The major differences in this condition are the presence of small blisters, or vesicles, on the external ear, significant pain in the jaw, ear face, and/or neck and hearing disturbances, but these findings may occasionally be lacking (zoster sine herpete). Reactivation of existing herpes zoster infection leading to facial paralysis in a Bells palsy type pattern is known as Ramsay Hunt syndrome type 2. The prognosis for Bells palsy patients is generally much better than for Ramsay Hunt syndrome type 2 patients. Treatment
Steroids have been shown to be effective at improving recovery in Bells palsy while antivirals have not. In those who are unable to close their eyes, eye protective measures are required. Management during pregnancy is similar to management in the non-pregnant. Steroids
Corticosteroids such as prednisone improve recovery at 6 months and are thus recommended. Early treatment (within 3 days after the onset) is necessary for benefit with a 14% greater probability of recovery. Antivirals
One review found that antivirals (such as aciclovir) are ineffective in improving recovery from Bells palsy beyond steroids alone in mild to moderate disease. Another review found a benefit when combined with corticosteroids but stated the evidence was not very good to support this conclusion.In severe disease it is also unclear. One 2015 review found no effect regardless of severity. Another review found a small benefit when added to steroids.They are commonly prescribed due to a theoretical link between Bells palsy and the herpes simplex and varicella zoster virus.
It is about equipotent in blocking beta1- and beta2- receptors.The amount of alpha to beta blockade depends on whether labetalol is administered orally or intravenously (IV). Orally, the ratio of alpha to β blockade is 1:3. Intravenously, alpha to β blockade ratio is 1:7. Thus, the labetalol can be thought to be a beta-blocker with some alpha-blocking effects. By comparison, labetalol is a weaker β-blocker than propranolol, and has a weaker affinity for alpha-receptors compared to Phentolamine.Labetalol possesses intrinsic sympathomimetic activity. In particular, it is a partial agonist at beta2- receptors located in the vascular smooth muscle. Labetalol relaxes vascular smooth muscle by a combination of this partial beta2- agonism and through alpha1- blockade. Overall, this vasodilatory effect can decrease blood pressure.Similar to local anesthetics and sodium channel blocking antiarrhythmics, labetalol also has membrane stabilizing activity. By decreasing sodium entry, labetalol decreases action potential firing and thus has local anesthetic activity. Physiological action
The physiological effects of labetalol when administered acutely (intravenously) are not predictable solely by their receptor blocking effect, i.e. blocking beta1- receptors should decrease heart rate, but labetalol does not. When labetalol is given in acute situations, it decreases the peripheral vascular resistance and systemic blood pressure while having little effect on the heart rate, cardiac output and stroke volume, despite its alpha1-, beta1- and beta2- blocking mechanism. These effects are mainly seen when the person is in the upright position.Long term labetalol use also has different effects from other beta-blocking drugs. Other beta-blockers, such as propranolol, persistently reduce cardiac output during exercise.