multiple sclerosis. However, there are medications that can reduce disease activity and disease progression for many individuals with relapsing forms of MS, including those with secondary progressive disease who continue to have relapses.

    Treatments are also available to treat acute attacks, manage MS symptoms, and improve overall function.

    Together, these treatments can enhance the quality of life of people with MS.
    Disease-Modifying Medications

    Disease-modifying medications is the name for a class of medications used for the treatment of multiple sclerosis that can reduce the frequency and severity of MS attacks. The National MS Society (NMSS) recommends that a disease-modifying treatment be started early before the disease causes significant and permanent damage.

    Reduce the Severity and Frequency of MS Attacks

    Most people using a disease-modifying drug have fewer and less severe MS attacks (relapses or exacerbations). In individual clinical trials comparing a drug versus an inactive placebo treatment, MS attacks were reduced by the different medications. In addition, most people were found to have fewer, smaller, or no new lesions developing within their central nervous system as visible in MRI scans.



    Prevent permanent damage

    Permanent damage to nerve fibers occurs early in the course of multiple sclerosis. Overall brain shrinkage (atrophy), can occur early in the disease, and damage can be ongoing even when the person has no symptoms of an attack and feels well. Therefore, MS specialists advise the early use of a drug that effectively limits lesion formation and brain atrophy, or shrinkage.



    There are currently seven disease-modifying therapies that are taken on a long-term basis. They offer the best defense available to slow down the natural course of multiple sclerosis.

    The goals of disease-modifying therapy are to:

    Reduce the frequency and severity of MS exacerbations
    Reduce the accumulation of brain and spinal lesions seen on MRI
    Slow down the accumulation of disabilities

    The selection of a particular medication is based on several factors, including a person’s response to previous treatments, clinical judgement of your physician, and personal preferences.

    It is important to keep in mind that none of these medications offer a cure for MS, nor will they prevent recurring MS symptoms, such as fatigue. However, all of them have proven records of partial to substantial success.

    The diseae modifying injections are administered through different routes on different schedules.

    Avonex® (interferon beta-1a). Administered via injection into the muscle (intramuscularly) once a week
    Betaseron® (interferon beta-1b). Administered via injection under the skin (subcutaneously) every other day.
    Copaxone® (glatiramer acetate), Administered via injection under the skin (subcutaneously) every day.
    Extavia® (interferon beta-1b). Administered via injection under the skin (subcutaneously) every other day.
    Gilenya (fingolimod). Taken by mouth once per day.
    Rebif® (interferon beta-1a), Administered via injection under the skin (subcutaneously) three times a week.
    Tysabri® (natalizumab), Administered through IV infusion in a registered infusion facility every four weeks.
    Novantrone® (Mitoxantrone), Administered through IV infusion four times a year in a medical facility. Lifetime cumulative dose limit of approximately 8-12 doses over 2-3 years.

    The four interferon medications (Avonex, Betaseron, Extavia and Rebif) can cause flu-like symptoms following injection. These might include fever, chills, sweating, muscle aches, fatigue, depression, and injection site reactions. For many people, these symptoms lessen over time. If you experience unacceptable side effects, you should discuss possible changes to another medication with your physician.
    Treating multiple sclerosis attacks

    An MS attack or flare is defined as a worsening of symptoms that lasts more than 24 hours and is separated from a previous attack by at least 30 days. These may occur even while a person is taking a disease-modifying therapy.

    Most attacks last from a few days to several weeks or even months. A particular attack can be mild, moderate or severe enough to interfere with a person’s ability to function at home and at work.

    Severe exacerbations may be treated with high-dose corticosteroids to reduce the degree of inflammation.
    Treating multiple sclerosis symptoms

    There are a variety of specific treatments available that may provide relief for the specific symptoms of MS. Your doctor will recommend medications, assistive devices and other therapies according to the symptom, its severity, and the response to past treatments.

