Objective To investigate Guillain Barre syndrome (GBS) combined with demyelinating neuropathy in central nervous system(CNS), and explore the possible mechanism and the relationship between the two.Methods 3 cases GBS combined with demyelinating neuropathy in CNS were observed clinically and the datum of laboratory were analysed.Results Case 1, a 28 year old man had symptoms of general flaccid paralysis and coma.The result of blood gas analysis was normal. CSF showed an albuminocytological dissociation, delayed nerve conduction velocity and missed F waves. Brain MRI showed multifocal T 2 Wight Image high signs in white matter of bilateral brain and cervical spinal cord. The patient is getting recovery by treatment with plasma and immunoglobulin. Case 2 , a 5 year old girl with progressive weakness of her limbs and respiratory arrest, appeared confusion,dully light reflex and absent corneal reflex, at last she died because of rejecting treatment.Case 3,a 12 year old boy with progressive weakness of his limbs and the difficult of relieving the bowels.Brain MRI was normal.Spinal MRI showed multifocal T 2 weight imagine hight signs from T 5 to L 4.CSF showed an albuminocytological dissociation.EMG showed a delayed nerve conduction velocity.Conclusion GBS combined with disorders of consciousness are mostly severe, the pathological mechanism is unclear. It is suggested that auto immunoreaction caused by P 1 myelin basic protein can relate to around and CNS demyelination.

Objective To study the risk of recurrence after a first unprovoked seizure and analyze the potential predictors of recurrence. Methods 150 patients with one or more recently unprovoked seizures who attended our hospital from October, 1998 to June, 2000, which included 66 patients having a first unprovoked seizure, were followed up for 2 years. Recurrence rate was estimated by Kaplan-Meier curves. Univariate and multivariate analyses of the potential predictors of recurrence were performed for the first unprovoked seizure patients using the Cox proportional hazards model.Results All the 150 patients had 109 relapses in 2 years, Kaplan-Meier estimate of recurrence rate was 73%(?3.6%), while 66 first unprovoked seizure patients had 36 relapses, with the recurrence rate 54%(?6.1%). Cox Univariate and multivariate analyses showed that symptomatic etiology increased the risk of recurrence, and other predictors of recurrence included abnormal electroencephalogram, the occurrence of seizures during sleep and first seizure lasting longer than 10 minutes, whereas an age of 3 to 12 years decreased this risk.Conclusion The recurrence risk after the first unprovoked seizure is lower than those who have two or more recent seizures. Several factors enable us to predict the recurrence risk after a first unprovoked seizure.

BACKGROUND: Status epilepticus can result in neuronal injury.OBJECTIVE: To observe the mitochondrial ultrastructural damage and the changes of Fas, Bax and Caspase-3 expressions in hippocampal CA3 neurons of rats of different kindling, so as to provide theoretical evidence for the neuronal injury after epilepsy.DESIGN: A randomized c ntrol animal experiment.SETTINGS: Department of Neurology and Department of Anesthesiology,Qilu Hospital of Shandong University.MATERIALS: The experiments were carried out in the pathological laboratory of Shandong Academy of Medical Sciences between March and July2005. Totally 150 adult male SD rats of 260-300 g were provided by the experimental animal center of Shandong University (SCXK20030004), they were raised at room temperature and were free to the access of food and water.METHODS: The adult male Sprague Dawley (SD) rats were divided into intraperitoneal injection of kainic acid group and caudal venous injection of kainic acid group respectively ac cording to the method of random number table, and the rats were administrated by kainic acid injected intraperitoneally (12 mg/kg) and via caudal vein (10 mg/kg) respectively. Each group was divided into 5 subgroups, which were 3, 6, 24, 48 and 72 hours after status epilepticus groups respectively. Twelve successfully induced rats were selected from each subgroup, hippocampi were removed at different time points after the termination of status epilepticus, 2 were used for examination under electron microscope, 5 for the reverse transcription-polymerase chain reaction (RT-PCR) detection of Fas and Bax, and 5 for the immunohistochemical assay of Caspase-3. Another 12 rats were used as normal controls without any treatment. The materials were taken at24 hours after corresponding status epilepticus in the control group, and the specific distributions were the same as those in the subgroups. The mitochondrial structure was observed under electron microscope, the levels of Fas and Bax mRNA were detected with semi-quantitative RT-PCR, and the expression of Caspase-3 protein was determined with the immunohistochemical assay.MAIN OUTCOME MEASURES: ① Results of ultrathin section under transmission electron mcroscope; ② RT-PCR results; ③ Immunohistochemical results.RESULTS: Totally 132 rats were involved in the analysis of results. ①Mitochondrial structure under electron microscope: In the intraperitoneal injection group, the mitochondria swelled, and the neurons showed characters of apoptosis. In the caudal venous injection group, the mitochondria swelled, and accompanied by the membranous collapse, and the neurons manifested the necrosis. ② No expression of Fas and Bax was detected in the control group and caudal venous injection. In the intraperitoneal injection group, Fas expression appeared at 6 hours after status epilepticus, increased at 24 hours, reached the peak value at 48 hours, and lasted till 72 hours. ③ The Caspase-3 expressions began to increase 6 hours after status epilepticus in both the intraperitoneal injection group and caudal venous injection group(10.27±0.34, 15.21±0.34; P ＜ 0.001), and reached the peak values at 24 hours (25.36±0.47, 28.23±0.47; P ＜ 0.001); The higher expression of Caspase-3 lasted till 72 hours in the intraperitoneal injection group, but sharply decreased in the caudal venous injection group.CONCLUSION: Two different methods of administration result in different severity of mitochondrial damage and different expressions of Fas, Bax and Caspase-3, which further determines the molecular mechanisms of neuronal death.

