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What are the symptoms of Radio-ulnar synostosis type 2 ?
What are the signs and symptoms of Radio-ulnar synostosis type 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Radio-ulnar synostosis type 2. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal dominant inheritance - Dislocated radial head - Limited elbow extension - Radioulnar synostosis - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What are the symptoms of Fanconi renotubular syndrome ?
What are the signs and symptoms of Fanconi renotubular syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Fanconi renotubular syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal dominant inheritance - Glycosuria - Hypokalemia - Hypophosphatemia - Lacticaciduria - Muscle weakness - Osteomalacia - Proteinuria - Renal insufficiency - Renal tubular dysfunction - Rickets - Short stature - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What are the symptoms of Malignant hyperthermia susceptibility type 3 ?
What are the signs and symptoms of Malignant hyperthermia susceptibility type 3? The Human Phenotype Ontology provides the following list of signs and symptoms for Malignant hyperthermia susceptibility type 3. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Alcohol-induced rhabdomyolysis - Anesthetic-induced rhabdomylosis - Elevated serum creatine phosphokinase - Exercise-induced rhabdomyolysis - Fever - Heterogeneous - Hyperkalemia - Hyperphosphatemia - Hypertonia - Lactic acidosis - Malignant hyperthermia - Myopathy - Viral infection-induced rhabdomyolysis - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is (are) Prune belly syndrome ?
Prune belly syndrome, also called Eagle-Barrett syndrome, is a condition characterized by three main features: (1) a lack of abdominal muscles, causing the skin on the belly area to wrinkle and appear "prune-like"; (2) undescended testicles in males; and (3) urinary tract problems. The incidence of prune belly syndrome (PBS) is 1 in 40,000 births; 95% of cases occur in boys. The severity of symptoms in infants with prune belly syndrome can vary greatly from child to child. At one end of the spectrum, the condition may cause severe urogenital and pulmonary problems incompatible with life (resulting in stillbirth); at the other end of the spectrum, the condition may cause few, if any, urological abnormalities that require no treatment other than undescended testicle repair in males. The cause of the condition is unknown.
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What to do for High Blood Pressure and Kidney Disease ?
- Blood pressure is the force of blood pushing against blood vessel walls as the heart pumps out blood, and high blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the body. - High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys. - High blood pressure is the second leading cause of kidney failure in the United States after diabetes. - A health care provider diagnoses high blood pressure when multiple blood pressure testsoften repeated over several visits to a health care providers officeshow that a systolic blood pressure is consistently above 140 or a diastolic blood pressure is consistently above 90. - Kidney disease is diagnosed with urine and blood tests. - The best way to slow or prevent kidney damage from high blood pressure is to take steps to lower blood pressure. These steps include a combination of medication and lifestyle changes, such as - healthy eating - physical activity - maintaining a healthy weight - quitting smoking - managing stress - No matter what the cause of the kidney disease, high blood pressure can increase damage to the kidneys. People with kidney disease should keep their blood pressure below 140/90.
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What are the treatments for Bronchiectasis ?
Bronchiectasis often is treated with medicines, hydration, and chest physical therapy (CPT). Your doctor may recommend surgery if the bronchiectasis is isolated to a section of lung or you have a lot of bleeding. If the bronchiectasis is widespread and causing respiratory failure, your doctor may recommend oxygen therapy. The goals of treatment are to: Treat any underlying conditions and lung infections. Remove mucus (a slimy substance) from your lungs. Maintaining good hydration helps with mucus removal. Prevent complications. Early diagnosis and treatment of the underlying cause of bronchiectasis may help prevent further lung damage. In addition, any disease associated with the bronchiectasis, such as cystic fibrosisor immunodeficiency, also should be treated. Medicines Your doctor may prescribe antibiotics, bronchodilators, expectorants, or mucus-thinning medicines to treat bronchiectasis. Antibiotics Antibiotics are the main treatment for the repeated lung infections that bronchiectasis causes. Oral antibiotics often are used to treat these infections. For hard-to-treat infections, your doctor may prescribe intravenous (IV) antibiotics. These medicines are given through an IV line inserted into your arm. Your doctor may help you arrange for a home care provider to give you IV antibiotics at home. Expectorants and Mucus-Thinning Medicines Your doctor may prescribe expectorants and mucus thinners to help you cough up mucus. Expectorants help loosen the mucus in your lungs. They often are combined with decongestants, which may provide extra relief. Mucus thinners, such as acetylcysteine, loosen the mucus to make it easier to cough up. For some of these treatments, little information is available to show how well they work. Hydration Drinking plenty of fluid, especially water, helps prevent airway mucus from becoming thick and sticky. Good hydration helps keep airway mucus moist and slippery, which makes it easier to cough up. Chest Physical Therapy CPT also is called physiotherapy (FIZ-e-o-THER-ah-pe) or chest clapping or percussion. This technique is generally performed by a respiratory therapist but can be done by a trained member of