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Long term prognosis of symptomatic occipital lobe epilepsy ... - sepeap

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94 H. Montassir et al.<br />

Perinatal history and neurological sequelae (Table 2)................................................................. 94<br />

Characteristics <strong>of</strong> epileptic seizure and clinical course <strong>of</strong> <strong>epilepsy</strong> (Table 3 and Figs. 1 and 2)........................ 95<br />

EEG and MRI findings (Table 4 and Figs. 3—5) ......................................................................... 97<br />

Discussion ............................................................................................................... 97<br />

References .............................................................................................................. 99<br />

Introduction<br />

Glucose is essentially important for brain metabolism. It<br />

is well known that severe neonatal hypoglycemia results<br />

in posterior cerebral injury. The neurological sequelae<br />

<strong>of</strong> severe neonatal hypoglycemic encephalopathy include<br />

developmental delay, learning or behavioral problems,<br />

<strong>epilepsy</strong>, and visual impairment. Although the prevalence<br />

<strong>of</strong> <strong>epilepsy</strong> in neonatal hypoglycemic encephalopathy was<br />

quite high, studies about <strong>epilepsy</strong> secondary to neonatal<br />

hypoglycemia are sparse (Norden, 2001). Caraballo et<br />

al. (2004) reported that <strong>prognosis</strong> <strong>of</strong> <strong>symptomatic</strong> <strong>occipital</strong><br />

<strong>lobe</strong> <strong>epilepsy</strong> following neonatal hypoglycemia was<br />

mostly good. In our own experience, <strong>symptomatic</strong> <strong>occipital</strong><br />

<strong>lobe</strong> <strong>epilepsy</strong> secondary to neonatal hypoglycemia is<br />

intractable to treatment with high prevalence <strong>of</strong> status<br />

epilepticus in infancy but remits in late childhood. <strong>Long</strong>itudinal<br />

clinical course <strong>of</strong> <strong>epilepsy</strong> secondary to neonatal<br />

hypoglycemia are not fully described. In this study, we<br />

sought to examine the long-<strong>term</strong> <strong>prognosis</strong> and longitudinal<br />

clinical course <strong>of</strong> <strong>symptomatic</strong> <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong><br />

secondary to neonatal hypoglycemia.<br />

Subjects and methods<br />

We retrospectively extracted subjects from the database <strong>of</strong> outpatients<br />

who were referred to our child neurology clinic at Tottori<br />

University Hospital from 1980 to 2006 (12,463 patients). We<br />

extracted the data <strong>of</strong> 2028 epileptic patients from our database.<br />

Then, 81 patients with <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> were extracted.<br />

Patients with <strong>symptomatic</strong> <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> who had neonatal<br />

hypoglycemia were the subjects <strong>of</strong> this study. Occipital <strong>lobe</strong><br />

<strong>epilepsy</strong> was defined as having ictal semiology identical to <strong>occipital</strong><br />

<strong>lobe</strong> seizures, which include eye deviation or eye blinking with<br />

staring, ictal vomiting, or visual hallucination (Williamson et al.,<br />

1992), and interictal paroxysmal waves in the posterior derivation.<br />

Patients with <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong> who had <strong>occipital</strong> <strong>lobe</strong><br />

injuries other than neonatal hypoglycemia were excluded. Severe<br />

hypoxic-ischemic brain injury is a high risk for the occurrence <strong>of</strong><br />

<strong>epilepsy</strong> regardless <strong>of</strong> hypoglycemia, while the mild to moderate<br />

type is not (Zafeiriou et al., 1999; Pisani et al., 2009). Therefore,<br />

patients with severe cerebral palsy who are not able to walk independently<br />

were excluded, while those with mild cerebral palsy were<br />

included. Epilepsy patients with pre<strong>term</strong> birth (less than 35 weeks<br />

gestation) or those with inborn errors <strong>of</strong> metabolism, congenital<br />

anomalies, brain malformation, or chromosomal abnormality were<br />

also excluded, even if they had histories <strong>of</strong> neonatal hypoglycemia<br />

(Table 1).<br />

Neonatal hypoglycemia was defined as whole-blood glucose concentration<br />

below 35 mg/dL, 40 mg/dL, and 45 mg/dL during 0—3 h,<br />

3—24 h, and after 24 h after birth, respectively (Srinivasan et al.,<br />

1986).<br />

Onsets <strong>of</strong> <strong>epilepsy</strong>, major seizure types, and clinical course <strong>of</strong><br />

<strong>epilepsy</strong>, EEG and neuroimaging findings were studied from their<br />

medical records. Status epilepticus was defined as clinical seizure<br />

lasting more than 30 min. MRI (1.5 T or 3.0 T recently) was performed<br />

repeatedly and included T1-, T2-, and FLAIR imaging. Mental<br />

or intellectual status was evaluated using the Wechsler intelligence<br />

scale for children or the Enjoji development scale. ‘‘Normal’’ was<br />

defined when IQ or DQ was more than 70, ‘‘mild’’ mental retardation<br />

(MR) or developmental delay was defined when it was between<br />

50 and 70, ‘‘moderate’’ when it was between 20 and 50, and<br />

‘‘severe’’ when it was below 20. We also reviewed clinical and<br />

laboratory data during perinatal periods.<br />

This study was approved by the ethical committee in Tottori<br />

University.<br />

Results<br />

The most common epileptic syndrome <strong>of</strong> <strong>occipital</strong> <strong>lobe</strong><br />

<strong>epilepsy</strong> was idiopathic childhood <strong>occipital</strong> <strong>epilepsy</strong><br />

(Panayiotopoulos syndrome and Gastaut type) and this was<br />

found in 54 <strong>of</strong> the patients. Twenty-one patients with <strong>occipital</strong><br />

<strong>lobe</strong> <strong>epilepsy</strong> were excluded and finally 6 patients (5<br />

males and 1 female) were the subjects <strong>of</strong> the study (Table 2).<br />

Perinatal history and neurological sequelae<br />

(Table 2)<br />

Perinatal histories and neurological sequelae are shown in<br />

Table 2. Patients 1—4 were taken care <strong>of</strong> in our neonatal<br />

intensive care unit and Patients 5 and 6 were treated in other<br />

hospitals. Perinatal histories closely correlated with neonatal<br />

hypoglycemia were highly present: low birth weight for<br />

gestational age in 5, low Apgar score after 1 min in 3, and<br />

neonatal seizure in 5. Severe neonatal hypoglycemia with a<br />

serum glucose level <strong>of</strong> less than 15 mg/dL was reported in<br />

3 patients and hypoglycemia was prolonged more than 10 h<br />

Table 1<br />

Inclusion and exclusion criteria.<br />

Inclusion criteria (no. <strong>of</strong> patients)<br />

Exclusion criteria<br />

Outpatients (12,463)<br />

OLE with <strong>occipital</strong><br />

injuries other than<br />

neonatal<br />

hypoglycemia<br />

Epilepsy patients (2028)<br />

Severe CP with<br />

inability to walk<br />

Occipital <strong>lobe</strong> <strong>epilepsy</strong> (81) LBW (less than 35<br />

weeks <strong>of</strong> gestation)<br />

Neonatal hypoglycemia (6) Inborn errors <strong>of</strong><br />

metabolism<br />

Congenital anomalies<br />

Brain malformations<br />

Chromosomal<br />

abnormalities<br />

CP: cerebral palsy; no.: number; OLE: <strong>occipital</strong> <strong>lobe</strong> <strong>epilepsy</strong>;<br />

LBW: low birth weight.

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