View clinical trials related to Disease.
Filter by:Bacteria carry substances on their surface called antigens. When antigens come into contact with the right kinds of cells in the body an immune reaction is caused. This reaction is often the symptoms of sickness that a patient feels. In order for the body to fight off the attack of antigens, it creates substances called antibodies. Antibodies counter the action of antigens and make the bacteria harmless. However, the immune system must learn how to make the right antibodies for the right antigens. Sometimes the body creates antibodies that confuse normal tissues as foreign and attack them. This is called an autoimmune reaction and sometimes occurs when the body is exposed to certain bacteria. One bacteria known for causing autoimmune reactions is Group A beta-hemolytic Streptococcus (GABHS). This bacteria often causes throat infections commonly known as "strep throat". Some researchers believe that the autoimmune reaction associated with strep throat infections may cause neuropsychiatric disorders, like obsessive-compulsive disorder and/or tic disorder in children. As a result, each time a child with one of these disorders experiences an infection with GABHS his/her symptoms can reoccur or worsen. Researchers believe that by giving patients a certain antibiotic, they can prevent GABHS infection and thus prevent the return of symptoms. This study is designed to test the effectiveness of the antibiotic Amoxicillin for the treatment of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS). Patients will receive Amoxicillin for six weeks and placebos "inactive sugar pills" for six weeks in order to see if the medication is truly working. Effectiveness of the treatment will be based on the presence or absence of symptoms. If at the end of the study Amoxicillin is proven to be effective treatment for PANDAS patients may be offered the opportunity to continue taking the medication for an additional six months.
The purpose the study is to determine the genetic causes of specific voice disorders that run in families. Researchers are particularly interested in two conditions; 1. Spasmodic dysphonia 2. Vocal fold paralysis Familial vocal fold paralysis can be a life-threatening disorder that can cause difficulty with vocal fold movement for breathing and voice and sometimes for swallowing. Studies are ongoing at the NIH to better understand the pathophysiology and to relate it to the genetic pattern of inheritance. Families are being recruited to participate in these studies and are being provided with further information on the disorder and genetic counseling if desired. Physician referral is requested for affected members of families with vocal fold paralysis of an unknown cause occurring over at least 2 generations. All travel, lodging, examination and counseling costs are covered for both affected and unaffected members of a family. Examinations include: voice, laryngeal, neurological, electrodiagnostic testing, genetic counseling, and radiological studies....
According to studies, speech disorders with unknown causes (idiopathic) affect approximately 5% of the population at some point in their life. Some of these disorders like, stuttering and cluttering, are known for being detected early, during speech development. Stuttering is characterized by sound and syllable repetitions and consonant/vowel prolongations. When stuttering is moderate to severe, it can interfere with a person's job and social activities. Speech articulation disorders are characterized by omissions, or substitutions of speech sounds. The speech of a person who clutters is often difficult to understand. People are often unaware of the errors they make when speaking causing treatment of the condition to be very difficult. The purpose of this research is to study an extended family whose members exhibit a pure form of speech articulation disorders In addition, the study will use data and information gathered from the study and use it to develop guidelines (criteria) for defining and differentiating patients with speech disorders.
The purpose of this study is to identify genes that affect susceptibility to obsessive-compulsive disorder (OCD). By identifying genes that increase or decrease the risk of OCD, researchers can better understand how the condition develops and ultimately improve treatment for people with OCD. OCD is a severe, familial condition that affects approximately 2% of the population. The way OCD is inherited is not clearly understood, but researchers believe it is complex and involves multiple genes. This study will detect and localize genes that increase or decrease susceptibility to OCD. The data collected from this study will be combined with data from other research studies to determine gene linkage and association.
This study is designed to evaluate repetitive transcranial magnetic stimulation (rTMS) as a potential treatment for depression. In rTMS, a rapidly changing magnetic field passes through your scalp and skull and generates a small electrical pulses in your brain. rTMS at lower intensities has helped some people with depression but we do not know what the results will be in your case using higher intensities, or whether you will be randomized to 3 weeks of high frequency (20 cycles er second), low frequency (1 cycle per second), or inactive (sham)rTMS. You will be assigned to receive one of these types of rTMS over the left front art of your brain five times per week for the three weeks. Each rTMS treatment session should take between 20-30 minutes of actual stimulation, but weekly ratings, memory testing, and blood sampling may require several hours per week. We will also ask you to have brain imaging procedures to see if these will predict response to high vs. low frequency rTMS. If you are randomized to the 3 weeks of sham rTMS, you will have the opportunity to receive one of the active stimulation frequencies for an additional 3 weeks. Responders to any phase will be offered an additional month of rTMS prior to study termination and recommendations of alternative treatments.