the family. It involves the therapist pounding your chest and back over and over with his or her hands or a device. Doing this helps loosen the mucus from your lungs so you can cough it up. You can sit with your head tilted down or lie on your stomach with your head down while you do CPT. Gravity and force help drain the mucus from your lungs. Some people find CPT hard or uncomfortable to do. Several devices can help with CPT, such as: An electric chest clapper, known as a mechanical percussor. An inflatable therapy vest that uses high-frequency air waves to force mucus toward your upper airways so you can cough it up. A small handheld device that you breathe out through. It causes vibrations that dislodge the mucus. A mask that creates vibrations to help break loose mucus from your airway walls. Some of these methods and devices are popular with patients and doctors, but little information is available on how well they actually work. Choice usually is based on convenience and cost. Several breathing techniques also are used to help move mucus to the upper airway so it can be coughed up. These techniques include forced expiration technique (FET) and active cycle breathing (ACB). FET involves forcing out a couple of breaths and then doing relaxed breathing. ACB is FET that involves deep breathing exercises. Other Treatments Depending on your condition, your doctor also may recommend bronchodilators, inhaled corticosteroids, oxygen therapy, or surgery. Bronchodilators Bronchodilators relax the muscles around your airways. This helps open your airways and makes breathing easier. Most bronchodilators are inhaled medicines. You will use an inhaler or a nebulizer to breathe in a fine mist of medicine. Inhaled bronchodilators work quickly because the medicine goes straight to your lungs. Your doctor may recommend that you use a bronchodilator right before you do CPT. Inhaled Corticosteroids If you also have wheezing or asthma with your bronchiectasis, your doctor may prescribe inhaled corticosteroids (used to treat inflammation in the airways). Oxygen Therapy Oxygen therapy can help raise low blood oxygen levels. For this treatment, you'll receive oxygen through nasal prongs or a mask. Oxygen therapy can be done at home, in a hospital, or in another health facility. (For more information, go to the Health Topics Oxygen Therapy article.) Surgery Your doctor may recommend surgery if no other treatments have helped and only one part of your airway is affected. If you have major bleeding in your airway, your doctor may recommend surgery to remove part of your airway or a procedure to control the bleeding. In very rare instances of severe bronchiectasis, your doctor may recommend that you receive a lung transplant replacing your diseased lungs with a healthy set of lungs.
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What are the symptoms of Ectopic Kidney ?
An ectopic kidney may not cause any symptoms and may function normally, even though it is not in its usual position. Many people have an ectopic kidney and do not discover it until they have tests done for other reasons. Sometimes, a health care provider may discover an ectopic kidney after feeling a lump in the abdomen during an examination. In other cases, an ectopic kidney may cause abdominal pain or urinary problems.
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What are the genetic changes related to aspartylglucosaminuria ?
Mutations in the AGA gene cause aspartylglucosaminuria. The AGA gene provides instructions for producing an enzyme called aspartylglucosaminidase. This enzyme is active in lysosomes, which are structures inside cells that act as recycling centers. Within lysosomes, the enzyme helps break down complexes of sugar molecules (oligosaccharides) attached to certain proteins (glycoproteins). AGA gene mutations result in the absence or shortage of the aspartylglucosaminidase enzyme in lysosomes, preventing the normal breakdown of glycoproteins. As a result, glycoproteins can build up within the lysosomes. Excess glycoproteins disrupt the normal functions of the cell and can result in destruction of the cell. A buildup of glycoproteins seems to particularly affect nerve cells in the brain; loss of these cells causes many of the signs and symptoms of aspartylglucosaminuria.
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How many people are affected by autosomal dominant vitreoretinochoroidopathy ?
ADVIRC is considered a rare disease. Its prevalence is unknown.
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How many people are affected by SADDAN ?
This disorder is very rare; it has been described in only a small number of individuals worldwide.
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What are the symptoms of X-linked congenital stationary night blindness ?
What are the signs and symptoms of X-linked congenital stationary night blindness? The Human Phenotype Ontology provides the following list of signs and symptoms for X-linked congenital stationary night blindness. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Congenital stationary night blindness - Hemeralopia - Severe Myopia - X-linked recessive inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is (are) Freiberg's disease ?
Freiberg's disease is rare condition that primarily affects the second or third metatarsal (the long bones of the foot). Although people of all ages can be affected by this condition, Freiberg's disease is most commonly diagnosed during adolescence through the second decade of life. Common signs and symptoms include pain and stiffness in the front of the foot, which often leads to a limp. Affected people may also experience swelling, limited range of motion, and tenderness of the affected foot. Symptoms are generally triggered by weight-bearing activities, including walking. The exact underlying cause of Freiberg's disease is currently unknown. Treatment depends on many factors, including the severity of condition; the signs and symptoms present; and the age of the patient.
