BACKGROUND: Elderly post-stroke secondary epilepsy is the main cause of elderly epilepsy, and has a certain effect on the rehabilitation and prognosis of stroke.OBJECTIVE: To probe into the association of post-stroke epileptic attack with the type, location and size of stroke.DESIGN: A case analysis.SETTING: the Department of Neurology, Qianfoshan Hospital of Shandong Province.PARTICIPANTS: Between January 1999 and December 2004, 68 inpatients (42 males and 26 females) with post-stroke secondary epilepsy, aged 60-83 years with an average of (68±7), were selected from the Department of Neurology, Qianfoshan Hospital of Shandong Province, and all the patients participated in the study voluntarily.METHODS: [1] According to the time of the first attack of post-stroke epilepsy, the patients were divided into early epilepsy (within 2 weeks post stroke) and delayed epilepsy (after 2 weeks post stroke), and the correlation between the time of epilepsy attack and types of stroke was analyzed. [2]Based on the imaging results, the ischemic stroke (including cerebral thrombosis and cerebral embolism) was divided into groups of ＜ 1/4, 1/4-1/2, ＞1/2 of unilateral hemisphere according to the infarcted size, and divided into groups of ＜ 20 mL, 20-40 mL, and ＞ 40 mL according to the amount of cerebral hemorrhage, and the association of epileptic attack with the stroke location and size was analyzed. [3] All the patients received symptomatic treatment, and they were followed up for 6 months to 4 years with an average of 21 months by means of reexamination. [4] The differences of the enumeration data were compared with the χ2 test.RESULTS: All the 68 patients with post-stroke epileptic attack were involved inthe analysis of results. [1] The correlation between the time of epileptic attack and type of stroke: The cases of cerebral hemorrhage and subarachnoid hemorrhage were obviously more in the patients with early epilepsy than in those with delayed epilepsy (10, 2 cases; 4, 0 case, P ＜ 0.05),and the cases of cerebral thrombosis were obviously fewer in the patients with early epilepsy than in those with delayed epilepsy (3, 36 cases, P ＜ 0.05). [2]The association of epileptic attack with the stroke location and size: There were more cases with the infarcted size of 1/4-1/2 and ＞1/2 of unilateral hemisphere than those with the infarcted size of ＜ 1/4 of unilateral hemisphere (26, 17, 9 cases, P＜ 0.05). There were more cases with the 20-40 mL and ＞ 40 mL cerebral hemorrhage than those with ＜ 20 mL cerebral hemorrhage (4, 9, 1 case, P ＜ 0.05). [3] The prognosis of epileptic attack: Of the 21patients with early epilepsy, epilepsy was the first symptom in 6 cases, and no re-attack occurred within 2 weeks in 15 cases. Of the 47 patients with delayed epilepsy, the disease after 1 year was completely controlled in 18 cases,better controlled in 23 cases, and the attack was frequent in 6 cases.CONCLUSION: [1] Early epilepsy is mainly manifested by cerebral hemorrhage, subarachnoid hemorrhage and cerebral embolism, and delayed epilepsy is mainly manifested by cerebral thrombosis. [2] The risk of epilepsy is obviously increased in the patients with the infarcted size over 1/4 of the unilateral hemisphere, and those with ＞ 40 mL cerebral hemorrhage. [3] The prognosis of early epilepsy is better.

Objective To investigate the effects of electric stimulation on motor function and expression of Rho kinase following cerebral infarction in rats. Methods Acute cerebral infarction was modeled in adult male Sprague-Dawley ( SD) rats using the permanent middle cerebral artery occlusion ( PMCAO) technique. The rats were randomly divided into sham operation, control, unilateral electric stimulation and bilateral electric stimulation groups ( each group had 36 rats). Electric stimulation was applied to the paralyzed ( unilateral or bilateral) limbs in the last two groups. Motor function recovery and the expression of Rho kinase were examined using a beam walking test ( BWT) and immunohistochemistry respectively at the 3rd, 7th, 14th and 21st day after stimulation. In addition, the cerebral infarction volume was also determined by 2, 3, 5-triphenyl tetrazolium chloride (TTC) staining at different time points. Results Motor function improved significantly in the electric stimulation groups compared with the control group, and the effect in the bilateral electric stimulation group was better than that in the unilateral electric stimulation group. The expression of Rho kinase decreased remarkably in the electric stimulation groups, and it was significantly lower in the bilateral group than in the unilateral electric stimulation group. No difference in cerebral infarction volume was found at the 3rd day. At the 21st day, the cerebral infarction volume had decreased significantly in both stimulation groups compared with the control group, but no difference was seen between the unilateral and bilateral electric stimulation groups. Conclusions Early electric stimulation, especially bilateral electric stimulation, can improve motor function after cerebral infarction and reduce cerebral infarction volume, which may be associated with down-regulation of the expression of Rho kinase in the border zone of the infarction.

