The likelihood that the facial palsy is caused by Lyme disease should be estimated, based on recent history of outdoor activities in likely tick habitats during warmer months, recent history of rash or symptoms such as headache and fever, and whether the palsy affects both sides of the face (much more common in Lyme than in Bells palsy). If that likelihood is more than negligible, a serological test for Lyme disease should be performed. If the test is positive, the diagnosis is Lyme disease. If no cause is found, the diagnosis is Bells Palsy. Classification
Facial nerve paralysis may be divided into supranuclear and infranuclear lesions. In a clinical setting, other commonly used classifications include: intra-cranial and extra-cranial; acute, subacute and chronic duration. Supranuclear and nuclear lesions
Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus. The facial nucleus itself can be affected by infarcts of the pontine arteries. These are corticobulbar fibers travelling in internal capsule. Infranuclear lesions
Infranuclear lesions refer to the majority of causes of facial palsy. Treatment
If an underlying cause has been found for the facial palsy, it should be treated. If it is estimated that the likelihood that the facial palsy is caused by Lyme disease exceeds 10%, empiric therapy with antibiotics should be initiated, without corticosteroids, and reevaluated upon completion of laboratory tests for Lyme disease. All other patients should be treated with corticosteroids and, if the palsy is severe, antivirals.
Toremifene has been reported to significantly improve symptoms of gynecomastia in men. Available forms
Toremifene is provided in the form of 60 mg oral tablets. Side effects
The side effects of toremifene are similar to those of tamoxifen. The most common side effect is hot flashes. Other side effects include sweating, nausea, vomiting, dizziness, vaginal discharge, and vaginal bleeding. In women with bone metastases, hypercalcemia may occur. Toremifene has a small risk of thromboembolic events. Cataracts, vision changes, and elevation of liver enzymes have been reported. The drug prolongs the QT interval and hence has a risk of potentially fatal dysrhythmias. The risk of dysrhythmias can be reduced by avoiding use in patients with hypokalemia, hypomagnesemia, pre-existing QT prolongation, and in those taking other QT-prolonging drugs. Because toremifene has estrogenic actions in the uterus, it can increase the risk of endometrial hyperplasia and endometrial cancer.Toremifene appears to be safer than tamoxifen. It has a lower risk of venous thromboembolism (VTE) (e.g., pulmonary embolism), stroke, and cataracts. The lower risk of VTE may be related to the fact tamoxifen decreases levels of the antithrombin III to a significantly greater extent than either 60 or 200 mg/day toremifene. Interactions
Toremifene is a substrate of CYP3A4, a cytochrome P450 enzyme, and hence drugs that induce or inhibit this enzyme can respectively decrease or increase levels of toremifene in the body. Pharmacology
Pharmacodynamics
Toremifene is a selective estrogen receptor modulator (SERM).