Benzodiazepines (BZD) are one of the most frequently used drugs to treat anxiety which acts on the gamma-amino butyric receptor A (GABA A receptor)- an inhibitory neurotransmitter. BZDs are also used as sedatives, light anesthesia in surgery, anticonvulsants, muscle relaxants and even insomnia. The teratogenicity of BZD remains a mystery among prenatal cases however recent study by Koren (2001) showed that there was no risk of major congenital malformations associated with BZD utilization. In contrary to Koren’s findings, case studies revealed significant high risk of major malformation (cleft palate or lip) with the use of BZD. Several studies have also likened the effects of BZD to fetal alcohol syndrome. The “benzodiazepine syndrome” is basically characterized by facial dysmorphism, hypotonia, and delayed motor development, polycystic kidney, submucous clef hard palate, microcephaly, varying degrees of mental retardation, convulsions and neonate abstinence syndrome. Some other studies that followed this hypothesis measure blood level of BZD and found out that elevated levels were evident after regular BZD treatment. Infants prenatally exposed to BZD were assessed in terms of their neuro-cognitive development. Among the infants that were assessed, the traits such as microcephaly, severe mental retardation, mild mental retardation, and normal intelligence were found to be evident on them. Authors also found out that prenatal exposure to BZD of 17 sampled children deviated in neurodevelopmental tests. Gross motor and fine motor development was delayed at 6 and 10 months follow-up. Delayed fine motor was still observed at 18 months follow-up and the children already had muscle tones deficits compared to the control group. The same group of children were then evaluated through cognitive testing with the use of Griffith’s developmental that measures locomotor, hearing and speech, eye and hand coordination, performance, practical reasoning, and
Benzodiazepines (BZD) are one of the most frequently used drugs to treat anxiety which acts on the gamma-amino butyric receptor A (GABA A receptor)- an inhibitory neurotransmitter. BZDs are also used as sedatives, light anesthesia in surgery, anticonvulsants, muscle relaxants and even insomnia. The teratogenicity of BZD remains a mystery among prenatal cases however recent study by Koren (2001) showed that there was no risk of major congenital malformations associated with BZD utilization. In contrary to Koren’s findings, case studies revealed significant high risk of major malformation (cleft palate or lip) with the use of BZD. Several studies have also likened the effects of BZD to fetal alcohol syndrome. The “benzodiazepine syndrome” is basically characterized by facial dysmorphism, hypotonia, and delayed motor development, polycystic kidney, submucous clef hard palate, microcephaly, varying degrees of mental retardation, convulsions and neonate abstinence syndrome. Some other studies that followed this hypothesis measure blood level of BZD and found out that elevated levels were evident after regular BZD treatment. Infants prenatally exposed to BZD were assessed in terms of their neuro-cognitive development. Among the infants that were assessed, the traits such as microcephaly, severe mental retardation, mild mental retardation, and normal intelligence were found to be evident on them. Authors also found out that prenatal exposure to BZD of 17 sampled children deviated in neurodevelopmental tests. Gross motor and fine motor development was delayed at 6 and 10 months follow-up. Delayed fine motor was still observed at 18 months follow-up and the children already had muscle tones deficits compared to the control group. The same group of children were then evaluated through cognitive testing with the use of Griffith’s developmental that measures locomotor, hearing and speech, eye and hand coordination, performance, practical reasoning, and