Objective To investigate the effects of electric stimulation on motor function and expression of microtubule-associated protein-2(MAP-2) and survivin of brain tissue in the cerebral infarction rats.Methods Cerebral infarction rat models were made using middle cerebral artery occlusion.After cerebral infarction for 24 h,the rats were respectively treated with electric stimulation on paralyzed(unilateral)or bilateral limbs for 3 d,7 d,14 d,21 d.By using beam walking test(BWT) and immunehistochemistry,the motor function and the expression of MAP-2 and survivin of brain tissue in the border of cerebral infarction area were examined at various time following treatment.Results Compared to control group,the electric stimulation groups showed significant increase in BWT scores after treatment 7 d(all P0.05).In the electric stimulation groups,the expression of survivin of brain tissue were obviously higher than those in the sham operation group at various time points(all P0.05).Conclusions Treatment with electric stimulation,in particular bilateral electric stimulation,can promote the recovery of motor function of paralyzed limbs and induce up-regulation of expression of MAP-2 and survivin in the brain tissue of cerebral infarction rats.

Objective To investigate the effects of orexin-A on learning and memory of pentyleneterazol (PTZ)-kindled epileptic rats.Methods Adult Wistar rats were randomly divided into control group(normal saline,NS)and PTZ group.The PTZ-kindled rats were randomly divided into,orexin-A group and NS group administrated by intracerebroventricular(i.c.v.)injection of 10μl orexin-A(1.4 nmol/μl)or 10μl NS.Using Morris water msze experiment,the ability of learning and memory was measured in all rats.Results Eighty percent of rats in PIZ group were kindled successfully after intraperitoneal injection of 35mg/kg PTZ every day for 30 days.Compared to control group,the escape latency in the PTZ-kindled rats was significantly increased in place navigation test(PNT)(F=200.956,P<0.01),whereas a remarkable reduction of time spent in the target quadrant and number of pool circlings in 120 seconds Was observed during probe trials.Following injection of orexin-A,the latency of escape platform was significantly declined in both PTZ-kindled((39.73±2.03)8,(33.76±2.96)s)and NS rats,increased the number of crossing the platform(10.83±1.80)vs(4.67±3.34).In addition,the treatment with orexin-A markedly increased swim velocity and number of pool circlings in beth groups(P<0.01),particularly to the PTZ-kindled rats.Conclusion Spatial learning and memory in the PIZ-kindled rats can be improved by treatment with orexin-A.

Objective To investigate the effects of unilateral and bilateral electrical stimulation of the upper and lower limbs on motor function following cerebral infarction and the expressions of microtubule-associated protein-2 (MAP-2) and survivin in the infarction border zone of rats. Methods Adult male Sprague-Dawley (SD) rats were randomly divided into sham operation, control, impaired limb and bilateral limbs electrical stimulation groups (each group included 32 rats). Acute cerebral infarction was mimicked using a middle cerebral artery occlusion tech-nique. After cerebral infarction for 24 h, the rats were treated daily with or without electrical stimulation. A beam walking test (BWT) was used to measure limbs motor function and immunohistochemistry and HE staining were used to detect the expressions of MAP-2 and survivin in the border zone of infarcted area after electrical stimulation treat-ment for 3, 7, 14 and 21 d. Results Comparet with the control group treatment with electric stimulation led to BWT scores increasing significantly, and bilateral stimulation was more potent in ameliorating motor function thanstimulating the impaired limb only. The expression of MAP-2 was significantly higher in eleetrieal stimulation groups than in control group from the 7th of treatment, and it was higher in bilateral stimulation group than that in unilateral stimulation group from tbe 14th day of treatment. There was no significant difference in MAP-2 expression between bi-lateral stimulation group and sham operation group at the 21st day of treatment. In electrical stimulation groups, at every time point the expressions of survivin were obviously higher than that in sham operation group, and it was higher than that in control group and peaked at the 7tb and 14th day of treatment and in bilateral stimulation group it was no-tably higher than that in unilateral stimulation group. At the 21st d of treatment the level of survivin expression drop-per; however, there was no significant difference between unilateral and bilateral electrical stimulation groups. Con-clusions Treatment with electrical stimulation, particularly in bilateral limbs stimulation, could induce MAP-2 and survivin expressions in the infarction border zone of rats. It also could promote the recovery of motor function in para-lyzed limbs after cerebral infarction of rats. The improvement might involve the up-regulation of MAP-2 and survivin expressions.

