What is F.A.C.S

The Problem

Fetal Anti-Convulsant Syndrome occurs when anti-convulsant medicine (also known as Anti-Epileptic Drugs, or AEDs) taken during pregnancy affects the developing baby. The level of risk depends on the specific drug and dose — this is covered on the Risks & Diagnosis page.

Fetal anticonvulsant syndrome(s) are/is not a 'genetic' condition in the usual sense, but current opinion is that the way these drugs are metabolised by some pregnant women, and/or their affected children, predisposes the unborn baby to damage.

Fetal Valproate Spectrum Disorder (FVSD)

Where the medicine involved is sodium valproate, the condition is now often called Fetal Valproate Spectrum Disorder (FVSD). FVSD describes the range of physical, sensory, social, and cognitive differences that someone may have if they were exposed to sodium valproate in the womb.

The type and level of differences vary from person to person, and can be influenced by the amount of medication taken during pregnancy, the stage of pregnancy when exposure occurred, genetic background, and other health conditions. Every person with FVSD has their own individual strengths and support needs, and care should always be tailored to the person.

There is no single test for FVSD — it is diagnosed by a team of specialists, and effects on learning and behaviour are described separately. See Risks & Diagnosis and Neurodevelopmental effects.

Characteristics of Fetal Anti-Convulsant Syndrome

Some characteristics of foetal anticonvulsant syndrome involve the following areas:

• Spina bifida
• Cleft lip and palate
• Facial and skull
• Limb defects
• Ear malformations
• Skeletal malformation
• Heart, kidney, urinary tract, and sexual organ malformations
• Distinctive facial features
• Growth and general health
• Joint hypermobility
• Genitourinary defects
• Low muscle tone

Important

Please remember there is NO SAFE dose-effect of Epilim (Valproate) in pregnancy.

Some history

Epilim (Sodium Valproate) has a history of adverse developmental effects. The drug is unusual in that its teratogenicity in humans was predicted from animal studies, without any knowledge of mechanism (Brown et al., 1980; Kao et al., 1981).

Valproic acid, first marketed in Europe in 1967, appeared to be without adversity to development over the initial 13 years following marketing. Then, in the early 1980s, Dalens and her associates made the initial association of VPA to birth defects (Dalens et al., 1980; Dalens, 1981). They reported an infant who died at 19 days of age, was growth retarded, and who had multiple malformations of the face and brain, heart, and skeleton, among other defects. The mother of the infant had taken 1000mg/day of VPA throughout gestation. These observations were followed by several case reports and other publications attesting to the malformation effects of the drug when administered to a pregnant mother during gestation.

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