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What causes Ehlers-Danlos syndrome, dermatosparaxis type ?
What causes Ehlers-Danlos syndrome, dermatosparaxis type? Ehlers-Danlos syndrome (EDS), dermatosparaxis type is caused by changes (mutations) in the ADAMTS2 gene. This gene encodes an enzyme that helps process several types of "procollagen molecules" (precursors of collagen). Collagen is a protein that provides structure and strength to connective tissues throughout the body. Mutations in ADAMTS2 lead to reduced levels of functional enzyme which interferes with the proper processing of procollagens. As a result, networks of collagen are not assembled properly. This weakens connective tissues and causes the many signs and symptoms associated with EDS, dermatosparaxis type.
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What are the symptoms of Limb-girdle muscular dystrophy, type 2C ?
What are the signs and symptoms of Limb-girdle muscular dystrophy, type 2C? The Human Phenotype Ontology provides the following list of signs and symptoms for Limb-girdle muscular dystrophy, type 2C. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal recessive inheritance - Calf muscle pseudohypertrophy - Elevated serum creatine phosphokinase - Flexion contracture - Gowers sign - Hyperlordosis - Muscle fiber necrosis - Muscular dystrophy - Pneumonia - Rapidly progressive - Restrictive lung disease - Right ventricular dilatation - Right ventricular hypertrophy - Scoliosis - Skeletal muscle atrophy - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What are the treatments for progressive supranuclear palsy ?
These resources address the diagnosis or management of progressive supranuclear palsy: - Gene Review: Gene Review: MAPT-Related Disorders - Genetic Testing Registry: Progressive supranuclear ophthalmoplegia - NHS Choices (UK): Diagnosis of Progressive Supranuclear Palsy - NHS Choices (UK): Treatment of Progressive Supranuclear Palsy - Partners in Parkinson's: Movement Disorder Specialist Finder - University of California, San Francisco (UCSF) Memory and Aging Center These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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Do you have information about Cochlear Implants
Summary : A cochlear implant is a small, complex electronic device that can help to provide a sense of sound. People who are profoundly deaf or severely hard-of-hearing can get help from them. The implant consists of two parts. One part sits on the outside of the body, behind the ear. A second part is surgically placed under the skin. An implant does not restore normal hearing. It can help a person understand speech. Children and adults can benefit from them. National Institute on Deafness and Other Communication Disorders
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How to diagnose Fanconi Anemia ?
People who have Fanconi anemia (FA) are born with the disorder. They may or may not show signs or symptoms of it at birth. For this reason, FA isn't always diagnosed when a person is born. In fact, most people who have the disorder are diagnosed between the ages of 2 and 15 years. The tests used to diagnose FA depend on a person's age and symptoms. In all cases, medical and family histories are an important part of diagnosing FA. However, because FA has many of the same signs and symptoms as other diseases, only genetic testing can confirm its diagnosis. Specialists Involved A geneticist is a doctor or scientist who studies how genes work and how diseases and traits are passed from parents to children through genes. Geneticists do genetic testing for FA. They also can provide counseling about how FA is inherited and the types of prenatal (before birth) testing used to diagnose it. An obstetrician may detect birth defects linked to FA before your child is born. An obstetrician is a doctor who specializes in providing care for pregnant women. After your child is born, a pediatrician also can help find out whether your child has FA. A pediatrician is a doctor who specializes in treating children and teens. A hematologist (blood disease specialist) also may help diagnose FA. Family and Medical Histories FA is an inherited disease. Some parents are aware that their family has a medical history of FA, even if they don't have the disease. Other parents, especially if they're FA carriers, may not be aware of a family history of FA. Many parents may not know that FA can be passed from parents to children. Knowing your family medical history can help your doctor diagnose whether you or your child has FA or another condition with similar symptoms. If your doctor thinks that you, your siblings, or your children have FA, he or she may ask you detailed questions about: Any personal or family history of anemia Any surgeries youve had related to the digestive system Any personal or family history of immune disorders Your appetite, eating habits, and any medicines you take If you know your family has a history of FA, or if your answers to your doctor's questions suggest a possible diagnosis of FA, your doctor will recommend further testing. Diagnostic Tests and Procedures The signs and symptoms of FA aren't unique to the disease. They're also linked to many other diseases and conditions, such as aplastic anemia. For this reason, genetic testing is needed to confirm a diagnosis of FA. Genetic tests for FA include the following. Chromosome Breakage Test This is the most common test for FA. It's available only in special laboratories (labs). It shows whether your chromosomes (long chains of genes) break more easily than normal. Skin cells sometimes