    For instance, spasticity may be treated in different ways depending on its severity and duration. Oral anti-spasmodics, such as Zanaflex, may provide relief for patients with mild, early spasticity. More severe or long-lasting spasticity may require use of botulinum toxin, or intrathecal baclofen.
    Promoting Function through Rehabilitation

    Rehabilitation programs focus on function. They are designed to help you improve or maintain your ability to perform effectively and safely at home and at work. Rehabilitation professionals focus on overall fitness and energy management, while addressing problems with accessibility and mobility, speech and swallowing, and memory and other cognitive functions.

    Rehabilitation is an important component of comprehensive, quality health care for people with MS, at all stages of the disease. Rehabilitation programs include:

    Physical Therapy
    Occupational Therapy
    Therapy for Speech and Swallowing Problems
    Cognitive Rehabilitation
    Vocational Rehabilitation

    Alternative therapies for multiple sclerosis

    Many people with multiple sclerosis will consider trying one or more alternative treatments to help manage the disease or its symptoms.

    This is understandable since there is no universally effective treatment and no known cause. However, MS has a natural tendency to improve spontaneously between flares. These episodes of improvements can be inappropriately credited to the alternative treatment. This opens the door to a variety of unsubstantiated claims.

    At one time or another, many ineffective and even potentially dangerous therapies have been promoted as treatments for multiples sclerosis. A partial list of these “therapies” includes: injections of snake venom, removal of the thymus gland, breathing pressurized (hyperbaric) oxygen in a special chamber, intravenous or oral calcium orotate (calcium EAP), removal of dental fillings containing silver or mercury amalgams, and surgical implantation of pig brain into the patient’s abdomen. None of these treatments is an effective therapy for multiple sclerosis or any of its symptoms.

  • Carpal tunnel syndrome

    Carpal tunnel syndrome occurs when the median nerve becomes squeezed within the wrist. The median nerve runs from the forearm into the hand. It senses touch on the palm side of hand, on the portion near the thumb and index finger, but not the little finger. It also controls the muscle that allow the forefinger and thumb to move.

    The “carpal tunnel” is a a narrow space near the wrist that tendons and the median nerve pass through to reach the hand. The tunnel is lined by ligaments and bone.

    Sometimes, the tunnel becomes narrow as a result of thickening from irritated tendons or other swelling. This narrowing causes the median nerve to become compressed.

    Carpal tunnel syndrome is the most common form of “entrapment neuropathy” in which the body’s peripheral nerves are compressed or traumatized.
    What are the symptoms of carpal tunnel syndrome?

    The classic symptoms of carpal tunnel syndrome are pain, tingling, weakness, or numbness in the hand and wrist, extending up the arm.

    Symptoms usually start slowly, with frequent burning, tingling, or itching numbness in the palm of the hand and the fingers. The symptoms are usually most prominent in the thumb, index finger and middle fingers. Some carpal tunnel sufferers say their fingers feel useless and swollen, even though little or no swelling is apparent.

    The symptoms may appear in one or both hands during the night, since many people sleep with flexed wrists. A person with carpal tunnel syndrome may wake up feeling the need to “shake out” the hand or wrist. As symptoms worsen, people might feel tingling during the day.

    Decreased grip strength may make it difficult to form a fist, grasp small objects, or perform other manual tasks. In chronic and/or untreated cases, the muscles at the base of the thumb may waste away. Some people are unable to tell between hot and cold by touch.

    Writer’s cramp is an ache and lack of muscle coordination in the fingers and wrist as a result of repetitive writing. Writer’s cramp is not a symptom of carpal tunnel syndrome.
    What are the causes of carpal tunnel syndrome?

    Carpal tunnel syndrome is usually the result of a combination of factors put pressure on the median nerve within the carpal tunnel. Some people have a carpal tunnel that is simply smaller in some people than in others. Other factors include injury to the wrist that causes swelling, such as a sprain, repetitive stress injury or fracture.

    There is little clinical data to prove whether repetitive and forceful movements of the hand and wrist during work or leisure activities can cause carpal tunnel syndrome. Repeated motions performed in the course of normal work or other daily activities can result in repetitive motion disorders such as bursitis and tendonitis.

    Medical conditions that are less commonly associate with carpal tunnel syndrome include; hypothyroidism, rheumatoid arthritis, fluid retention during pregnancy or menopause; or the development of a cyst or tumor in the canal.

