Characteristics of Epilepsies in Patients with Hypoxic‐Ischemic Encephalopathy (HIE) During the Neonatal Periods

Abstract

Purpose: The purpose of this study was to observe the characteristics of epilepsies in patients with a history of hypoxic‐ischemic encephalopathy (HIE) during the neonatal period, which is presumed to be etiologic. Patients and Methods: Clinical records of 1,295 outpatients, whose first visit to our hospital was between November 1989 and October 1994, and who were under our care at the time of this study, were reviewed. Patients were selected who satisfied all of the following criteria for possible incidence for HIE. (a) gestational age was >38 weeks; (b) at least one of the following: incidence of meconium aspiration, a low Apgar score (<5 at 1 min), a neonatal asphyxia manifested as prolonged insufficient respiration or cyanosis, or recurrent apneic attacks; and (c) medical treatment such as artificial ventilation or oxygen inhalation. Patients transferred to a neonatal intensive care unit or a pediatrician were included even if the details of the medical care were not available. Patients who had other causative disorders for their epilepsy, such as encephalitis and traumatic brain injury after the neonatal period, were excluded. The epilepsies were classified according to the criteria presented by the International League Against Epilepsy. Simultaneous video‐EEG recordings were available for 15 patients. Results: Twenty‐two (18 male and four female) patients, whose mean age was 18.0 years at the time of this study, satisfied the criteria described. Their mean age at the onset of epilepsy was 5.6 years, They had been diagnosed as having meconium aspiration syndrome in two patients, low Apgar score in five, neonatal asphyxia at birth in 14, and apneic attacks on the day after birth in one. For respiratory insufficiency, they received artificial respiration (four cases) or resuscitation other than artificial respiration (nine cases); nine patients were transferred to a neonatal intensive care unit or a pediatric unit. Convulsions were observed in seven patients during the neonatal period. At the time of their first visit, quadriplegia (four cases), hemiplegia (five cases), defects in the visual fields (two cases). and difficulty in hearing (one case) were observed. In 20 patients, their intellectual quotient was <70, and in four of them, it was <30. Based on neuroimaging, 21 patients had apparent abnormalities: bilateral and diffuse (five cases), bilateral but predominantly unilateral (three cases). bilateral parietooccipital (three cases). and unilateral parietooccipital (LO cases). Two (9%) patients were diagnosed as having symptomatic generalized epilepsy with tonic seizures and the remaining 20 (91%) as having symptomatic partial epilepsy. In the latter cases, 10 patients had visual symptoms and an additional one had conjugated eye deviation during the initial phase of the seizure. These 11 (55%) patients showed occipital spikes in their interictal EEGs and were diagnosed as having occipital lobe epilepsy (OLE). One patient who was diagnosed as having parietal lobe epilepsy had sensory symptoms in his right arm. The interictal EEGs revealed bilateral independent anterior temporal spikes. One patient had autonomic sensations with right anterior temporal interictal spikes and was diagnosed as having temporal lobe epilepsy. In six patients, the epileptogenic areas were not determined electroclinically. In 20 patients, seizures haw not been controlled. Sixteen of them have tonic, complex partial, or secondarily generalized tonic‐clonic seizures more than once a month. Conclusions: Most of our patients whose history suggested an incidence of HIE during the neonatal period have intractable symptomatic partial epilepsy. In SS% of patients, epileptogenic areas are believed to be located in the occipital lobe. In addition to our finding that patients with OLE have a greater incidence of perinatal difficulties than do those with temporal or frontal lobe epilepsy, this study suggests that the occipital lobe is more likely than the other lobes to become epileptogenic as a consequence of hypoxic insults.