Objective To investigate the correlation between spatial memory and sleep architecture and hippocampal volumes in patients with chronic insomnia disorder.Methods Twenty-two chronic insomnia patients and 17 normal sleepers (controls) were selected to evaluate the subjective insomnia using Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS), Insomnia Severity Index (ISI) and the objective insomnia by polysomnography (PSG).The cognitive function was measured by Montreal Cognitive Assessment (MoCA).Spatial memory and object-memory were measured by Nine-box Maze, and object-recognition memory was detected by picture recognition test.MRI was used to detect hippocampus volumes.Results Compared with controls, a significant reduction in total sleep time (328.3 (310.4, 387.9) min vs 418.0 (375.8, 45.5) min, Z=2.607, P=0.009), sleep efficiency (%) (77.7 (73.1, 84.0) vs 93.0 (87.2, 93.9), Z=3.739,P=0.000), proportion of N3 (%) (5.5 (0.4, 14.4) vs 13.7 (7.7, 18.3), Z=2.664, P=0.008) and proportion of rapid eye movement (REM) (%) (14.4 (10.7, 17.2) vs 17.3 (15.9, 23.3), Z=2.890, P=0.004) was seen in insomnia patients, whereas sleep latency was delayed.The error numbers of spatial working-memory (4.5 (2.0, 7.3) vs 1.0 (0.0, 3.0), Z=3.007, P=0.003) in chronic insomnia patients were more than those in controls.There was no statistically significant difference in object reference memory, spatial reference memory and object recognition in two groups.A significant reduction of the left (2 818.0 (2 534.9, 3 191.8) mm3 vs 3 453.3 (3 081.2, 3 764.4) mm3, Z=3.314, P=0.001), right (2 780.5 (2 451.2, 3 191.8) mm3 vs 3 479.8 (3 024.1, 3 786.7) mm3, Z=3.484,P=0.000) and whole hippocampal volumes (5 561.7 (4 956.6, 6 396.9) mm3 vs 6 898.9 (6 017.1, 7 540.1) mm3, Z=3.455, P=0.001) was seen in chronic insomnia patients compared with controls.The hippocampal volumes were negatively correlated with sleep latency (r=-0.432, P=0.006), but positively correlated with sleep efficiency, proportion of N3 (r=0.323, 0.376;P=0.045, 0.018).There was a negative correlation between the error numbers of spatial working-memory and hippocampal volumes (r=-0.351, P=0.029).The hippocampal volumes were negatively correlated with the duration of disease in chronic insomnia patients (r=-0.734, P<0.01).Conclusion The spatial memory may be associated with decreased proportion of REM and reduced hippocampal volumes in chronic insomnia patients.

Objectives To access the bacteriology in patients with sepsis due to biliary tract infection to provide a basis for empirical selection of proper antibiotic treatment.Methods This is a single-center retrospective study on 214 patients with biliary tract infection admitted from August 2014 to July 2016 to the surgical intensive care units (ICU) of The First Affiliated Hospital of Sun Yat-sen University.To study the demographic information,sequential organ failure assessment (SOFA),usage of antibiotics before ICU and duration of ICU were analyzed.Bile,peritoneal drainage and blood samples were collected.Results 47 septic shock patients and 25 septic patients due to biliary tract infection were enrolled in the trial.The two groups (the shock group vs.the sepsis group) had a significant difference in the duration of ICU stay [(6.4 ± 4.6) d vs.(2.3 ± 1.8) d,P ＜ 0.05].48 strains of pathogens were isolated from the bile samples.The major pathogens were Escherichia coli (E.coli) (n =23,47.9％),Enterococcus faecalis (n =8,16.7％) and Enterococcus faecium (n =2,4.2％).80 strains of pathogens were isolated from the peritoneal drainage culture samples.E.coli,pseudomonas aeruginosa,and Klebsiella pneumoniae ranked the top 3 species,accounting for 26.3％,11.3％ and 7.5％,respectively.The sensitivity of E.coli isolated from bile to amikacin,imipenem and panipenem were all over 90.0％.Conclusions E.coli was the principal gram-negative bacterium in biliary infection induced sepsis.Early administration of carbapenemes may reduce the occurrence of septic shock in these patients.