    In some cases no cause of carpal tunne syndrome can be found.
    How is carpal tunnel syndrome diagnosed?

    A physical examination of the hands, arms, shoulders, and neck can help determine if the symptoms are the result of an underlying disorder. Routine laboratory tests and X-rays may reveal diabetes, arthritis, and fractures.

    The Tinel test may be performed during which the doctor taps on or presses on the median nerve in the patient’s wrist. The test is positive when tingling in the fingers or a resultant shock-like sensation occurs.

    The Phalen, or wrist-flexion test involves having the patient hold his or her forearms upright by pointing the fingers down and pressing the backs of the hands together. The presence of carpal tunnel syndrome is suggested if one or more symptoms, such as tingling or increasing numbness, is felt in the fingers within 1 minute.

    Often it is necessary to confirm the diagnosis by use of electrodiagnostic tests. In a nerve conduction study, electrodes are placed on the hand and wrist. Small electric shocks are applied and the speed with which nerves transmit impulses is measured. In electromyography, a fine needle is inserted into a muscle; electrical activity viewed on a screen can determine the severity of damage to the median nerve.

    Ultrasound imaging can show impaired movement of the median nerve. Magnetic resonance imaging (MRI) can show the anatomy of the wrist but to date has not been especially useful in diagnosing carpal tunnel syndrome.
    How is carpal tunnel syndrome treated?

    Early treatment of carpal tunnel syndrome are important to avoid permanent damage to the median nerve.

    Initial treatment generally involves resting the affected hand and wrist for at least 2 weeks, avoiding activities that may worsen symptoms, and immobilizing the wrist in a splint to avoid further damage from twisting or bending. If there is inflammation, applying cool packs can help reduce swelling.

    Underlying disorders, such as diabetes or arthritis, must also be treated.

    Medications

    Some medications may be prescribed to ease the pain and swelling associated with carpal tunnel syndrome.

    Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, ibuprofen, and other nonprescription pain relievers, may ease symptoms that have been present for a short time or have been caused by strenuous activity.

    Orally administered diuretics (“water pills”) can decrease swelling. Corticosteroids (such as prednisone) or the drug lidocaine can be injected directly into the wrist or taken by mouth (in the case of prednisone) to relieve pressure on the median nerve and provide immediate, temporary relief to persons with mild or intermittent symptoms.

    Additionally, some studies show that vitamin B6 (pyridoxine) supplements may ease the symptoms of carpal tunnel syndrome.

    Exercise

    Stretching and strengthening exercises can be helpful in people whose symptoms have abated. These exercises may be supervised by a physical therapist, who is trained to use exercises to treat physical impairments, or an occupational therapist, who is trained in evaluating people with physical impairments and helping them build skills to improve their health and well-being.

    Surgery

    Carpal tunnel release is one of the most common surgical procedures. It involves severing the band of tissue around the wrist to reduce pressure on the median nerve. Surgery may be recommended if symptoms last for 6 months or longer. Surgery is done under local anesthesia and does not require an overnight hospital stay. Many patients require surgery on both hands.

    The following are types of carpal tunnel release surgery:

    Open release surgery, the traditional procedure used to correct carpal tunnel syndrome, consists of making an incision up to 2 inches in the wrist and then cutting the carpal ligament to enlarge the carpal tunnel. The procedure is generally done under local anesthesia on an outpatient basis, unless there are unusual medical considerations.
    Endoscopic surgery may allow faster functional recovery and less postoperative discomfort than traditional open release surgery. The surgeon makes two incisions (about ½” each) in the wrist and palm, inserts a camera attached to a tube, observes the tissue on a screen, and cuts the carpal ligament (the tissue that holds joints together). This two-portal endoscopic surgery, generally performed under local anesthesia, is effective and minimizes scarring and scar tenderness, if any. One-portal endoscopic surgery for carpal tunnel syndrome is also available.

    Although symptoms may be relieved immediately after surgery, full recovery from carpal tunnel surgery can take months. Some patients may have infection, nerve damage, stiffness, and pain at the scar. Occasionally the wrist loses strength because the carpal ligament is cut. Patients should undergo physical therapy after surgery to restore wrist strength. Some patients may need to adjust job duties or even change jobs after recovery from surgery.

