目的 了解北京市某医院神经内科患者睡眠障碍、焦虑、抑郁的发生率及其现状,为临床早期干预及治疗提供依据.方法 采用横断面调查方法,对431例神经内科就诊患者使用匹兹堡睡眠质量量表(PSQI)、汉密尔顿焦虑量表14项(HAMA-14)、汉密尔顿抑郁量表24项(HAMD-24)进行他评式问卷调查.结果 被调查的431例患者睡眠障碍的发生率高达84.69％,68.91％ 的患者存在不同程度的焦虑或抑郁,其中32.2％ 的患者肯定有焦虑,30.6％的患者有明显抑郁,23.9％ 的患者焦虑抑郁共病.PSQI平均分为(12.12±4.17)分,HAMA-14的平均分为(10.97±6.95)分,HAMD-24的平均分为(15.29±10.15)分.女性睡眠质量较男性差,更容易患焦虑(P<0.05);住院患者睡眠效率明显低于门诊患者(P<0.05);有焦虑或抑郁的患者睡眠质量显著低于一般患者(P<0.01).结论 神经内科患者睡眠障碍与焦虑抑郁发生率较高,女性高于男性,住院患者睡眠效率更差,应引起医护人员的足够重视,并对患者进行早期预防及治疗.

Objective To investigate the clinical and electrophysiological features and treatments for thallium poisoning. Methods Twelve cases of thallium poisoning patients were from hospital 307 of PLA between June 2012 and October 2017 and their data were retrospectively analyzed. Twelve sex-and age-matched healthy subjects were selected as control group. Result The clinical manifestations of thallium poisoning were mainly symptoms of nervous and gastrointestinal systems as well as hair loss. Thallium poisoning compromised function of motor nerves including the prolonged distal latency of ulnar and common peroneal nerve, the decreased amplitude and slowed nerve conduction velocity of common peroneal nerve and tibial nerve, which were statistically different from control group (P<0.05). Thallium poisoning also impaired function of sensory nerve including the prolonged distal latency and decreased amplitude of median , ulnar and sural nerve, the slowed nerve conduction velocity of median , ulnar, radial and sural nerve which were statistically different from control group (P<0.05 or P<0.01 ). Electroencephalogram (EEG) of 7 cases revealed mild abnormality EEG in 6 cases and moderate abnormality EEG in one case. Patients received potassium supplementation, diuresis, oral Prussian blue, intramuscular injection of sodium dimercaptopropanesulfonate and other treatment. Severe cases had good outcome after hemoperfusion and plasma exchange. Conclusions Thallium poisoning is rare in clinic and typical clinical features and electrophysiological examination are helpful to the diagnosis and differential diagnosis of diseases. Timely increasing thallium excretion and symptomatic support treatment can effectively improve the prognosis of the patients.

Objective To observe the effects of sleep deprivation on the antioxidant activity and autophagy in the neurons in the locus coeruleus of mice.Methods Fifty-four adult male C57BL/6 mice (8-12 weeks old,weighing 23-26 g) were randomized into total sleep deprivation (induced by gentle stimulation) for 6 h group (n =8),total sleep deprivation for 12 h group (n =8),and rapid eye movement sleep deprivation (RSD;induced using a modified multiple platform method) group (n =11),and each group was assigned a normal control group with the same number of mice.Western blotting was used to detect the expression levels of superoxide dismutase 2 (SOD2),catalase,microtubule-associated protein 1 light chain 3 Ⅱ (LC3-Ⅱ) and P62 (also known as SQSTM1),and immunofluorescence staining was used to detect the expression of lysosomal-associated membrane protein 1 (LAMP-1) in the locus coeruleus and the lateral hypothalamus of the mice.Results The protein levels of SOD2 and catalase were significantly increased in the neurons of the locus coeruleus in the mice after sleep deprivation for 6 h (P ＜ 0.05),but showed no further increment after sleep deprivation for 12 h.RSD significantly decreased the protein levels of SOD2 and catalase in the locus coeruleus neurons (P ＜ 0.05).In the lateral hypothalamic neurons,sleep deprivation resulted in no significant changes in the expression levels of catalase or SOD2.Sleep deprivation for 6 and 12 h did not significantly affect the expression of LC3-Ⅱ and P62 in the locus coeruleus,whereas RSD caused a significant decrease in LC3-Ⅱ expression (P ＜ 0.05),increased P62 level (P ＜ 0.05) and reduced LAMP-1 level in the locus coeruleus neurons (P ＜ 0.05).Sleep deprivation did not affect the expression levels of LC3-Ⅱ or P62 in the lateral hypothalamic neurons.Conclusion Short-term total sleep deprivation causes a transient increase in the antioxidant activity whereas has no significant effect on autophagy in the locus coeruleus neurons.Long-term RSD significantly reduces both the antioxidant activity and autophagy in the locus coeruleus neurons of mice.