N-methyl-D-aspartate receptor (NMDAR) encephalitis in combination with acute peripheral nerve damage is rare. A young female patient with anti-NMDAR encephalitis was admitted to Qianfoshan Hospital in Shandong Province on October 23, 2022. The main manifestations were abnormal mental behavior, consciousness disorders, and flaccid paralysis. Electromyography indicated axonal damage to the upper and lower extremities. Patient was in critical condition and admitted to the ICU with tracheal intubation for central hypoventilation. A combination of critical polyneuropathy was considered. The prognosis was good after hormone shock, immunosuppressive therapy, surgical therapy, anti-infection, respiratory support and symptomatic support. The diagnosis of anti-NMDAR encephalitis with acute peripheral nerve damage is difficult. Immune factors need to be considered and paraneoplastic syndrome should be differentially diagnosed.

Chinese guidelines for diagnosis and treatment of narcolepsy (2022) as the second edition of Chinese guidelines for narcolepsy, had made important updates compared with the 2015 edition in some aspects, such as epidemiology, pathogenesis, clinical manifestations, scale assessment and laboratory examination, diagnostic criteria and treatment. This article will focus on the above updated content.

Objective To explore the effects of N-butylphthalide on the expressions of ZO-1 and claudin-5 in blood-brain barrier (BBB) in rats with acute carbon monoxide (CO) poisoning. Methods A total of 144 adult healthy male Sprague-Dawley (SD) rats were randomly divided into normal control group, CO poisoning group, and NBP treatment group, with 48 rats in each group. The acute CO poisoning model was reproduced in hyperbaric oxygen chamber, and all model rats were given hyperbaric oxygen therapy once daily. The rats in the normal control group were free to breathe fresh air. The rats in NBP treatment group were administered orally NBP 60 mg/kg twice a day at 2 hours after poisoning until death. The rats in normal control group and CO poisoning group were treated with equal amount of pure olive oil. Four rats were sacrificed from each group at 1, 3, 7, 14 days after model reproducing, respectively. The changes in ultrastructure of BBB were observed under transmission electron microscope. The expressions of ZO-1 and claudin-5 proteins were determined by immunofluorescence staining and Western Blot. The localization of the two target proteins was observed by immunofluorescence double staining. The correlation between the two proteins was analyzed by linear regression. Results The ultrastructure of BBB was normal in normal control group, some ZO-1 and a large number of claudin-5 positive cells were observed. The ultrastructure of BBB was seriously injured, ZO-1 and claudin-5 positive cells in brain tissue were significantly decreased, and the expressions of ZO-1 and claudin-5 proteins in brain tissue at 1 day after poisoning in CO poisoning group were significantly lower than those of normal control group (ZO-1 protein:3.38±0.30 vs. 24.50±5.62, claudin-5 protein: 11.38±0.93 vs. 46.35±6.88, both P < 0.05), and although gradually restored, they were maintained at relatively lower levels until 14 days as compared with those in normal control group (ZO-1 protein: 10.35±0.80 vs. 24.63±3.57, claudin-5 protein: 32.35±3.11 vs. 46.43±7.20, both P < 0.05). NBP treatment could significantly alleviate the ultrastructure injury of BBB induced by acute CO poisoning, the amount of ZO-1 and claudin-5 positive cells in brain tissue were significantly increased, as well as the expressions of ZO-1 and claudin-5 proteins were significantly increased, which were significantly higher than those of CO poisoning group from 1 day and 3 days on, respectively (1-day ZO-1 protein: 7.57±0.69 vs. 3.38±0.30, 3-day claudin-5 protein:20.46±1.42 vs. 11.43±0.86, both P < 0.05), and which showed an increase tendency with time prolongation. The results of immunofluorescence double staining showed that ZO-1 and claudin-5 proteins could not only coexist in the same cell, but also could be expressed separately in different cells. Linear regression analysis showed the positive correlation between the expressions of ZO-1 and claudin-5 proteins in brain tissue of rats with acute CO poisoning (R2= 0.917, P = 0.022). Conclusion NBP could markedly improve the ultrastructure and functional integrity of BBB through up-regulating the expressions of ZO-1 and claudin-5 proteins, and then reduce brain damage caused by CO poisoning.