Objective To analyse the clinical features in general paresis of insane(GPI)as to offering an early diagnosis. Methods A retrospective analysis of 2 cases of GPI was focused on their clinical manifestations. Results The clinical features of GPI showed: (1) Chronic onset, progressive development in 2 cases; (2) Dementia was key symptom.Hasegawa dementia scales were 4 and 17 in 2 cases.2 cases accompanied with abnormal mentality,such as delusion of grandeur ,euphoria and so on;(3)GPI have features of pupil change,dysarthria,muscular tension,abnormal reflection; (4) Serum and cerebrospinal fluid (CSF) syphilis antibody reaction manifested positive, CSF protein content was increased significantly, and cells increased ( with lymph cell mainly ); (5) Head MRI manifested: cerebral atrophy in 2 cases, multiple abnormal signals in cerebral parenchyma in 1 case. Conclusions GPI misdiagnosis rate is high. Important basis of diagnosis remains on clinical manifestations, laboratory and imaging examinations.

BACKGROUND: More and more researches prove that cell apoptosis could be induced by glutamine, also there are more researches on studying the indirect and direct nervous-protective effects of insulin, but the nervous-protective effects of insulin on impairment induced by glutamine, as well as its mechanism still need further investigation.OBJECTIVE: To investigate the nervous-protective effects of insulin on impairment induced by glutamine in PC12 cells, and to explore its molecular mechanism.DESIGN: A prospective controlled study based on cells.SETTING: Department of Neurology, Zhejiang Hospital; Department of Neurology of Sun Yat-wen University Hospital.MATERIALS: The study was carried out at the Laboratory of the Third Affiliated Hospital and the Experimental Animal Center of Sun Yat-sen University from March 2002 to March 2003. PC12 cells were purchased from the same animal center.METHODS: Traumatic models were made in PC 12 cells by treated with 0.5 mmol/L glutamine for 20 minutes, and the insulin of different concentration were used for protection, after 24 hours, protective effects of insulin were assessed with MTT method, Hoechst33258 fluorescence staining, DNA agar gelatin electrophoresis, meanwhile the expression of PKB/Akt protein were also detected./Akt protein in experimental group.RESULTS: The A value of50 mU/L, 100 mU/L, 200 mU/L, 400 mU/L insulin groups were 0. 214 ±0. 062, 0. 234 ±0. 067, 0. 260 ±0. 076 and 0. 265 ± 0. 069, respectively, but the value of single glutamine group was 0. 201 ± 0. 079, statistical analysis indicated that compared with single glutamine group, there were no significant difference in 50 mU/L, 100 mU/L insulin groups( P > 0.05), but 200 mU/L, 400 mU/L insulin groups were found statistically different from single glutamine group(t=-2.398,-2. 716, P < 0.05); "DNA Ladder" could not be observed in 400 mU/L insulin group by electrophoresis;It was proved that Insulin could enhance the expression of PKB/Akt protein.CONCLUSION: Insulin has nervous-protective effects on impairment induced by glutamine in PC12 cells, furthermore it also has property of anti-apoptosis, and its protective mechanism might be associated with enhancement of the expression of PKB/Akt protein.