are used for the test. Usually, though, a small amount of blood is taken from a vein in your arm using a needle. A technician combines some of the blood cells with certain chemicals. If you have FA, the chromosomes in your blood sample break and rearrange when mixed with the test chemicals. This doesn't happen in the cells of people who don't have FA. Cytometric Flow Analysis Cytometric flow analysis, or CFA, is done in a lab. This test examines how chemicals affect your chromosomes as your cells grow and divide. Skin cells are used for this test. A technician mixes the skin cells with chemicals that can cause the chromosomes in the cells to act abnormally. If you have FA, your cells are much more sensitive to these chemicals. The chromosomes in your skin cells will break at a high rate during the test. This doesn't happen in the cells of people who don't have FA. Mutation Screening A mutation is an abnormal change in a gene or genes. Geneticists and other specialists can examine your genes, usually using a sample of your skin cells. With special equipment and lab processes, they can look for gene mutations that are linked to FA. Diagnosing Different Age Groups Before Birth (Prenatal) If your family has a history of FA and you get pregnant, your doctor may want to test you or your fetus for FA. Two tests can be used to diagnose FA in a developing fetus: amniocentesis (AM-ne-o-sen-TE-sis) and chorionic villus (ko-re-ON-ik VIL-us) sampling (CVS). Both tests are done in a doctor's office or hospital. Amniocentesis is done 15 to 18 weeks after a pregnant woman's last period. A doctor uses a needle to remove a small amount of fluid from the sac around the fetus. A technician tests chromosomes (chains of genes) from the fluid sample to see whether they have faulty genes associated with FA. CVS is done 10 to 12 weeks after a pregnant woman's last period. A doctor inserts a thin tube through the vagina and cervix to the placenta (the temporary organ that connects the fetus to the mother). The doctor removes a tissue sample from the placenta using gentle suction. The tissue sample is sent to a lab to be tested for genetic defects associated with FA. At Birth Three out of four people who inherit FA are born with birth defects. If your baby is born with certain birth defects, your doctor may recommend genetic testing to confirm a diagnosis of FA. For more information about these defects, go to What Are the Signs and Symptoms of Fanconi Anemia? Childhood and Later Some people who have FA are not born with birth defects. Doctors may not diagnose them with the disorder until signs of bone marrow failure or cancer occur. This usually happens within the first 10 years of life. Signs of bone marrow failure most often begin between the ages of 3 and 12 years, with 7 to 8 years as the most common ages. However, 10 percent of children who have FA aren't diagnosed until after 16 years of age. If your bone marrow is failing, you may have signs of aplastic anemia. FA is one type of aplastic anemia. In aplastic anemia, your bone marrow stops making or doesn't make enough of all three types of blood cells: red blood cells, white blood cells, and platelets. Aplastic anemia can be inherited or acquired after birth through exposure to chemicals, radiation, or medicines. Doctors diagnose aplastic anemia using: Family and medical histories and a physical exam. A complete blood count (CBC) to check the number, size, and condition of your red blood cells. The CBC also checks numbers of white blood cells and platelets. A reticulocyte (re-TIK-u-lo-site) count. This test counts the number of new red blood cells in your blood to see whether your bone marrow is making red blood cells at the proper rate. Bone marrow tests. For a bone marrow aspiration, a small amount of liquid bone marrow is removed and tested to see whether it's making enough blood cells. For a bone marrow biopsy, a small amount of bone marrow tissue is removed and tested to see whether it's making enough blood cells. If you or your child is diagnosed with aplastic anemia, your doctor will want to find the cause. If your doctor suspects you have FA, he or she may recommend genetic testing. For more information, go to the Health Topics Aplastic Anemia article.
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What is (are) Autoimmune Diseases ?
Your body's immune system protects you from disease and infection. But if you have an autoimmune disease, your immune system attacks healthy cells in your body by mistake. Autoimmune diseases can affect many parts of the body. No one is sure what causes autoimmune diseases. They do tend to run in families. Women - particularly African-American, Hispanic-American, and Native-American women - have a higher risk for some autoimmune diseases. There are more than 80 types of autoimmune diseases, and some have similar symptoms. This makes it hard for your health care provider to know if you really have one of these diseases, and if so, which one. Getting a diagnosis can be frustrating and stressful. Often, the first symptoms are fatigue, muscle aches and a low fever. The classic sign of an autoimmune disease is inflammation, which can cause redness, heat, pain and swelling. The diseases may also have flare-ups, when they get worse, and remissions, when symptoms get better or disappear. Treatment depends on the disease, but in most cases one important goal is to reduce inflammation. Sometimes doctors prescribe corticosteroids or other drugs that reduce your immune response.
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What are the symptoms of Polyglucosan body disease, adult ?