    Recurrence of carpal tunnel syndrome following treatment is rare. The majority of patients recover completely.

    Alternative Therapies

    Acupuncture and chiropractic care have benefited some patients but their effectiveness remains unproved. An exception is yoga, which has been shown to reduce pain and improve grip strength among patients with carpal tunnel syndrome.
    Who is at risk of developing carpal tunnel syndrome?

    Carpal tunnel syndrome usually occurs only in adults. Women are three times more likely than men to develop carpal tunnel syndrome. This may be due to the carpal tunnel itself being smaller in women than in men. A person’s dominant handout (right or left) is usually affected first and produces the most severe pain.

    People with diabetes or other metabolic disorders are at greater risk of developing symptoms.

    The risk of developing carpal tunnel syndrome is not confined to people in a single industry or job, but is especially common in those performing routine manual labor, including manufacturing, sewing, finishing, cleaning, and meat, poultry, or fish packing. Carpal tunnel syndrome is three times more common among assembly line workers than among data-entry personnel who use computers.

    A 2001 study by the Mayo Clinic found heavy computer use (up to 7 hours a day) did not increase a person’s risk of developing carpal tunnel syndrome.

    An estimated three of every 10,000 workers lost time from work because of carpal tunnel syndrome. Half of these workers missed more than 10 days of work.
    How can carpal tunnel syndrome be prevented?

    At the workplace, workers can do on-the-job conditioning, perform stretching exercises, take frequent rest breaks, wear splints to keep wrists straight, and use correct posture and wrist position. Wearing fingerless gloves can help keep hands warm and flexible.

    Workstations, tools and tool handles, and tasks can be redesigned to enable the worker’s wrist to maintain a natural position during work. Jobs can be rotated among workers. Employers can develop programs in ergonomics, the process of adapting workplace conditions and job demands to the capabilities of workers. However, research has not conclusively shown that these workplace changes prevent the occurrence of carpal tunnel syndrome.

  • Fibromyalgia (FMS)

    Fibromyalgia (FMS) is a common and chronic disorder with three main symptoms.

    widespread muscle pain
    fatigue
    multiple tender points

    Although fibromyalgia is often considered to be related to arthritis, it is not truly a form of arthritis (a disease of the joints) because it does not cause inflammation or damage to the joints, muscles, or other tissues. Like arthritis, however, fibromyalgia can cause significant pain and fatigue, and it can interfere with a person’s ability to carry on daily activities.

    In addition to pain and fatigue, people who have fibromyalgia may experience:

    Sleep disturbances
    Morning stiffness
    Headaches
    Irritable Bowel Syndrome (IBS)
    Painful menstrual periods
    Numbness or tingling of the extremities
    Restless legs syndrome (RLS)
    Temperature sensitivity
    Cognitive and memory problems (sometimes referred to as “fibro fog”)

    Fibromyalgia Tender points

    Symptoms vary widely among individuals and tend to wax and wane over time. An illness, injury, cold weather or emotional stress may trigger a fibromyalgia episode or make ongoing symptoms worse. (See Fibromyalgia Symptoms)

    In medical terms, fibromyalgia is referred to as a “syndrome”, not as a “disease”, because its cause remains unknown. A syndrome is a collection of symptoms (what the patient feels) and signs (abnormalities detected by a physician) that tend to appear together. Of course, no matter how the symptoms are classified, they can severely impact a person’s life.
    Who Gets Fibromyalgia?

    After rheumatoid arthritis and osteoarthritis, fibromyalgia is the most common rheumatological diagnosis.

    Fibromyalgia affects as many as one in 50 Americans. For unknown reasons, between 80 and 90 percent of those diagnosed with fibromyalgia are women. However, men and children also can be affected. Most people are diagnosed during middle age, although the symptoms often present earlier in life.

    See Who Gets Fibromyalgia
    How Is Fibromyalgia Diagnosed?

