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Clinical course and serial neuroimaging findings are not fully described in children who have had neurological sequelae following status epilepticus. We found four patients who had neurological sequelae out of 42 children with status epilepticus in 2004. MRI studies were reviewed with specific attention to diffusion-weighted images (DWI) and the apparent diffusion coefficient (ADC). Proinflammatory cytokines, including tumor necrosis factor-alpha and interleukin-6, were measured in the cerebrospinal fluid (CSF) (3 patients). The clinical course showed biphasic; initial status epilepticus and neurological exacerbation along with seizure recurrence four to five days after onset. Within three days after initial status epilepticus, CT (all patients) and MRI (2 patients) did not show any abnormalities. From four to ten days after onset, MRI demonstrated diffuse hyperintensity in the cerebral white matter on DWI and hypointensity on ADC maps in all patients. Diffuse brain atrophy progressed thereafter. Tumor necrosis factor-alpha or interleukin-6 was elevated in all patients. A biphasic clinical course may be a specific feature for neurological sequelae. The preferential white matter involvement on MRI and elevated CSF cytokines indicate that glial dysfunction may play an important role in the pathophysiology of status epilepticus-associated cerebral damage.

Using a two-site enzyme-linked immunosorbent assay, we measured nerve growth factor (NGF) levels in cerebrospinal fluid (CSF) from 40 patients with or without brain atrophy due to various neurologic disorders. White matter and cortical atrophies were assessed by frontal horn index (FHI) and subarachnoid space area/inner skull space area (SSA/ISSA) ratio, respectively. CT findings of 40 patients were classified into 4 grades: normal (< mean + 2SD), grade I (mean + 2SD < or = or < mean + 4SD), grade II (mean + 4SD < or = < mean + 8SD), and grade III (mean + 8SD < or =). NGF levels in CSF were significantly elevated in 3 of 6 patients with grade III cortical atrophy and normal in 2 with grade II atrophy, 4 with grade I atrophy and 28 without atrophy. Cortical atrophy was progressive in the 3 with NGF elevation in CSF. With respect to white matter atrophy, NGF elevation was observed in none of 3 with grade III white matter atrophy, two of 4 with grade II atrophy, none of 3 with grade I atrophy and one of 30 without atrophy. The symptoms of the two of three with NGF elevation were progressive at the time of obtaining the CSF samples, while those of other patients without NGF elevation were non-progressive. The present study suggests that NGF elevation in CSF may reflect extensive cortical degenerative change.