Eye Pressure Test

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Watch that video to know the Premature Ejaculation Cures

Wernicke's aphasia is a neurological disorder typically caused by stroke. It affects the Wernicke's region in the brain's left hemisphere which is reasoned to be responsible for processing of meaning, especially as it relates to verbal communication, hence the problems with speech witnessed in these patients

Psoriasis: treatment options related issues

Comedone Extraction Video

How to treat a burn - How to treat burns at home

Electroconvulsive ECT Psychiatric Therapy Information

Many U.S. hospitals still perform traditional surgery, over minimally invasive procedures, according to Johns Hopkins University researchers. Also, a new study on HPV vaccines. Wendy Gillette reports on the day's top health stories.

This video demonstrates why ears become clogged and why ear popping helps. The video also explains why ear popping may become difficult resulting in a persistent clogged or muffled ear especially after an ear infection.

Testing for the four features of Gerstmann Syndrome in this patient with two separate left sided strokes (left frontoparietal ischaemic stroke followed by left posterior parietal haemorrhagic stroke). He exhibits (i) acalculia, (ii) agraphia, (iii) left-right disorientation, and (iv) finger agnosia. Complicating the issue is his obvious nonfluent aphasia (expressive dysphasia) with paraphasic errors (replacing words with associated words (e.g. says 'fork' instead of 'spoon')) and some comprehension issues.

What are the classifications of burns? Burns are classified as first-, second-, or third-degree, depending on how deep and severe they penetrate the skin's surface. First-degree (superficial) burns. First-degree burns affect only the epidermis, or outer layer of skin. The burn site is red, painful, dry, and with no blisters. Mild sunburn is an example. Long-term tissue damage is rare and usually consists of an increase or decrease in the skin color. Second-degree (partial thickness) burns. Second-degree burns involve the epidermis and part of the dermis layer of skin. The burn site appears red, blistered, and may be swollen and painful. Third-degree (full thickness) burns. Third-degree burns destroy the epidermis and dermis and may go into the subcutaneous tissue. The burn site may appear white or charred Fourth degree burns. Fourth degree burns also damage the underlying bones, muscles, and tendons. There is no sensation in the area since the nerve endings are destroyed.

Doctor makes magic - Doctor hace magia (Sorprendente) - Doctor Magic

Basic Surgical Instrumentation

Watch that video to know about The Most Disgusting Parasites That Can Infect The Human Body

Biceps tenodesis surgery is performed when the biceps tendon is damaged, or the rotator cuff tendon or cartilage ring in the shoulder is torn. The biceps tendon is a strong rope‐like structure connecting the upper end of the biceps muscle to the bones in the shoulder. In biceps tenodesis surgery, the biceps tendon is separated from the shoulder and reattached to the humerus, or the upper arm bone.

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? 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This video describes the various positions a baby may be in prior to delivery.