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 of the middle ear and carries taste sensations from the anterior two-thirds of the tongue.
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As such, common characteristics include facial drooping on the affected side, an inability to control movement of the facial muscles, hypersensitivity to sound and impaired taste. Normally simple functions such as blinking and closing the eye, smiling, lacrimation, salivation, raising an eyebrow all become paralyzed. With the involvement of the lacrimal gland, tear production often decreases and the lack of lubrication and constant exposure to the environment may lead to eye irritation and corneal abrasions. More rare, long-term complications may include permanent facial weakness with muscle contractures. However, most patients recover spontaneously and recuperate completely. In terms of duration, the onset of symptoms to maximal weakness usually occurs within three days to within one week. If left untreated, 85% of patients show at least partial recovery within three weeks of clinical onset. Reconsideration of the diagnosis of Bell’s palsy is usually necessary when the progression of symptoms continues to worsen beyond two weeks.
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A gradual onset of symptoms beyond two weeks is strongly suggestive of a mass lesion. Medical history should include any extraneous symptoms outside of the unilateral facial weakness directly related to Bell’s palsy. Careful inspection may evaluate for any recent rashes, arthralgia, or fevers, history of peripheral nerve palsy, exposure to influenza vaccine or other medications, and exposure to ticks or presence in areas where Lyme disease is endemic. All of these atypical signs and symptoms should prompt further evaluation from a physician and neurologist.
Bell’s palsy is thought to be caused by inflammation of the facial nerve at the geniculate ganglion, which may cause compression and possible ischemia and demyelination of the nerve. Historically, the syndrome has...
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