Cases reported "Facial Nerve Diseases"

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1/2. poland-Moebius syndrome: a case report.

    BACKGROUND: The primary site of pathology in Moebius syndrome is still unknown, although several studies have variably localized the lesion in the extraocular muscles, cranial nerves, or central nervous system. CASE: A 24-year-old man with poland-Moebius syndrome and acquired progressive bilateral paralytic lower eyelid ectropion is described. OBSERVATIONS: In this patient, magnetic resonance imaging studies revealed a barely detectable pontine hypoplasia and normal recti muscles. Nerve conduction studies of the facial nerves showed a severe demyelinating or dysmyelinating type of neuropathy. Bilateral lower eyelid ectropium of the patient was successfully corrected by canthal tightening procedures. CONCLUSION: Contrary to many reported cases, this patient serves as a rare example of a progressive type of poland-Moebius syndrome presumably resulting from a combination of a brainstem abnormality and a peripheral neural degenerative process.
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keywords = demyelinating
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2/2. guillain-barre syndrome.

    guillain-barre syndrome (GBS) is an acute, demyelinating polyneuropathy involving the spinal roots, peripheral nerves, and often the cranial nerves. Although its exact mechanism remains unclear, an autoimmune etiopathology is theorized. It is characterized by rapidly progressing, symmetrical muscular weakness starting in the legs and ascending to the trunk and arms. Additionally, deep tendon reflexes are lost. Approximately half of the patients with GBS have cranial nerve palsies, with unilateral or bilateral facial nerve (CN VII) palsy being the most common. paralysis of the muscles of the tongue, lips, palate, larynx, and pharynx from lesions involving cranial nerves IX, X, and XI and weakness of the muscles of mastication (CN V) are the next most common cranial nerve abnormalities. Ocular muscle palsy is not common, only occurring in approximately 10% of patients. The Miller Fisher variant of GBS is a distinct syndrome in which the only neurologic deficits are oculomotor palsies, areflexia, and ataxia. We present the rare case of a 45-year-old woman with GBS whose ocular muscles were affected. The oculomotor disturbance and limb weakness occurred within a few days of one another. Basic anatomic considerations are reviewed along with the pathophysiology and clinical features of GBS.
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keywords = demyelinating
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