What are the signs and symptoms of Polyglucosan body disease, adult? The Human Phenotype Ontology provides the following list of signs and symptoms for Polyglucosan body disease, adult. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal pyramidal signs 90% Abnormal renal physiology 90% Cognitive impairment 90% Erectile abnormalities 90% Gait disturbance 90% Hemiplegia/hemiparesis 90% Hypertonia 90% Muscle weakness 90% Peripheral neuropathy 90% Behavioral abnormality 50% Skin ulcer 50% Abnormality of extrapyramidal motor function 7.5% Developmental regression 7.5% EMG abnormality 7.5% Incoordination 7.5% Limitation of joint mobility 7.5% Abnormal upper motor neuron morphology - Abnormality of metabolism/homeostasis - Adult onset - Autosomal recessive inheritance - Distal sensory impairment - Paresthesia - Slow progression - Tetraparesis - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is the outlook for Tourette Syndrome ?
Although TS can be a chronic condition with symptoms lasting a lifetime, most people with the condition experience their worst symptoms in their early teens, with improvement occurring in the late teens and continuing into adulthood. As a result, some individuals may actually become symptom free or no longer need medication for tic suppression.
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How many people are affected by SOX2 anophthalmia syndrome ?
SOX2 anophthalmia syndrome is estimated to affect 1 in 250,000 individuals. About 10 percent to 15 percent of people with anophthalmia in both eyes have SOX2 anophthalmia syndrome.
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How to diagnose Urinary Incontinence ?
The first step in treating urinary incontinence is to see a health care provider. He or she will give you a physical exam and take your medical history. The provider will ask about your symptoms and the medicines you use. He or she will want to know if you have been sick recently or have had surgery. Your provider also may do a number of tests. These might include - urine tests - tests that measure how well you empty your bladder, usually by ultrasound. urine tests tests that measure how well you empty your bladder, usually by ultrasound. In addition, your health care provider may ask you to keep a daily diary of when you urinate and when you leak urine. Your family provider may also send you to a urologist or urogynecologist, a doctor who specializes in urinary tract problems. Learn more about how urinary incontinence is diagnosed in men and women.
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What is (are) Stroke ?
One test that helps doctors judge the severity of a stroke is the standardized NIH Stroke Scale, developed by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health, or NIH. Health care professionals use the NIH Stroke Scale to measure a patient's neurological deficits by asking the patient to answer questions and to perform several physical and mental tests. Other scales include the Glasgow Coma Scale, the Hunt and Hess Scale, the Modified Rankin Scale, and the Barthel Index.
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What are the symptoms of Spondylometaphyseal dysplasia with cone-rod dystrophy ?
What are the signs and symptoms of Spondylometaphyseal dysplasia with cone-rod dystrophy? The Human Phenotype Ontology provides the following list of signs and symptoms for Spondylometaphyseal dysplasia with cone-rod dystrophy. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of retinal pigmentation 90% Abnormality of color vision 50% Astigmatism 50% Hyperlordosis 50% Hypermetropia 50% Myopia 50% Nystagmus 50% Photophobia 50% Scoliosis 50% Visual impairment 50% Brachydactyly syndrome 7.5% Limitation of joint mobility 7.5% Abnormality of macular pigmentation - Autosomal recessive inheritance - Cone/cone-rod dystrophy - Coxa vara - Cupped ribs - Dental malocclusion - Femoral bowing - Hypoplastic inferior ilia - Joint stiffness - Metaphyseal cupping - Metaphyseal irregularity - Metaphyseal widening - Narrow greater sacrosciatic notches - Ovoid vertebral bodies - Postnatal growth retardation - Progressive visual loss - Recurrent otitis media - Rhizomelia - Severe platyspondyly - Short finger - Short metacarpal - Spondylometaphyseal dysplasia - Tibial bowing - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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How to diagnose Stenotrophomonas maltophilia infection ?
How is Stenotrophomonas maltophilia infection diagnosed? Stenotrophomonas maltophilia (S. maltophilia) infection is usually diagnosed by examining a small sample of blood, mucus, and/or urine. When an infection is suspected, possible sites of infection including wounds, intravenous (vein) catheters, urinary catheters, and breathing machines should also be tested for the presence of S. maltophilia bacteria.
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What is (are) Juvenile dermatomyositis ?
Juvenile dermatomyositis has some similarities to adult dermatomyositis and polymyositis. It typically affects children ages 2 to 15 years, with symptoms that include weakness of the muscles close to the trunk of the body, inflammation, edema, muscle pain, fatigue, skin rashes, abdominal pain, fever, and contractures. Children with juvenile dermatomyositis may have difficulty swallowing and breathing, and the heart may also be affected. About 20 to 30 percent of children with juvenile dermatomyositis develop calcium deposits in the soft tissue. Affected children may not show higher than normal levels of the muscle enzyme creatine kinase in their blood but have higher than normal levels of other muscle enzymes.
