Infection
Lyme disease, an infection caused by Borrelia burgdorferi bacteria and spread by ticks, can account for about 25% of cases of facial palsy in areas where Lyme disease is common. In the U.S., Lyme is most common in the New England and Mid-Atlantic states and parts of Wisconsin and Minnesota, but it is expanding into other areas. The first sign of about 80% of Lyme infections, typically one or two weeks after a tick bite, is usually an expanding rash that may be accompanied by headaches, body aches, fatigue, or fever. In up to 10-15% of Lyme infections, facial palsy appears several weeks later, and may be the first sign of infection that is noticed, as the Lyme rash typically does not itch and is not painful. Lyme disease is treated with antibiotics.Reactivation of herpes zoster virus, as well as being associated with Bells palsy, may also be a direct cause of facial nerve palsy. Reactivation of latent virus within the geniculate ganglion is associated with vesicles affecting the ear canal, and termed Ramsay Hunt syndrome type II. In addition to facial paralysis, symptoms may include ear pain and vesicles, sensorineural hearing loss, and vertigo. Management includes antiviral drugs and oral steroids. Otitis media is an infection in the middle ear, which can spread to the facial nerve and inflame it, causing compression of the nerve in its canal.
Middle cerebral artery syndrome is a condition whereby the blood supply from the middle cerebral artery (MCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the lateral aspects of frontal, temporal and parietal lobes, the corona radiata, globus pallidus, caudate and putamen. The MCA is the most common site for the occurrence of ischemic stroke.Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with MCA syndrome. More distal blockages tend to produce milder deficits due to more extensive branching of the artery and less ischemic response. In contrast, the most proximal occlusions result in widespread effects that can lead to significant cerebral edema, increased intracranial pressure, loss of consciousness and could even be fatal. In such occasions, mannitol (osmotic diuretic) or hypertonic saline are given to draw fluid out of the edematous cerebrum to minimise secondary injury. Hypertonic saline is better than mannitol, as mannitol being a diuretic will decrease the mean arterial pressure and since cerebral perfusion is mean arterial pressure minus intracranial pressure, mannitol will also cause a decrease in cerebral perfusion. Contralateral hemiparesis and hemisensory loss of the face, upper and lower extremities is the most common presentation of MCA syndrome. Lower extremity function is more spared than that of the faciobrachial region. The majority of the primary motor and somatosensory cortices are supplied by the MCA and the cortical homunculus can, therefore, be used to localize the defects more precisely.