ABSTRACT
Introduction: This study aims to explore the clinical features and prognostic factors for relapse of acute disseminated encephalomyelitis (ADEM) in adults. Material and methods: 56 patients with ADEM were retrospectively analyzed. The epidemiological characteristics, clinical manifestations, laboratory features, magnetic resonance imaging (MRI), treatment and prognosis data of these patients were analyzed using the χ2 test for categorical variables and Mann-Whitney U-test for continuous variables. Then, the clinical characteristics and recurrence factors were summarized. Results: 56 patients with ADEM, based on the criteria of the International Pediatric Multiple Sclerosis Study Group, were recruited to the study. Among these patients, 31 were male and 25 were female. Furthermore, 13 patients had multiphasic ADEM, and 29 patients (52%) had definite incentive factors before onset. The commonest presenting symptoms and signs were fever (36%), disturbance of consciousness (52%), mental disorder (38%), seizure (14%), headache and dizziness (43%), optic neuritis (34%), autonomic nervous system symptoms (43%), limb paralysis or abnormal sensation (73%), and unilateral or bilateral pyramidal tract signs (48%). Inflammatory changes in the cerebrospinal fluid were prominent. MRI T2-weighted and fluid-attenuated inversion recovery images displayed multiple or large flaky high signals, and the lesions were usually different in the number and distribution of these lesions. Intravenous corticosteroids and/or immunoglobulin were still important treatments in the acute phase. After treatment, 38 patients completely recovered, 9 patients had neurologic deficits, and 9 patients died. Conclusions: ADEM in adults is not uncommon, its clinical features are complex and varied, and some of these are multiphasic. There may be some potential clinical predictors at first onset.
ABSTRACT
OBJECTIVE: To investigate the effects of estrogen 17beta-estradiol on beta-amyloid protein 25-35 (Abeta25-35) -induced neurotoxicity and possible mechanism thereof. METHODS: Primary cortical neurons were obtained from the brain of a SD rat and cultured and treated with Abeta25-35 and 17beta-estradiol. I order to investigate the possible mechanism of antagonism of estrogen against the neurotoxicity of Abeta25-35, Akt- I, a specific Akt inhibitor and ICI-182780, an inhibitor of estrogen receptor were added before the addition of estrogen. The Abeta32-35 induced cell viability and lactate dehydrogenase (LDH) release into the cell media was detected with spectrophotometer. Western blotting was used to detect the level of phosphorylated Akt, a cell-protecting factor, and level of nonphosphorylated Akt in different conditions. RESULTS: 20 micromol/L Abeta25-35 decreased the cell viability of the rat cortical neurons to 40.4% (P < 0.01) as compared with the control group and the cell viability of the group with the addition of 17beta-estradiol was 84.2%, significantly higher than that of the Abeta25-35 group (P < 0.01). The LDH secretion level of the Abeta25-35 was 172.5% as high as that of the control group (P < 0.01), while that of the 17beta-estradiol preincubation group was only 118.5% that of the control group (P < 0.01). Both Akt inhibitor and estrogen receptor antagonist partially antagonized estrogen's protective effects against Abeta25-35 in cell viability. Abeta25-35 decreased the phosphorylated Akt level to 69.5% (P < 0.01), while estrogen 17beta-estradiol pretreatment antagonized this effect to 94.7% (P < 0.01), and the addition of Akt inhibitor partially blocked the estrogen's rescue effect (75.4%, P < 0.05). Estrogen treatment alone increased Akt phosphorylation, but this phosphorylation could be partially blocked by the estrogen receptor antagonist, the latter alone had no effect on Akt phosphorylation. Under all circumstances, the amount of nonphosphorylated Akt didn't change significantly. CONCLUSION: The estrogen 17beta-estradiol partially alleviates the Abeta25-35-induced neurotoxicity and Akt activation may be involved in estrogen's neuroprotective effect. Estrogen receptor may play a role in estrogen induced Akt activation.