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What is the outlook for Hereditary Neuropathies ?
The prognosis for individuals with hereditary neuropathies depends upon the type of neuropathy. Some hereditary neuropathies have very mild symptoms and may go undiagnosed for many years. Other types are more severe and are associated with more disabilities. Genetic counseling is important to understand further details about the disease and prognosis.
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What is (are) Klippel Feil Syndrome ?
Klippel-Feil Syndrome is a rare disorder characterized by the congenital fusion of two or more cervical (neck) vertebrae. It is caused by a failure in the normal segmentation or division of the cervical vertebrae during the early weeks of fetal development. The most common signs of the disorder are short neck, low hairline at the back of the head, and restricted mobility of the upper spine. The fused vertebrae can cause nerve damage and pain in the head, neck, or back. Associated abnormalities may include scoliosis (curvature of the spine), spina bifida (a birth defect of the spine), cleft palate, respiratory problems, and heart malformations. Other features may include joint pain; anomalies of the head and face, skeleton, sex organs, muscles, brain and spinal cord, arms, legs, and fingers; and difficulties hearing. Most cases are sporadic (happen on their own) but mutations in the GDF6 (growth differentiation factor 6) or GDF3 (growth differentiation factor 3) genes can cause the disorder. These genes make proteins that are involved in bone development and segmentation of the vertebrae.
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What are the treatments for genitopatellar syndrome ?
These resources address the diagnosis or management of genitopatellar syndrome: - Gene Review: Gene Review: KAT6B-Related Disorders - Genetic Testing Registry: Genitopatellar syndrome These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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What is (are) congenital insensitivity to pain with anhidrosis ?
Congenital insensitivity to pain with anhidrosis (CIPA) has two characteristic features: the inability to feel pain and temperature, and decreased or absent sweating (anhidrosis). This condition is also known as hereditary sensory and autonomic neuropathy type IV. The signs and symptoms of CIPA appear early, usually at birth or during infancy, but with careful medical attention, affected individuals can live into adulthood. An inability to feel pain and temperature often leads to repeated severe injuries. Unintentional self-injury is common in people with CIPA, typically by biting the tongue, lips, or fingers, which may lead to spontaneous amputation of the affected area. In addition, people with CIPA heal slowly from skin and bone injuries. Repeated trauma can lead to chronic bone infections (osteomyelitis) or a condition called Charcot joints, in which the bones and tissue surrounding joints are destroyed. Normally, sweating helps cool the body temperature. However, in people with CIPA, anhidrosis often causes recurrent, extremely high fevers (hyperpyrexia) and seizures brought on by high temperature (febrile seizures). In addition to the characteristic features, there are other signs and symptoms of CIPA. Many affected individuals have thick, leathery skin (lichenification) on the palms of their hands or misshapen fingernails or toenails. They can also have patches on their scalp where hair does not grow (hypotrichosis). About half of people with CIPA show signs of hyperactivity or emotional instability, and many affected individuals have intellectual disability. Some people with CIPA have weak muscle tone (hypotonia) when they are young, but muscle strength and tone become more normal as they get older.
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What is (are) PDGFRA-associated chronic eosinophilic leukemia ?
PDGFRA-associated chronic eosinophilic leukemia is a form of blood cell cancer characterized by an elevated number of cells called eosinophils in the blood. These cells help fight infections by certain parasites and are involved in the inflammation associated with allergic reactions. However, these circumstances do not account for the increased number of eosinophils in PDGFRA-associated chronic eosinophilic leukemia. Another characteristic feature of PDGFRA-associated chronic eosinophilic leukemia is organ damage caused by the excess eosinophils. Eosinophils release substances to aid in the immune response, but the release of excessive amounts of these substances causes damage to one or more organs, most commonly the heart, skin, lungs, or nervous system. Eosinophil-associated organ damage can lead to a heart condition known as eosinophilic endomyocardial disease, skin rashes, coughing, difficulty breathing, swelling (edema) in the lower limbs, confusion, changes in behavior, or impaired movement or sensations. People with PDGFRA-associated chronic eosinophilic leukemia can also have an enlarged spleen (splenomegaly) and elevated levels of certain chemicals called vitamin B12 and tryptase in the blood. Some people with PDGFRA-associated chronic eosinophilic leukemia have an increased number of other types of white blood cells, such as neutrophils or mast cells. Occasionally, people with PDGFRA-associated chronic eosinophilic leukemia develop other blood cell cancers, such as acute myeloid leukemia or B-cell or T-cell acute lymphoblastic leukemia or lymphoblastic lymphoma. PDGFRA-associated chronic eosinophilic leukemia is often grouped with a related condition called hypereosinophilic syndrome. These two conditions have very similar signs and symptoms; however, the cause of hypereosinophilic syndrome is unknown.
