Abstract Paralysis of a facial nerve (i.e. CN VII) is frequently diagnosed as Bell’s palsy. Patients who suffer from Bell’s palsy often experience unilateral loss of facial muscle function which presents as drooping of the eyelid and corner of mouth, impaired taste, hypersensitive hearing, and general loss of facial muscle function on the affected side of the face. Loss of nerve function occurs as a result of inflammation at the geniculate ganglion which causes nerve damage and may eventually lead to loss of function of the areas of the face innervated by that nerve. While the etiology of the disease is unknown, recent studies have shown that Lyme disease or positive HSV-1 titers, along with other diseases, are more prevalent in patients with Bell’s palsy and may indirectly be the cause of this paralysis. Medication therapy for Bell’s palsy includes the use of corticosteroids, Botox or surgery to return the patient to normal function in the occasional occurrence where the patient does not undergo spontaneous recovery. While Bell’s palsy is a disorder in its own right, other diseases such as tumors or stroke should be ruled out for confirmation of the diagnosis.
Bell’s Palsy Syndrome
Bell’s palsy is a paralysis of the facial nerve. Patients often experience a unilateral facial weakness, drooping eyelid and corner of the mouth, impaired taste and other devastating, but often acute, symptoms. This research paper will discuss the clinical presentation of the disorder, its complications, investigate its etiology and various treatment options.
Bell’s palsy was named after Sir Charles Bell (1774-1842), who described the clinical findings of the syndrome and its neuropathic effects on the facial nerve. As the diagram below illustrates, the nerve is responsible for innervating all of the muscles of facial expression and contains parasympathetic fibers to the lacrimal and salivary glands. It also innervates the stapedial (stapes) muscles
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