The incidence of congenital hypothyroidism, dyshormonogenesis and the associated malformations and diseases are higher than those reported in the literature. Cord blood as a screening method is associated with a significant number of missed cases.

Carbamazepine has been used in adults and children for over 30 years. In spite of an excellent therapeutic and side-effect profile in older children, it has never been used as a primary anticonvulsant in neonates. This is the first report of the long-term use of carbamazepine in neonates. Ten full-term neonates with two or more seizures due to hypoxic-ischemic encephalopathy were given 10 mg/kg of carbamazepine as a loading dose via nasogastric tube. Twenty-four hours later, the first five patients began a maintenance regimen of 21 mg/kg/daily, and the remaining five patients began a maintenance regimen of 15 mg/kg/daily, all via nasogastric tube. Therapy was continued for 3 to 9 months. Drug levels were monitored every 2 to 4 hours during the first 24 hours, and on days 2, 4, 8, 15, 30, 45, and 60, and monthly thereafter. Absorption of carbamazepine was excellent even in sick neonates. Therapeutic levels were reached in 2 to 4 hours in all patients. Peak levels were achieved in 4 to 16 hours (mean, 9.2 +/- 4.2). Elimination half-life was 24.5 hours. Levels dropped precipitously around 8 to 15 days and thereafter declined slowly over the next 3 months. Seizure control was excellent; only two patients had one seizure each during the first 10 hours. There were no gastrointestinal, hepatic, hematologic, renal, or dermatologic side effects. This preliminary study shows that carbamazepine may be an effective anticonvulsant for neonatal seizures.

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Focal cerebral infarction remains an uncommon diagnosis in full term unstressed babies despite advancement in radiological techniques. However, it is not rare in autopsy series. In 1979 Barmada et al [1] reported a 5.4% incidence of focal cerebral infarction acquired perinatally in full term neonates in an autopsy series. Review of current literature thus far has revealed around 35 full term babies with focal infarctions, mostly in the territory of the left middle cerebral artery. Most of these babies have experienced significant perinatal asphyxia. Thus far, only seven babies, unstressed and apparently normal with good Apgar scores, have developed focal cerebral infarction. PLEDS has not been reported in any of these babies. Prognosis of these babies, including ours, has been better as compared to those who suffered perinatal asphyxia [2]. Case ReportA full term female baby was delivered at Riyadh Armed Forces Hospital (RKH) to a 24-year-old gravida 4, para 3, whose pregnancy was uncomplicated. The baby's birth weight was 3.3 kg, OFC 34.5 cm, and Apgars were 9 and 10 at one and five minutes. No active resuscitation was required. The placenta looked grossly normal and weighed 600 gm. At 18 h of age, clonic movements of the right half of the body were noted which lasted for approximately one-half h. These seizures recurred four times within the ensuing 24 h. Physical examination revealed a baby in no apparent distress, pink on room air, who was well perfused. Fontanelles were normal. Pupils were equal and reactive. Doll's eye movements were normal. Tone was normal and equal in all extremities. Deep tendon reflexes (DTRs) were symmetrical. The infant had a symmetrical Moro reflex. Examination of the cardiovascular system did not reveal any murmurs. Laboratory investigations revealed hematocrit of 0.47. Septic screen including lumbar puncture was normal. Glucose was 4.5 mmol/L, calcium 2.24 mmol/L, and magnesium 0.72 mmol/L. Coagulation screen was normal. Protein C and S were normal. Electrocardiogram was normal for age. Echocardiogram was normal. Cranial ultrasound did not reveal any bleeds. Ventricle size was normal. There was no evidence of cerebral edema or focal lesions. Computerized tomographic (CT) scan performed at the age of five days revealed an area of low attenuation in the left parietal region (Figure 1). There was no mass effect. The lesion was suggestive of infarction in the distribution of left middle cerebral artery. Electroencephalogram revealed periodic lateralizing epileptiform discharges arising from the left side (Figure 2). The baby was loaded with phenobarbitone 20 mg/kg. She also required additional doses of diazepam 0.3 mg/kg within the first 24 h. The seizures did not recur after the first day. There was no sign of focal neurological deficit. She was gradually taken off the anticonvulsant without recurrence of symptoms. The baby has been seen in the follow-up clinic on several occasions. She has no neurological deficit or recurrence of seizures. Her development, including speech and langu...