Abstract

P E R I I-I E R A L facial paralysis was described as early as 1821 by Charles Bell , 1 and the term is still in general use. The term has been applied to any facial palsy of the peripheral type, the etiology of which is obscure. 2, 3 I t is usually unilateral and results from an intrinsic lesion of the seventh cranial nerve. Sudden peripheral facial paralysis in children is similar to that seen in the adult; weakness is often preceded by upper respiratory infection, with sore throat, otitis media, or exposure to extreme cold. About 24 hours before the onset of weakness and paralysis there may be prickly sensations and numbness on that side of the face. When circumstances have permitted exploration, the nerve has been found to be swollen and inflamed. In the very few instances in which histologic examination was possible, a hemorrhagic interstitial neuritis was noted. Bell's palsy is rare in children under the age of 2 years, so that indications of facial paralysis in this age group are of greater concern, since they suggest involvement of the central nervous system which is of a serious nature. Treatment of Bell's palsy is largely supportive, including protection of the cornea and prevention of stretching of the facial muscles during recovery. Any existing infection such as otitis media must be brought under control. In some instances, corticosteroids employed early in the course have been considered useful in reducing edema and are thought by some to speed recovery. Prognosis in general is good; however, recovery may be slow, requiring weeks or even months f o r full resolution of the manifestati0ng. In rare instances asymmetry of }he face may persist in the pediatric age group. Multiple recurrence of Bell's palsy with facial edema (Melkersson's syndrome 4' ~) has been recorded infrequently. Melkersson ~ first described this complex of symptoms in 1928. The syndrome is characterized by chronic facial edema, by peripheral facial paralysis which may be bilateral and tends to be recurrent, and in some instances by fissured tongue. Usually the disease has its initial onset in childhood or youth. In 1965 Kunstadter G described a Caucasian male child, 5 ~ years of age, in whom this clinical entity first appeared at the age of 2 ~ years. Otitis media was suspected as a possible contributing cause in the first attack, although history of infection was n o t elicited in subsequent attacks. The disease began at 2 89 years of age with facial edema and rightsided Bell's palsy. The condition cleared in approximately 3 weeks. Several months later spontaneous palsy on the left side with swelling was diagnosed initially as possible mumps. T h e facial swelling subsided i n about 10 days, but improvement in the palsy required between 3 and 4 weeks. The syndrome recurred at 4 ~ years of age. This child was seen last at the age Of 5 ~ years; he appeared well and had not experienced recurrence for 7 months. Treatment in each instance included antibiotic drugs and steroids with potassium chloride as indicated. In this syndrome, the paralysis may be of sudden onset, often precedes the swelling, and is indistinguishable from Bell's palsy. An evaluation of prognosis and treatment in Bell's palsy appears in a recent issue of Acta paediatrica scandinavica. This informative r e p o r t b y Salam and Elyahky T is based on a study of 150 children (82 males and 68 females) who were referred to the Departments of Pediatrics and Radiology of the

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