Facial Clefts Among Epileptic Patients

Friis, Mogens Laue; Broeng-Nielsen, Bodil; Sindrup, E; Lund, M.; Fogh‐Andersen, Poul; Hauge, M.

doi:10.1001/archneur.1981.00510040053008

Cited by 26 publications

(15 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…10,12,17,18 Association of facial clefting in infants of epileptic mothers has been well documented. 10,[19][20][21] In our study, history of epilepsy or anticonvulsant drug intake was not present in any of the cases. It has been suggested that a genetic link with both epilepsy and the effect of anticonvulsants may be the etiologic factor in facial clefting.…”

Section: Discussionmentioning

confidence: 45%

Facial Clefting in Arab Infants

Mir

Soni²,

Kishan³

et al. 1988

Ann Saudi Med

View full text Add to dashboard Cite

Over a period of two years, 32,332 consecutive live-born babies were surveyed for facial clefts. A total of 17 patients with facial clefts were identified. After exclusion of the cases with other major congenital anomalies, the overall incidence of the facial clefts was 0.28/1,000 live births (alveolar, 0.12; postalveolar, 0.09; and prealveolar 0.06/1,000 live births). Maternal history of epilepsy and/or anticonvulsant drug intake was not present. There was a family history of facial clefts in four infants. Advanced maternal age and high parity were observed in seven (P < 0.05) and six (P < 0.05) cases, respectively. Six of the eight infants with major malformations died, with an overall mortality of 35.3%.NA Mir, ASJ Kishan, W Galczek, Facial Clefting in Arab Infants. 1988; 8(3): 206-208 MeSH KEYWORDS: Cleft palate-in infancy and childhood Perinatal mortality remains high in developing countries, 1,2 and congenital malformations are ranked as the leading cause of perinatal deaths.3 Facial clefts, one of the major congenital malformations, 4 result from interference with normal development and fusion of the embryonic frontonasal and maxillary processes.5 There is a strong genetic component in their etiology, but environmental factors have also been suggested from epidemiologic and experimental animal data.6-8 These malformations are readily recognized at birth and occur throughout the world with variable frequency. The epidemiology of facial clefting in the Arab population has not been reported previously. This prospective study surveyed the incidence and pattern of this congenital malformation in an Arab population. Subjects and MethodsThe subjects of this prospective study were all live-born babies born at Jamahiria Maternity Hospital, Benghazi, Libya, between 1 January 1982 and 31 December 1983. The hospital is the main maternity center in the eastern part of Libya, and over 96% of the deliveries in this region occur in this hospital. Standard physical examination of all newborns, including assessment of gestational age by the Dubowitz method, 9 was carried out by a qualified pediatrician or a senior pediatric resident within 48 hours of birth. The clefts were classified as (1) prealveolar, when only the upper lip was clef ting, varying from a notch in the red margin of the lip to a cleft extending into the floor of the nostrils; (2) postalveolar, when only palate was involved; and (3) alveolar, when clefting involved the upper lip, alveolus, and palate. Various clinical factors, such as maternal age and parity, gestation, mode of delivery, sex,

show abstract

Section: Discussionmentioning

confidence: 45%

Facial Clefting in Arab Infants

Mir

Soni²,

Kishan³

et al. 1988

Ann Saudi Med

View full text Add to dashboard Cite

show abstract

“…One of the nine mothers was not on anticonvulsants; three had a family history of epilepsy. Friis et a1 [37] explored the relationship of clefting to epilepsy. They identified 3,203 epileptic probands and found that 11 had a facial cleft, twice the expected number if there were no association between clefting and epilepsy.…”

Section: Specific Malformations and Maternal Epilepsymentioning

confidence: 99%

Teratogenicity of anticonvulsant drugs. I: Review of the literature

Kelly

1984

Am. J. Med. Genet.

129

View full text Add to dashboard Cite

“…However, the proportions of exposed nonexposed children in the CHD-affected group (18) and the non-CHD group (2,443) were not significantly different (P >.10). Two children with CHD of the eight epilep¬ tic fathers have had their genome exposed to phenytoin and five chil¬ dren of four epileptic mothers were exposed to phenytoin, phénobarbital, primidone, and sulthiame in utero in different combinations.…”

Section: Resultsmentioning

confidence: 89%