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What is (are) Neck Injuries and Disorders ?
Any part of your neck - muscles, bones, joints, tendons, ligaments, or nerves - can cause neck problems. Neck pain is very common. Pain may also come from your shoulder, jaw, head, or upper arms. Muscle strain or tension often causes neck pain. The problem is usually overuse, such as from sitting at a computer for too long. Sometimes you can strain your neck muscles from sleeping in an awkward position or overdoing it during exercise. Falls or accidents, including car accidents, are another common cause of neck pain. Whiplash, a soft tissue injury to the neck, is also called neck sprain or strain. Treatment depends on the cause, but may include applying ice, taking pain relievers, getting physical therapy or wearing a cervical collar. You rarely need surgery.
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Do you have information about Pulmonary Rehabilitation
Summary : Pulmonary rehabilitation (rehab) is a medically supervised program to help people who have chronic breathing problems, including - COPD (chronic obstructive pulmonary disease) - Sarcoidosis - Idiopathic pulmonary fibrosis - Cystic fibrosis During pulmonary rehab you may do exercise training and learn breathing techniques. You'll also get tips on conserving your energy and advice on nutrition and coping. These can't cure your lung disease or completely ease your breathing problems. But it can help you function better in your daily life. NIH: National Heart, Lung, and Blood Institute
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What are the genetic changes related to myosin storage myopathy ?
Mutations in the MYH7 gene cause myosin storage myopathy. The MYH7 gene provides instructions for making a protein known as the cardiac beta ()-myosin heavy chain. This protein is found in heart (cardiac) muscle and in type I skeletal muscle fibers, one of two types of fibers that make up the muscles that the body uses for movement. Cardiac -myosin heavy chain is the major component of the thick filament in muscle cell structures called sarcomeres. Sarcomeres, which are made up of thick and thin filaments, are the basic units of muscle contraction. The overlapping thick and thin filaments attach to each other and release, which allows the filaments to move relative to one another so that muscles can contract. Mutations in the MYH7 gene lead to the production of an altered cardiac -myosin heavy chain protein, which is thought to be less able to form thick filaments. The altered proteins accumulate in type I skeletal muscle fibers, forming the protein clumps characteristic of the disorder. It is unclear how these changes lead to muscle weakness in people with myosin storage myopathy.
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Do you have information about Ebola
Summary : Ebola hemorrhagic fever is caused by a virus. It is a severe and often fatal disease. It can affect humans and other primates. Researchers believe that the virus first spreads from an infected animal to a human. It can then spread from human to human through direct contact with a patient's blood or secretions. Symptoms of Ebola may appear anywhere from 2 to 21 days after exposure to the virus. Symptoms usually include - Fever - Headache - Joint and muscle aches - Weakness - Diarrhea - Vomiting - Stomach pain - Lack of appetite Other symptoms including rash, red eyes, and internal and external bleeding, may also occur. The early symptoms of Ebola are similar to other, more common, diseases. This makes it difficult to diagnose Ebola in someone who has been infected for only a few days. However, if a person has the early symptoms of Ebola and there is reason to suspect Ebola, the patient should be isolated. It is also important to notify public health professionals. Lab tests can confirm whether the patient has Ebola. There is no cure for Ebola. Treatment involves supportive care such as fluids, oxygen, and treatment of complications. Some people who get Ebola are able to recover, but many do not. Centers for Disease Control and Prevention
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What is (are) Meralgia Paresthetica ?
Meralgia paresthetica is a disorder characterized by tingling, numbness, and burning pain in the outer side of the thigh. The disorder is caused by compression of the lateral femoral cutaneous nerve, a sensory nerve to the skin, as it exits the pelvis. People with the disorder often notice a patch of skin that is sensitive to touch and sometimes painful. Meralgia paresthetica should not be associated with weakness or radiating pain from the back.
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What are the symptoms of Hairy Cell Leukemia ?
Signs and symptoms of hairy cell leukemia include infections, tiredness, and pain below the ribs. These and other signs and symptoms may be caused by hairy cell leukemia or by other conditions. Check with your doctor if you have any of the following: - Weakness or feeling tired. - Fever or frequent infections. - Easy bruising or bleeding. - Shortness of breath. - Weight loss for no known reason. - Pain or a feeling of fullness below the ribs. - Painless lumps in the neck, underarm, stomach, or groin.
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What is (are) distal arthrogryposis type 1 ?