Objective To study the role of gap junctions in epileptiform activity. Methods The epileptiform activity was induced by zero-Mg 2+ medium in cultured hippocampal neurons of newborn rats. Immunocytochemistry and real time RT-PCR were introduced to evaluate the expression of gap junction Cx32 and Cx43. Results The level of Cx32 mRNA increased quickly one hour after the neurons were treated with zero-Mg 2+ medium and was raised by 10 times 5 hours later, while Cx32 protein began to develop at the 2nd hour (21.80?1.74) and was raised by 5 times at the 8th hour (47.30?5.75). The expression of Cx43 mRNA went up obviously 5 hours later, and Cx43 protein developed visibly 8 hours later. Carbenoxolone depressed the expressions of Cx32 and Cx43. Conclusions The expression of Cx32 and Cx43 increases dramatically after epileptic discharges and carbenoxolone inhibits both the discharges and the expression of gap junctions, which indicates that gap junction could contribute to epileptogenesis.

Objective To investigate the value of gradient echo T2'* -weighted imaging for detection of familial cerebral cavernous malformation (FCCM). Methods Twenty-six members in 2 families of FCCM were examined at 3.0 T by using CT, conventional MRI and GRE T2'*2'-WI sequences to detect numbers of FCCM. Results Twelve cases of FCCM were found by GRE T2'*-WI sequences. These patients all had multiple lesions(average of 23). The lesions were mainly located in ganglia area, followed by cortico-subcortical, thalamus, cerebellar and brain stem. These lesions appeared as special reticulated core of mixed signal intensity with a surrounding rim of decreased signal intensity representing bemosiderin from previous hemorrhages. The numbers of lesions (average of 5-17) and cases of FCCM (average of 3-9) examined by the conventional MRI were decreasing in the order of SE, DWI, T2FLAIR, T1WI and T2WI, each less than GRE T2'*-WI. CT only identified 3 cases with big lesions combined with hemorrhage and calcification.Conclusions GRE T2'*-WI could be a better choice of MRI sequence in diagnosing FCCM compared with CT and conventional MRI.

Objective To study the role of calcium homeostatic and kinetics in the epileptogenesis activity. Methods Hippocampal neurons were acutely isolated from controls and status epilepticus (SE) models induced by lithium-pilocarpine at different time point. The [Ca2+]i levels were detected by laser scanning confocal microscope. And the ability to restore resting [Ca2+]i levels after a brief exposure to 5 μmol/L glutamate in control and epileptic neurons were evaluated. Results The [Ca2+]i level of acute separated hippocampal neurons in the control rats was (95.4±22. 1) nmol/L After injection of lithium pilocarpine, the [Ca2+]i level in hippecampal neurons increased dramatically to (867.6±35.2) nmol/L, and decreased to (292.8 ± 18.3) nmol/L on the 7th day, lasting for about 30 days ((220. 8± 17.6) nmol/L), it is higher than that in the control group (t = 12. 55, P < 0.01). The distribution of neuronal [Ca22+]i showed that 92% of control neurons were in the normal range of [Ca2+]i level (25-150 nmol/L) ; After 6 hours, however [Ca2+]i levels of all SE neurons increased, and 85% of which were higher than 500 nmol/L; After 7, 14 and 30 days, there were 75%, 60% and 52% of SE neurons still manifested an elevated [Ca22+]i level, but less than 500 nmol/L. After the exposure to 5 μmol/L glutamate treatment for 2 minutes, [Ca2+]i of the control neurons restored to baseline values in (9. 5±3.4) minutes, whereas the SE rats of acute, latent and chronic phases did not (t = 5.08, 4. 56, 4. 21, all P < 0. 01). Conclusion Lithium-pilocarpine induced epilepsy causes a long-term alteration of calcium homeostatic mechanisms of hippocampus neurons, which may play an important role in the development and maintenance of spontaneous recurrent seizures.

