94 H. Montassir et al. Perinatal history and neurological sequelae (Table 2)................................................................. 94 Characteristics <strong>of</strong> epileptic seizure and clinical course <strong>of</strong> <strong>epilepsy</strong> (Table 3 and Figs. 1 and 2)........................ 95 EEG and MRI findings (Table 4 and Figs. 3—5) ......................................................................... 97 Discussion ............................................................................................................... 97 References .............................................................................................................. 99 Introduction Glucose is essentially important for brain metabolism. It is well known that severe neonatal hypoglycemia results in posterior cerebral injury. The neurological sequelae <strong>of</strong> severe neonatal hypoglycemic encephalopathy include developmental delay, learning or behavioral problems, <strong>epilepsy</strong>, and visual impairment. Although the prevalence <strong>of</strong> <strong>epilepsy</strong> in neonatal hypoglycemic encephalopathy was quite high, studies about <strong>epilepsy</strong> secondary to neonatal hypoglycemia are sparse (Norden, 2001). Caraballo et al. (2004) reported that <strong>prognosis</strong> <strong>of</strong> <strong>symptomatic</strong> <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> following neonatal hypoglycemia was mostly good. In our own experience, <strong>symptomatic</strong> <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> secondary to neonatal hypoglycemia is intractable to treatment with high prevalence <strong>of</strong> status epilepticus in infancy but remits in late childhood. <strong>Long</strong>itudinal clinical course <strong>of</strong> <strong>epilepsy</strong> secondary to neonatal hypoglycemia are not fully described. In this study, we sought to examine the long-<strong>term</strong> <strong>prognosis</strong> and longitudinal clinical course <strong>of</strong> <strong>symptomatic</strong> <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> secondary to neonatal hypoglycemia. Subjects and methods We retrospectively extracted subjects from the database <strong>of</strong> outpatients who were referred to our child neurology clinic at Tottori University Hospital from 1980 to 2006 (12,463 patients). We extracted the data <strong>of</strong> 2028 epileptic patients from our database. Then, 81 patients with <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> were extracted. Patients with <strong>symptomatic</strong> <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> who had neonatal hypoglycemia were the subjects <strong>of</strong> this study. Occipital <strong>lobe</strong> <strong>epilepsy</strong> was defined as having ictal semiology identical to <strong>occipital</strong> <strong>lobe</strong> seizures, which include eye deviation or eye blinking with staring, ictal vomiting, or visual hallucination (Williamson et al., 1992), and interictal paroxysmal waves in the posterior derivation. Patients with <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> who had <strong>occipital</strong> <strong>lobe</strong> injuries other than neonatal hypoglycemia were excluded. Severe hypoxic-ischemic brain injury is a high risk for the occurrence <strong>of</strong> <strong>epilepsy</strong> regardless <strong>of</strong> hypoglycemia, while the mild to moderate type is not (Zafeiriou et al., 1999; Pisani et al., 2009). Therefore, patients with severe cerebral palsy who are not able to walk independently were excluded, while those with mild cerebral palsy were included. Epilepsy patients with pre<strong>term</strong> birth (less than 35 weeks gestation) or those with inborn errors <strong>of</strong> metabolism, congenital anomalies, brain malformation, or chromosomal abnormality were also excluded, even if they had histories <strong>of</strong> neonatal hypoglycemia (Table 1). Neonatal hypoglycemia was defined as whole-blood glucose concentration below 35 mg/dL, 40 mg/dL, and 45 mg/dL during 0—3 h, 3—24 h, and after 24 h after birth, respectively (Srinivasan et al., 1986). Onsets <strong>of</strong> <strong>epilepsy</strong>, major seizure types, and clinical course <strong>of</strong> <strong>epilepsy</strong>, EEG and neuroimaging findings were studied from their medical records. Status epilepticus was defined as clinical seizure lasting more than 30 min. MRI (1.5 T or 3.0 T recently) was performed repeatedly and included T1-, T2-, and FLAIR imaging. Mental or intellectual status was evaluated using the Wechsler intelligence scale for children or the Enjoji development scale. ‘‘Normal’’ was defined when IQ or DQ was more than 70, ‘‘mild’’ mental retardation (MR) or developmental delay was defined when it was between 50 and 70, ‘‘moderate’’ when it was between 20 and 50, and ‘‘severe’’ when it was below 20. We also reviewed clinical and laboratory data during perinatal periods. This study was approved by the ethical committee in Tottori University. Results The most common epileptic syndrome <strong>of</strong> <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> was idiopathic childhood <strong>occipital</strong> <strong>epilepsy</strong> (Panayiotopoulos syndrome and Gastaut type) and this was found in 54 <strong>of</strong> the patients. Twenty-one patients with <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> were excluded and finally 6 patients (5 males and 1 female) were the subjects <strong>of</strong> the study (Table 2). Perinatal history and neurological sequelae (Table 2) Perinatal histories and neurological sequelae are shown in Table 2. Patients 1—4 were taken care <strong>of</strong> in our neonatal intensive care unit and Patients 5 and 6 were treated in other hospitals. Perinatal histories closely correlated with neonatal hypoglycemia were highly present: low birth weight for gestational age in 5, low Apgar score after 1 min in 3, and neonatal seizure in 5. Severe neonatal hypoglycemia with a serum glucose level <strong>of</strong> less than 15 mg/dL was reported in 3 patients and hypoglycemia was prolonged more than 10 h Table 1 Inclusion and exclusion criteria. Inclusion criteria (no. <strong>of</strong> patients) Exclusion criteria Outpatients (12,463) OLE with <strong>occipital</strong> injuries other than neonatal hypoglycemia Epilepsy patients (2028) Severe CP with inability to walk Occipital <strong>lobe</strong> <strong>epilepsy</strong> (81) LBW (less than 35 weeks <strong>of</strong> gestation) Neonatal hypoglycemia (6) Inborn errors <strong>of</strong> metabolism Congenital anomalies Brain malformations Chromosomal abnormalities CP: cerebral palsy; no.: number; OLE: <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong>; LBW: low birth weight.
<strong>Long</strong>itudinal clinical course 95 Table 2 Perinatal histories and neurological sequelae. Patient no., sex, current age Gestational age (weeks) Birth weight (g) APGAR (1 min) Neonatal seizure Neonatal hypoglycemia Neurological sequelae Lowest level Duration (h) (IQ/DQ, examined age) 1, m, 13 years 39 2100 9 + 35 24 Normal 2, f, 17 years 42 2790 3 +
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