Expression of estrogen receptor alpha and beta in reactive astrocytes at the male rat hippocampus after status epilepticus.

Estrogen is neuroprotective against status epilepticus (SE)-induced hippocampal damage in female animals. In male animals, estrogen is converted from testosterone via aromatization the activity of which is upregulated by brain damage. However, it is controversial whether estrogen is neuroprotective or neuroinvasive against male hippocampal damage after SE. In order to understand the role of estrogen, it is important to elucidate the distribution manner of estrogen receptor (ER)alpha and beta as the targets of estrogen. In this study, we examined the time course changes of ERs in adult male rat hippocampus after SE using anti-ERalpha antibodies (MC-20 and PA1-309) and anti-ERbeta antibodies (PA1-310B and PA1-311). In control rats, both ERalpha and beta were expressed in the pyramidal cells predominantly at CA1 and CA3. ERalpha was expressed in the cytoplasm and the nucleus, whereas ERbeta was expressed in the cytoplasm of the pyramidal cells. After SE, according to the pyramidal cell loss at CA1, the number of ERalpha- and beta-immunoreactive pyramidal cells decreased up to day 21. On the other hand, reactive astrocytes, which newly appeared after SE and formed gliosis at CA1, were confirmed to express both ERs in the nucleus, cytoplasm, and process. There were no differences in immunoreactivity between antibodies. Our results indicate that endogenous estrogen affects the pyramidal cells through ERalpha and beta under normal circumstances in adult male rats, whereas the targets of estrogen shift to the reactive astrocytes through ERalpha and beta after SE.

[A child with non-herpetic acute limbic encephalitis affecting the claustrum and hippocampus].

We experienced an 8-year-old-boy with non-herpetic acute limbic encephalitis (NHALE), who developed headache, convulsion, consciousness disturbance, and ataxia following cold like symptoms. Disturbance of short term memory and a change of character were recognized. Myoclonic seizures and generalized tonic clonic convulsions developed, that responded to antiepileptic agents. Although other symptoms resolved spontaneously, short term memory disturbance persisted. Brain MRI demonstrated the lesion involving the bilateral claustrum and right hippocampus. Three months later, the lesion in the claustrum disappeared, but the hippocampus still showed slight hyperintensity on FLAIR image of MRI. Autoantibodies against glutamine receptor were detected in the cerebrospinal fluid and plasma, which suggested the involvement of immunologic disturbances in this disease. In NHALE, many cases have been reported in adults but not in children, and the further attentions should be paid to childhood-onset NHALE.

Time course changes of estrogen receptor alpha expression in the adult rat hippocampus after kainic acid-induced status epilepticus.

Although estrogens possess neuroprotective and epileptogenic properties, the expression pattern of the estrogen receptor (ER) following status epilepticus (SE) remains unclear. We therefore examined the expression pattern of ER alpha in the adult rat hippocampus after SE. SE was induced in rats by kainic acid (KA; 12 mg/kg, i.p.). ER alpha expression was assessed by immunostaining and Western blotting at various times (24 h, and 7, 14, and 21 days) after SE onset. Immunohistochemistry disclosed ER alpha expression in the CA1 and CA3 pyramidal cells of control rats, whereas, after SE, ER alpha-immunoreactive neurons decreased in number due to neuronal death in the CA1 from days 7 to 21. On the other hand, ER alpha-immunoreactive cells with astrocytic morphology were observed in the CA1 beginning on day 7 after SE. This immunoreactivity increased in proportion to the hypertrophy of astrocytes up to day 21. Western blotting revealed a significant decrease in ER alpha expression on day 7 after SE in comparison with control level. However, ER alpha expression on days 14 and 21 were similar when comparing KA-treated and control rats. These results indicate that reactive astrocytes are important sites of estrogen action in the hippocampal CA1 after SE.

An infant with idiopathic orbital myositis poorly responsive to steroid therapy: a case report.

A 9-month-old girl developed subacute limited adduction of the left eye, presenting with blepharoptosis. An orbital magnetic resonance imaging (MRI) 2 months after the onset revealed swelling of the left lateral rectus muscle, with increased intensity on T2-weighted images with fat saturation, which was enhanced with gadolinium. She was diagnosed with idiopathic orbital myositis based on history, physical examination, and MRI findings. Swelling of the left lateral rectus muscle was partially reduced by pulse steroid therapy. This is the first reported case of an infant orbital pseudotumor with clinical and MRI findings consistent with subacute orbital myositis. We propose that a fibrotic change of the orbital muscle may occur during a subacute course and would be incompletely responsive to steroid therapy.

[Multicenter study of occipital lobe epilepsy in childhood: clinical characteristics].

We investigated the clinical characteristics of 54 patients with childhood onset occipital lobe epilepsy (OLE). There were 25 patients of symptomatic OLE (cortical dysplasia, post encephalitis or encephalopathy, brain tumor and so on), and 29 cases of cryptogenic OLE. Eighteen patients had positive visual symptoms such as flash light, bright spots and sparks of light, 23 patients had negative ones such as scotoma, hemianopia and amaurosis and 10 patients had other complicated visual symptoms such as change of the shape or colors. Young children complained of simple visual phenomena. The youngest patient who could explain visual symptom was 3 years old. All 3 patients with visual field defects had cortical dysplasia in occipital lobe. Ictal SPECT study showed wide hyperperfusion areas in the temporo-parieto-occipital lobe in most of patients with abnormal MRI findings. CBZ and VPA were prescribed in most cases, and were effective in 65% and 60% of the patients, respectively. Seizure prognosis was relatively good. Seizures disappeared in 56% of the patients with symptomatic OLE and 79% of those with cryptogenic OLE.

Usefulness of somatosensory evoked magnetic field dipole measurements by magnetoencephalography for assessing spinal cord function.

OBJECT: Objective assessment of sensory function disorders is difficult. In the present study, the authors investigated the possibility of assessing cervical myelopathy-induced sensory disorders by using magnetoencephalography (MEG) to measure somatosensory evoked magnetic fields (SSEMFs). METHODS: In 12 patients with cervical myelopathy, SSEMFs were measured before and after surgery by using a 160-channel helmet-type MEG system to stimulate the median nerve, and the intensity and latency of N20m (first response occurring 20 msec after stimulation) were then determined. Additionally, the severity of the sensory disorder was assessed before and after surgery by obtaining sensory scores determined using the Neurosurgical Cervical Spine Scale. Furthermore, in 11 healthy individuals (control group), the intensity and latency of N20m were measured in the same fashion. Analysis of the results showed that the preoperative intensity of N20m in the 12 patients with cervical myelopathy was significantly lower than that demonstrated in the control patients (p < 0.005, Student t-test). In addition, of six patients in whom sensory scores improved postoperatively, there were significant increases in the intensity of N20m (p < 0.005, paired t-test). Furthermore, there was a significant correlation between sensory scores and dipole intensity (p < 0.001, Spearman correlation coefficient by rank test). CONCLUSIONS: Somatosensory evoked magnetic field measurements determined by MEG are useful in objectively and noninvasively assessing sensory disorders caused by cervical myelopathy.