Multiple sclerosis (MS) involves an immune-mediated process in which an abnormal response of the body’s immune system is directed against the central nervous system (CNS). The CNS is made up of the brain, spinal cord and optic nerves. Within the CNS, the immune system causes inflammation that damages myelin — the fatty substance that surrounds and insulates the nerve fibers — as well as the nerve fibers themselves, and the specialized cells that make myelin. When myelin or nerve fibers are damaged or destroyed in MS, messages within the CNS are altered or stopped completely. Damage to areas of the CNS may produce a variety of neurological symptoms that will vary among people with MS in type and severity The damaged areas develop scar tissue which gives the disease its name – multiple areas of scarring or multiple sclerosis. The cause of MS is not known, but it is believed to involve genetic susceptibility, abnormalities in the immune system and environmental factors that combine to trigger the disease. People with MS typically experience one of four disease courses. There are over a dozen treatments to help modify the MS disease process.

It sounds like you're questioning whether or not your water may have broken, and this can actually be a hard thing for a lot of women to tell. Usually if your water breaks, it's just a trickle of fluid, and you're afraid to admit it to anyone because you think you peed your pants. And it is normal to pee your pants when you're pregnant because the bladder is right below the uterus, and if the baby moves just right, it might kick out a little bit of urine. So if you feel a trickle or a little tiny gush of fluid, what you want to do is put a pad or a pantie-liner on after going to the bathroom and emptying your bladder, and wait an hour and see if fluid continues to come out. And if it does, then you're not having bladder leakage issues - your water is probably broken.

USMLE Step 2 CS - Pain Seeking This is just preview video. To get full access please visit our website : www.usmletutoring.com

Systemic Lupus Erythematosus Animation 3d

EKG/ECG Interpretation Explained Clearly

Watch that video of 232 Teeth Removal From Indians' Boy Mouth

Dialysis Fistula clip from full video on Dialysis Options

Laparoscopic Resection of Ovary Dermoid Cyst

Foreceps Delivery Birth Video

kin grafting is a type of graft surgery involving the transplantation of skin. The transplanted tissue is called a skin graft. Skin grafting is often used to treat: Extensive wounding or trauma Burns Areas of extensive skin loss due to infection such as necrotizing fasciitis or purpura fulminans[2] Specific surgeries that may require skin grafts for healing to occur - most commonly removal of skin cancers Skin grafts are often employed after serious injuries when some of the body's skin is damaged. Surgical removal (excision or debridement) of the damaged skin is followed by skin grafting. The grafting serves two purposes: reduce the course of treatment needed (and time in the hospital), and improve the function and appearance of the area of the body which receives the skin graft.

It depends upon which ligament is injured. If it is medial collateral ligament you feel pain when you walk ,sit and stand and you will be liming as well. If it is anterior cruciate ligament you feel pain when you walk on uneven ground.

Researchers have received approval to bring 20 brain-dead humans back to life.