The purpose of this study is to improve the understanding of the genetic causes of specific neurologic and psychiatric disorders. The study will focus on conditions of mental retardation, childhood onset schizophrenia, attention deficit hyperactivity disorder (ADHD), atypical psychosis of childhood, and bipolar affective disorder. The study addresses the belief that there may be several genes contributing to the illness. Researchers intend to use several molecular genetic techniques in order to identify the areas of chromosomes containing genes responsible for the development of these disorders. Patients will be selected to participate in this study based on an early age of onset of their condition as well as the severity of the illness and the frequency of the illness among family members. Researchers will collect DNA samples from patients as well as affected and unaffected family members of each patient. The DNA samples collected will be analyzed for a variety of genetic abnormalities including; triplet repeat expansions, chromosome rearrangements, and polymorphisms.
Dehydroepiandrosterone (DHEA) is a hormone produced by the adrenal gland. As humans grow older the levels of DHEA naturally decrease. Low levels of DHEA have been associated with a variety of harmful effects, including increased heart disease, decreased immune system function, decreased bone density (osteoporosis), high cholesterol, and increased fat to muscle ratio. Blood levels of DHEA and its sulfate form, DHEA-S, begin dropping when humans are in their 20's. By the time humans are in their 40's and 50's, levels of DHEA and DHEA-S levels are at 50% of their peak. Previous studies have shown that levels of these hormones are associated with feelings of "well-being" and enjoyment of "leisure" activities. In this study researchers are interested in the effects on mood and behavior of DHEA in men and women with mid-life related mood disorders. Specifically, researchers would like to find out if increasing levels of DHEA will lessen the symptoms associated with these disorders.
This study will compare the effectiveness of relatively new antidepressants which have different mechanisms of action. Buproprion (Wellbutrin) works on dopamine and the dopaminergic pathway. Sertraline (Zoloft) works as a selective serotonin reuptake inhibitor (SSRI). Venlafaxine (Effexor) works as a mixed serotonin, norepinephrine, and dopamine reuptake inhibitor. Subjects enrolled in this study will be patients diagnosed with a bipolar disorder who are presently taking medication to prevent the symptoms of the disease (prophylactic treatment), but have had breakthrough episodes of depression despite taking their medication. Patients will receive any one of the three antidepressant medications as noted above plus a placebo inactive sugar pill, in order to mask which antidepressant is being prescribed) in addition to their regular medication for bipolar disorder. All of the doses will be calculated as effective for the treatment of a unipolar major depressive disorder. The patient will continue receiving the medication for ten weeks. The effectiveness of the drug treatment will be measured by using three different scales; 1. Inventory for Depressive Symptoms - Clinicians form (IDS-C) 2. Clinical Global Impression scale(CGI-BP) 3. Life Charting Methodology (LCM) Patients who do not respond to their medication within ten weeks from the beginning of the study will be considered as non-responders and be offered the opportunity to start the study again, taking one of the two remaining medications. For example, if a patient was assigned to take Wellbutrin but it was ineffective, he/she could re-enter the study and be given either Zoloft or Effexor. Patients that do respond in the first ten weeks of the study will be eligible to continue taking the medication for one year to assess the long term effectiveness of the drug on preventing episodes of depression and to assess for any possible differential induction of mania.
This clinical study compares the effectiveness of two anticonvulsants Lamotrigine (Lamictal) Monotherapy and Gabapentin (Neurontin) in patients with treatment resistant affective disorders. We initially have found that the response rate to lamotrigine (51%) exceeded that of gabapentin (28%) or placebo (21%). In this study the placebo phase has been dropped so that we examine possible clinical and biological factors predictors of response. The drugs will be given in a randomized order for six weeks each and you will not know when you are on a given one. There will be a 2-4 week "washout" period between treatments. If you respond well to one of these treatments, a longer open continuation period will be offered at the end of this study. This would involve one or both drugs in combination. A variety of rating scales and brain imaging procedures will also be offered before and during each drug evaluation. Both lamotrigine and gabapentin are generally well tolerated. A serious potentially life threatening rash occurs in about 1/500 patients treated with lamotrigine, however. Common side effects are rash, dizziness, unsteadiness, double vision, blurred vision, nausea, vomiting, insomnia, sedation, and headache. These side effects are usually mild, and resolve with continued time on the drug or a decrease in dosage.
The purpose of this study is to evaluate people with mild memory problems, those with dementia, those at risk for developing Alzheimer's disease (AD), and healthy volunteers to identify markers of AD before the changes that occur with the disease begin. The origin and markers of progression for Alzheimer's disease (AD) are relatively obscure. Despite increased understanding of the underlying biology of AD, its clinical diagnosis is still made only after progressive cognitive decline; definitive diagnosis is confirmed at autopsy. This study will examine biomarker changes over time in a distinct cohort of people with an increased risk of developing AD. The study will also identify and track biological changes that occur with progressive dementia and compare those changes to the known cognitive and emotional disturbances that characterize AD. Individuals with a first-degree relative with AD will be recruited into an at-risk cohort. They will be followed and compared to a group of healthy volunteers for a minimum of 8 years.