Effects Of Epileptic Drugs On Pregnancy
Epilepsy, also known as seizure disorder, is one of the biggest health issue in the world, as it affect people from all races and in all age groups. Epilepsy can simply be defined as an illness of repetitive uncontrollable seizures(Banerjee et al.,2009) or in a much scientific manner as “a brain disorder in which clusters of nerve cells, or neurons, in the brain sometimes signal abnormally causing strange sensations, emotions, and behaviour, or sometimes convulsions, muscle spasms, and loss of consciousness”(Cunha,n.d.).
The aetiology (the cause or set of causes) of epilepsy include genetics (heritable genes), brain injuries, developmental disability (like defective neuronal migration in the brain, or imbalances in neuromodulators and neurotransmitters), central nervous system infections, neurodegenerative diseases, cerebrovascular disease, brain tumors, and perinatal insult (is defined as brain damage immediately before birth. This due to mainly asphyxia as the reduction of the uterine or umbilical circulation) (Berger et al., 2000., Cunha, n.d, Annegers et al, 1996)
Treatment of epilepsy normally include prescribed medication referred as anti-epileptic drugs, AEDs. There are many anti-epileptic drugs but the commonly used are carbamazepine, valproate, lamotrigine, gabapentin and topiramate (Cunha,n.d.). Other treatments include vagus nerve stimulation (Ben-Menachem, E., 2002)
Almost 1% of all pregnancies are women with epilepsy and need to continue taking their medication to prevent epileptic episodes which may harm the mother and her fetus (Tomson et al, 2011). As there are numerous occurrences of epilepsy and pregnancy, it is likely the influence of AEDs on the developing fetus that increases the risks of congenital defects or abnormalities (Morrow et al, 2006).The longer the women are exposed to the anti-epileptic drugs as well as an increase in the dose of these drugs, the greater the risks of congenital defects (Tomson et al., 2011, Campbell et al., 2014). Epileptic women risks of congenital defects are doubled from a contextual risk of congenital defects (Campbell et al., 2014).
Ornoy et al.(1996) reported that carbamazepine is used to treat several nervous system disorders such as cyclic manic-depressive disorder (bipolar disorder) and trigeminal neuralgia and mostly common in epileptic women . No variations in gestational age, birth weight, and average age, also similar average height and head circumference between test group and the control were observed in their examination. Major findings were facial dysmorphic features (carbamazepine syndrome) as upslanting palpebral fissure, epicanthic folds, micrognathia, broad nasal bridge, high arched palate, or cleft palate. Some children also had strabismus, and hypoplasia of the toe nails; dilation of the pelvis of the kidney, ventricular septal defects, visual impairments, nystagmus and mental retardation associated with hydrocephalus. It was found that these children had an IQ below 90 .Jones et al.(1989) reported that 11% of cases had craniofacial defects, 26% had fingernail hypoplasia, and 20% had developmental delays as prenatal growth deficiency, microcephaly and narrow bifrontal diameter, tetralogy of fallot ,ventricular septal defects and hydrocephalus with a ventriculoperitoneal shunt. Rosa (1991) findings were cases of spina bifida only.
Used to balance chemicals in the brain that may cause seizures (Durbin, 2018). Weinstock et al (2001) concluded that no direct involvement of clonazepam in congenital birth defects as no cases of orofacial anomalies, benzodiazepine withdrawal syndrome, neonate apnea or other autonomic dysregulations were observed. Lin et al (2004) also reported that exposure to clonazepam did not show an increase in malformations at birth but malformations as growth retardation, dysmorphic features and tetralogy of fallot were observed.
Ethosuximide rarely cause major malformation, the only common malformations observed associated with ethosuximide are cleft palate (Sullivan et al, 1976). Kuhnz et al (1984) reported two major malformations as bilateral clefting and hare-lip. Also it was found that behavioural complications occurred in several neonates.
Exposure to both these drugs using monotherapy had low risks to major and manor malformations as it the risks equal that of the general population group but exposure to polytherapy with lamotrigine and levetiracetam drastically increases the risks, independently (Cunnington et al, 2005, Hunt et al, 2006)
This drug is used to treat tonic-clonic, partial seizures and migraines by the United States (Margulis et al, 2012). Margulis et al (2012) reported that there are major structure malformations associated with topiramate like cleft lip, patent foramen ovale, or patent ductus arteriosus and palate and undescended testis. Hunt et al (2008) research resulted in abnormalities including oral clefts both cleft lip and palate and cases of hypospadias. Ornoy et al (2008) findings were congenital anomalies involving genetics and structural abnormality. Their findings were genetic cases of DiGeorge Syndrome and Prader Willis syndrome. These were verified by finding microdeletion of 22q and genetic studies, respectively. Structural anomalies include multiple brain cysts and pulmonary artery stenosis.
Valproic acid is considered as the human teratogen as it is mostly highly susceptible in humans and because of its highly teratogenic effects it should be avoid during pregnancy( Ornoy, A.,2009, Jentink et al, 2010, koren et al, 2006). koren et al(2006) reported that valproic acid increases the risks by three fold causes malformations such as cardiac and limbs anomalies but mostly neural tube defects. Ornoy, A.,(2009) finding showed that valproic acid is mainly associated with spina bifida with cases of craniofacial, anencephaly, cadiac, limb and skeletal defects rarely occurring.
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