Distal arthrogryposis type 1 is a disorder characterized by joint deformities (contractures) that restrict movement in the hands and feet. The term "arthrogryposis" comes from the Greek words for joint (arthro-) and crooked or hooked (gryposis). The characteristic features of this condition include permanently bent fingers and toes (camptodactyly), overlapping fingers, and a hand deformity in which all of the fingers are angled outward toward the fifth finger (ulnar deviation). Clubfoot, which is an inward- and upward-turning foot, is also commonly seen with distal arthrogryposis type 1. The specific hand and foot abnormalities vary among affected individuals. However, this condition typically does not cause any signs and symptoms affecting other parts of the body.
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What is (are) Scoliosis ?
Scoliosis causes a sideways curve of your backbone, or spine. These curves are often S- or C-shaped. Scoliosis is most common in late childhood and the early teens, when children grow fast. Girls are more likely to have it than boys. It can run in families. Symptoms include leaning to one side and having uneven shoulders and hips. Doctors use your medical and family history, a physical exam, and imaging tests to diagnose scoliosis. Treatment depends on your age, how much more you're likely to grow, how much curving there is, and whether the curve is temporary or permanent. People with mild scoliosis might only need checkups to see if the curve is getting worse. Others might need to wear a brace or have surgery. NIH: National Institute of Arthritis and Musculoskeletal and Skin Diseases
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Is Type 1 plasminogen deficiency inherited ?
Is plasminogen deficiency, type 1 inherited? If so, in what manner? Plasminogen deficiency, type 1 is inherited in an autosomal recessive fashion, which means that an individual must inherit two disease-causing mutated copies of the plasminogen gene in order to have the condition and exhibit symptoms.
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Is Nicolaides-Baraitser syndrome inherited ?
How is Nicolaides-Baraitser syndrome inherited? Nicolaides-Baraitser syndrome (NCBRS) is inherited in an autosomal dominant manner. This means that having a change (mutation) in only one of the two copies of the responsible gene in each cell is enough to cause features of the condition. All known cases of NCBRS have been sporadic. This means it is thought that the mutation occurred for the first time in each affected person (called a de novo mutation). There have not been reports of NCBRS being inherited from a parent, or recurring in any family (with the exception of one pair of identical twins).
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What are the treatments for optic atrophy type 1 ?
These resources address the diagnosis or management of optic atrophy type 1: - Gene Review: Gene Review: Optic Atrophy Type 1 - Genetic Testing Registry: Dominant hereditary optic atrophy - MedlinePlus Encyclopedia: Optic Nerve Atrophy - MedlinePlus Encyclopedia: Visual Acuity Test These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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What are the treatments for Diagnosis of Diabetes and Prediabetes ?
People can manage their diabetes with meal planning, physical activity, and if needed, medications. More information about taking care of type 1 or type 2 diabetes is provided in the NIDDK health topics: - What I need to know about Diabetes Medicines - What I need to know about Eating and Diabetes - Your Guide to Diabetes: Type 1 and Type 2 These NDIC publications are available at http://www.niddk.nih.gov/health-information/health-topics/Diabetes/Pages/default.aspx or by calling 18008608747.
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Is ataxia with oculomotor apraxia inherited ?
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
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Do you have information about Radon
Summary : You can't see radon. And you can't smell it or taste it. But it may be a problem in your home. Radon comes from the natural breakdown of uranium in soil, rock, and water. Radon is the second leading cause of lung cancer in the United States. There are low levels of radon outdoors. Indoors, there can be high levels. Radon can enter homes and buildings through cracks in floors, walls, or foundations. Radon can also be in your water, especially well water. Testing is the only way to know if your home has elevated radon levels. It is inexpensive and easy. You can buy a test kit at most hardware stores or hire someone to do a test. Radon reduction systems can bring the amount of radon down to a safe level. The cost depends on the size and design of your home.
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How to diagnose Familial isolated hyperparathyroidism ?
How is familial isolated hyperparathyroidism diagnosed? The diagnosis of familial isolated hyperparathyroidism (FIHP) is primarily a diagnosis of exclusion. This means that it is diagnosed when no symptoms or genetic features of other forms of familial hyperparathyroidism are present. FIHP may be the only feature of another condition that is not manifesting completely, or it may be a distinct condition due to mutations in genes that have not yet been identified. Clinical exams, laboratory tests, and histological (microscopic) findings are needed before making a diagnosis of FIHP. A diagnosis of FIHP may include the findings of: hypercalcemia (defined as a serum calcium level greater than 10.5 mg/dL) inappropriately high parathyroid hormone (PTH) concentrations parathyroid adenomas exclusion of multiple endocrine neoplasia type 1 (MEN 1) and hyperparathyroidism-jaw tumor syndrome (HPT-JT) In the majority of people with FIHP, genetic mutations are not found. However, in some people, mutations in the MEN1, CASR, and CDC73 (HRPT2) genes have been reported. At this time, no gene has been associated exclusively with FIHP.
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