Objective To investigate clinicopathological and neuroimaging features of meninheal malignant melanosis.Methods The cytologic study of cerebrospinal fluid(CSF)and neuroimaging examination and meningeal histochemistry were performed in 3 cases of meningeal malignant melanosis. Results Three patients were found to have initial onsets of headache.followed by meningeal irritation.One case had huge malignant melanoma on skin.The second patient had diabrotic malignant melanoma on her face,which did not healed for a long time.The third patient had no malignant melanoma on skin and viscera.The MRI enhanced scanning of all 3 cases showed abnormal enhancement of meninge.There were a large number of abnormal shape cells in CSF.The meninxes were blackbrown or brown.The tumor cells were in various shapes with big and round irregular nucleus and rich cytoplasm.There were a great quantitv of melanosomes.The tumor cells were disarranged. Immunohistochemistry analyses found S-100 protein and Vim and HMB-45 were positive reaction. Conclusions The patients with meningeal malignant melanosis have an initial onset of headache,followed by meningeal irritation,and MRI enhanced scanning plays a valueble role in the diagnosis.A lage number of tumor cells in abnormal shape have been found in CSF.Thetumour cells of meninx presents different shapes with big and round or irregular nucleus.There are a great quantity of mellanosomes,and the tumour cells are arranged in a state of chaos.

Objective To investigate the clinical and neuroimaging futures of chorea due to nonketotic hyperglycemia.Methods Seven cases of chorea due to nonketotic hyperglycemia were clinically examined and underwent brain CT and MRI as well.Results Investigations revealed uncontrolled diabetes with absent ketones of 7 cases.They all presented with sudden onset hemiachorea or bilateral chorea or generalized chorea.The CT scan of brain could find abnormal lesions in our cases.Hyperintense lesions in the basal ganglia,on T1 WI of MRI were demonstrated in our study.Pure drugs was unable to control chorea.The symptoms of chorea and neuroimaging lesions were normal after the hyperglycemia being controlled.Conclusions Chorea caused by nonketotic hyperglycemia is mainly found in aged people with diabetes mellitus in a mechanism of causing striatal neuronal dysfunction,presenting charicristic CT scan or MRI of brain.Chorea should be considered potentially reversible when associated with nonketotic hyperglycemia,for rapid detection and early correction of hyperglycemia could lead to complete recovery of these involuntary movements.

Objective To investigate the clinical and neuroimaging features of hypoglycemia encephalopathy in the elderly. Methods The history and clinical features of 36 patients who had undergone brain CT and MRI were analyzed retrospectively. Results Twenty-seven patients had infections and fevers as a trigger, presenting all kinds of symptoms. Eleven cases were found to have abnormal signals in bilateral caudate nucleus and lenticular nucleus in MRL But CT examination showed no new lesions in corresponding position. Hypoglycemia encephalopathy were commanly found in the elderly who had diabetes mellitus and treated with drugs. After being followed up for 6 months, their neuroimaging did not change. Conclusions Because the patients often present unconsciousness and weakness with a sudden onset, hypoglycemia is easily mistaken for other disorders, especially in the elderly. For those with consciousness, we should pay more attations to hypoglycemia. Brain CT has no value of diagnosing hypoglycemia encephalopathy, while MRI plays an impotant role in diagnosing the disease. The characteristic MRI features predicts a bad prognosis.

Objective: To investigate an optimal chemotherapy regimen for patients diagnosed with lung adenocarcinoma harboring common EGFR mutations. Methods: Clinical data of 4,021 patients diagnosed with advanced primary lung adenocarcinoma who were admitted to Guangdong Lung Cancer Institute from June 2007 to June 2014 were retrospectively collected. The efficacy of the standard chemotherapy regimen in patients diagnosed with luny adenocarcinoma harboring common EGFR mutations was analyzed. Results: In total, 205 patients were included in the study, and 119, 60 and 81 patients received gemcitabine plus platinum, pemetrexed plus platinum, and paclitaxel plus platinum regimens, respectively. Statistical difference was not observed in the objective response rate (ORR,25.2%, 25.0%, 30.8%, respectively) and progression free survival (PFS, 5.5, 5.2, 6.2 months, respectively) between these three treatment regimens (P=0.979, P=0.811). Conclusions: Platinum-based chemotherapy regimens based on gemcitabine, pemetrexed, and paclitaxel have similar efficacy in patients diagnosed with advanced primary lung adenocarcinoma harboring common EGFR mutations.