    It often takes many doctor visits before someone is diagnosed with fibromylagia. The diagnosis of fibromyalgia can take months or even years because the main symptoms, pain and fatigue, overlap with many other medical conditions. Therefore, doctors have to rule out other possible causes of these symptoms before making a diagnosis of fibromyalgia. Another reason that diagnosis may be delayed is that there are currently no laboratory tests for fibromyalgia. Standard tests cannot yet reveal the reason for pain.

    A doctor familiar with fibromyalgia, can make a diagnosis based on two criteria:

    A history of widespread pain lasting more than 3 months. Pain is considered to be widespread when it affects all four quadrants of the body; that is, you must have pain in both your right and left sides as well as above and below the waist to be diagnosed with fibromyalgia.
    The presence of tender points. 18 sites on the body have been designated as possible tender points. For a fibromyalgia diagnosis, a person must have 11 or more tender points. One of these predesignated sites is considered a true tender point only if the person feels pain (not just tenderness) upon the application of 4 kilograms of pressure to the site. People who have fibromyalgia certainly may feel pain at other sites, too, but those 18 standard possible sites on the body are the criteria used for classification.

    What Causes Fibromyalgia?

    The cause of fibromyalgia remains unknown.

    Identifying a single abnormality as a cause is difficult, in part, because fibromyalgia comprises a range of symptoms, including widespread muscle pain, fatigue and abnormal sleep patterns. These varied symptoms cannot be explained by any single factor.

    Another difficulty is that fibromyalgia may not be caused by an external factor but instead may be an underlying abnormality unmasked by any one of a number of triggers. Triggers can include a flu-like illness or a traumatic event, such as divorce, an auto accident or the death of a spouse.

    In the past, symptoms of fibromyalgia were labeled as “fibrositis” or “muscular rheumatism”. These diagnostic terms were based on incorrect assumptions about the cause being located within the muscle fiber, or related to arthritis (a disease of the joints). Like arthritis, fibromyalgia can cause significant pain and fatigue, and it can interfere with a person’s ability to carry on daily activities. However it does not cause inflammation or damage to the joints, muscles, or other tissues.

    Today most research on the cause of fibromyalgia is focused on how the central nervous system (the brain and spinal cord) processes pain.
    How Is Fibromyalgia Treated?

    There is presently no cure for fibromyalgia, but there are several treatments available that can help to reduce the pain and fatigue and bring other symptoms under control, leading to a more active life.

    In treating fibromyalgia, most physicians combine medications with non-pharmacologic treatments, such as maintaining a healthy sleep and exercise regimen. The importance of getting sufficient sleep and exercise cannot be overlooked.

    Several interventions, such as exercise and acupuncture, can help alleviate fibromyalgia symptoms without any medications.

    No single therapy stands out as the most effective because comparative studies have not been done. These alternative therapies–whether hypnosis or biofeedback, exercise or acupuncture–require your willingness to incorporate them into daily life. For instance, to truly benefit from fitness training, you must exercise at least three times a week. If you stop exercising after three or six months, you will lose any ground gained.

    Because of the commitment required, select a therapy that fits into your schedule, appeals to your understanding of fibromyalgia, is reasonably priced, and takes advantage of community resources such as specialized healthcare providers.

    Realize that a new therapy may take time to work; stick with the it. If your symptoms have not improved within a reasonable trial period, even three to four months, discuss the problem with the person who is overseeing your therapy. There may be ways they can help you maximize the benefits.

    Keep in mind, though, that you are the best judge of “effectiveness.” What helps someone else may not help you. Once you have allowed enough time for a treatment to prove itself, think about its impact on you. Be critical of therapies that do not make you feel better, especially if the person recommending the treatment benefits financially from your continued use of it.

    People with fibromyalgia also may benefit from a combination of physical and occupational therapy, from learning pain-management and coping techniques, and from properly balancing rest and activity.
    Medications for Fibromyalgia

    There are now several FDA-approved medications for the treatment of fibromyalgia that have been shown to be effective at reducing pain and improving function.

    Cymbalta® (duloxetine)
    Lyrica® (pregabalin)
    Savella® (milnacipran)

    Your doctor may prescribe one of these medications to help get fibromyalgia symptoms under control.

    Other medications may also be prescribed to bring specific symptoms under control.