Thrombosis of the venous channels in the brain is an uncommon cause of cerebral infarction relative to arterial disease, but it is an important consideration because of its potential morbidity. (See Prognosis.) Knowledge of the anatomy of the venous system is essential in evaluating patients with cerebral venous thrombosis (CVT), since symptoms associated with the condition are related to the area of thrombosis. For example, cerebral infarction may occur with cortical vein or sagittal sinus thrombosis secondary to tissue congestion with obstruction. (See Presentation.) Lateral sinus thrombosis may be associated with headache and a pseudotumor cerebri–like picture. Extension into the jugular bulb may cause jugular foramen syndrome, while cranial nerve palsies may be seen in cavernous sinus thrombosis as a compressive phenomenon. Cerebral hemorrhage also may be a presenting feature in patients with venous sinus thrombosis. (See Presentation.) Imaging procedures have led to easier recognition of venous sinus thrombosis (see the images below), offering the opportunity for early therapeutic measures. (See Workup.) Left lateral sinus thrombosis demonstrated on magn Left lateral sinus thrombosis demonstrated on magnetic resonance venography (MRV). This 42-year-old woman presented with sudden onset of headache. Physical examination revealed no neurologic abnormalities. View Media Gallery Axial view of magnetic resonance (MR) venogram dem Axial view of magnetic resonance (MR) venogram demonstrating lack of flow in transverse sinus. View Media Gallery The following guidelines for CVT have been provided by the American Heart Association and the American Stroke Association [1] : In patients with suspected CVT, routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time should be performed. Screening for potential prothrombotic conditions that may predispose a person to CVT (eg, use of contraceptives, underlying inflammatory disease, infectious process) is recommended in the initial clinical assessment. Testing for prothrombotic conditions (including protein C, protein S, or antithrombin deficiency), antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden can be beneficial for the management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2-4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute setting or in patients taking warfarin. In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be continued for 3-6 months, with a target international normalized ratio of 2.0-3.0. In patients with unprovoked CVT, vitamin K antagonists may be continued for 6-12 months, with a target international normalized ratio of 2.0-3.0. For patients with recurrent CVT, venous thromboembolism (VTE) after CVT, or first CVT with severe thrombophilia (ie, homozygous prothrombin G20210A; homozygous factor V Leiden; deficiencies of protein C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), indefinite anticoagulation may be considered, with a target international normalized ratio of 2.0-3.0. For women with CVT during pregnancy, low-molecular-weight heparin (LMWH) in full anticoagulant doses should be continued throughout pregnancy, and LMWH or vitamin K antagonist with a target international normalized ratio of 2.0-3.0 should be continued for ≥6 weeks postpartum (for a total minimum duration of therapy of 6 months). It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated. Further investigations regarding the underlying cause and a formal consultation with a hematologist or maternal fetal medicine specialist are reasonable. It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than unfractionated heparin. For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum period is reasonable. Next: Etiology What to Read Next on Medscape Related Conditions and Diseases Quiz: Do You Know the Complications, Proper Workup, and Best Treatment Practices for Ischemic Stroke? Quiz: How Much Do You Know About Hypothyroidism? Quiz: Do You Know the Risk Factors, Symptoms, and Potential Treatments for Alzheimer Disease? Quiz: How Much Do You Know About Hypertension? Quiz: Test Your Knowledge of Epilepsy and Seizure-related Conditions A 25-Year-Old Man With Painless Diplopia NEWS & PERSPECTIVE Temporal Trends and Factors Associated With Diabetes Mellitus Among Patients Hospitalized With Heart Failure Watchful Waiting Tied to Worse Outcomes in LVAD Patients With Hemolysis Age of Transfused Blood Impacts Perioperative Outcomes Among Patients Who Undergo Major Gastrointestinal Surgery TOOLS Drug Interaction Checker Pill Identifier Calculators Formulary SLIDESHOW Chronic Alcohol Abuse: Complications and Consequences Most Popular Articles According to Neurologists DHA Supplements Linked to Less Progression to Alzheimer's in APOE4 Carriers Heading in Soccer Linked to CNS Symptoms 'Transient Smartphone Blindness' Misdiagnosed as Multiple Sclerosis? New Advances in Traumatic Brain Injury FDA Clears Deflazacort (Emflaza) for DMD View More Overview Background

External jugular vein cannulation is an integral part of modern medicine and is practiced in virtually every health care setting. Venous access allows sampling of blood, as well as administration of fluids, medications, parenteral nutrition, chemotherapy, and blood products. [1] This topic describes placement of an intravenous (IV) catheter into the external jugular vein. A similar technique can be used for placement of IV catheters at different anatomic sites.

Hemodialysis, also called dialysis, is the most common treatment for kidney failure. A dialysis machine is an artificial kidney which cleanses the blood. During dialysis, blood is drawn from the patient into the dialysis machine, circulated through the machine, and then returned to the patient. Two needles are inserted into the patient's bloodstream to allow this process to occur. Hemodialysis is normally performed three times a week and the purpose of vascular access is to provide reliable sites where the bloodstream can be easily accessed each time. There are three major types of vascular access: arteriovenous fistula, arteriovenous graft, and venous catheter. The great majority of vascular accesses are created in the arm, but they can also be created in the leg.

Watch that video to know if you have Trypophobia

Symptoms of serotonin syndrome include a classic triad of mental status changes (eg, anxiety, delirium, confusion, restlessness), autonomic dysregulation (eg, diaphoresis, tachycardia, hypertension, hyperthermia, diarrhea, mydriasis), and neuromuscular hyperactivity (eg, hyperreflexia, tremor, rigidity, myoclonus, ocular clonus). Serotonin syndrome is clinically diagnosed and laboratory tests are used to rule out other etiologies. It usually occurs due to inadvertent interactions between drugs, therapeutic use of multiple serotonergic agents, or serotonergic medication overdose. Treatment involves discontinuation of serotonergic drugs, supportive measures, and sedation with benzodiazepines. In severe cases, a serotonin antagonist (cyproheptadine) may be used.