    Nonsteroidal Anti-Inflammatory Drugs (NSAIDs). As their name implies, nonsteroidal anti-inflammatory drugs, including aspirin, ibuprofen (Advil®, Motrin®), and naproxen sodium (Anaprox®, Aleve®), are used to treat inflammation. Although inflammation is not a symptom of fibromyalgia, NSAIDs also relieve pain. The drugs work by inhibiting substances in the body called prostaglandins, which play a role in pain and inflammation. These medications, some of which are available without a prescription, may help ease the muscle aches of fibromyalgia. They may also relieve menstrual cramps and the headaches often associated with fibromyalgia.

    Antidepressants. Perhaps the most useful medications for fibromyalgia are several in the antidepressant class. Antidepressants elevate the levels of certain chemicals in the brain, including serotonin and norepinephrine (which was formerly called adrenaline). Low levels of these chemicals are associated not only with depression, but also with pain and fatigue. Increasing the levels of these chemicals can reduce pain in people who have fibromyalgia.

    Tricyclic antidepressants—When taken at bedtime in dosages lower than those used to treat depression, tricyclic antidepressants can help promote restorative sleep in people with fibromyalgia. They also can relax painful muscles and heighten the effects of the body’s natural pain-killing substances called endorphins.Tricyclic antidepressants have been around for almost half a century. Some examples of tricyclic medications used to treat fibromyalgia include amitriptyline (Elavil®), cyclobenzaprine (Flexeril®), doxepin (Sinequan®), and nortriptyline (Pamelor®). Both amitriptyline and cyclobenzaprine have been shown to be effective for the treatment of fibromyalgia.
    Selective serotonin reuptake inhibitors (SSRIs)—If a tricyclic antidepressant fails to bring relief, doctors sometimes prescribe a newer type of antidepressant called a selective serotonin reuptake inhibitor (SSRI). As with tricyclics, doctors usually prescribe these for people with fibromyalgia in lower dosages than are used to treat depression. By promoting the release of serotonin, these drugs may reduce fatigue and some other symptoms associated with fibromyalgia. The group of SSRIs includes fluoxetine (Prozac®), paroxetine (Paxil®), and sertraline (Zoloft®). SSRIs may be prescribed along with a tricyclic antidepressant. Because they make people feel more energetic, they also interfere with sleep, which often is already a problem for people with fibromyalgia. Studies have shown that a combination therapy of the tricyclic amitriptyline and the SSRI fluoxetine resulted in greater improvements in the study participants’ fibromyalgia symptoms than either drug alone.
    Mixed reuptake inhibitors—Some newer antidepressants raise levels of both serotonin and norepinephrine, and are therefore called mixed reuptake inhibitors. Examples of these medications include venlafaxine (Effexor®) and nefazadone (Serzone®).

    Benzodiazepines. Benzodiazepines help some people with fibromyalgia by relaxing tense, painful muscles and stabilizing the erratic brain waves that can interfere with deep sleep. Benzodiazepines also can relieve the symptoms of restless legs syndrome, which is common among people with fibromyalgia. Restless legs syndrome is characterized by unpleasant sensations in the legs as well as twitching, particularly at night. Because of the potential for addiction, doctors usually prescribe benzodiazepines only for people who have not responded to other therapies. Benzodiazepines include clonazepam (Klonopin®) and diazepam (Valium®).

    Other medications. Doctor may prescribe others medication depending on a person’s specific symptoms or fibromyalgia-related conditions. For example, tegaserod (Zelnorm®) and alosetron (Lotronex®) have been approved by the FDA for the treatment of irritable bowel syndrome which many people with fibromyalgia may also experience. Other symptom-specific medications include sleep medications, muscle relaxants, and headache treatments.
    Will Fibromyalgia Get Better With Time?

    Fibromyalgia is a chronic condition, meaning it lasts a long time — possibly a lifetime. However, it may comfort you to know that fibromyalgia is not a progressive disease. It is never fatal, and it won’t cause damage to your joints, muscles, or internal organs. In many people, the condition does improve over time.

 

 

This information is intended for educational and informational purposes only. It should not be used in place of an individual consultation or examination or replace the advice of your health care professional and should not be relied upon to determine diagnosis or course of treatment.