BACKGROUND: Attention deficit and hyperkinetic disorder (ADHD) isfrequently treated with psychostimulant medications, which had beenshown to improve both cognitive and behavioral outcomes for most chil dren. OBJECTIVE: To compare the efficacy and adverse effects of olanzapinevs methylphenidate treatment in childhood hyperkinetic syndrome.DESIGN: Clinical comparative study. SETTING: Department of Psychiatry, Beijing Huilongguan Hospital; De partment of Mental Psychiatry, Shangdong Mouping People's Hospital. PARTICIPANT S: Sixty children with hyperkinetic syndrome from theclinics of the Department of Psychiatry,Beijing Huilongguan Hospital andthe Department of Mental Psychiatry of Shandong Mouping People's Hos pital between March 2002 and April 2004 were enrolled into this prospec tive study after obtaining the consents from their guardians.The patientswere randomly divided into 2 group: the olanzapine group (n=30) and themethylphenidate group (n=30). METHODS: In the olanzapine group olanzapine 2.5-7.5 mg per day wasgiven as a single dose in every evening.In the methylphenidate groupmethylphenidate 5-15 mg per day was given in divided dose in everymorning and evening.The dosage ofolanzapine and methylphenidatewere adjusted according to age, body mass and patient's clinical condi tions. And the period of treatment for either drug was 12 weeks. Conners teachers scale was used before and at the end of the 12 weektreatment(①hyperkinetic index consisted of 10 items②hyperkinetic behavior factorconsisted of 7 items. Each item was rated “none=0, a little=1, quite alot=2, and very much=3 ). Side effect scale was used to evaluate the hy perkinetic symptom and adverse reactions which consisted of behavior toxicity, abnormal laboratory tests , symptoms of the nervous system, au tonomic nervous system, cardiovascular system and skin etc with. 0=none; 1 =suspicious or very mild, 2=mild, 3 =moderate, 4=severe. The highestscore was 22,and the lowest was 0 with a score over 2 being positivefinding). MAIN OUTCOME MEASURES:Hyperkinetic syndrom score and ad verse reaction score at the end of the 12 weeks treatment. RESULTS:All 60 children completed the study and their results wereentered into the data analysis① At the end of the 12th week treat ment, the total hyperkinetic index score and total behavior score in boththe olanzapine group and the methylphenidategroup were significantly lower than those before the treatment as shown in Table 1 (t=8.16-15.26, P ＜ 0.05-0.01 )]; The total hyperkinetic behavior score in the olanzap inegroup was significantly lower than that in the methylphenidategroup (t=2.69, P ＜ 0.05 ). ② The adverse reaction score of patients inthe olanzapine group and the methylphenidategroup was 10.3±4.5and 10.9±3.8 respectively ,with no significant difference(P ＞ 0.05)between the two groups. CONCLUSION: Olanzapine produced similar effect as methylphenidatein the treatment of the hyperkinetic symptoms and attention deficits with a better efficacy in treating the behavior disorder than methylphenidate.

Objective To investigate the risk factors of cognitive dysfunction in patients with traumatic brain injury. Methods From March to September, 2021, 556 hospitalized patients with traumatic brain injury were selected from a multicenter study. A 1∶1 sex-matched case-control study design was used. After assessment by Montreal Cognitive Assessment (MoCA), those with cognitive impairment were as case group and those without cognitive impairment were as control group. They were collected general data and assessed with Social Support Rating Scale (SSRS) and Hospital Anxiety and Depression Scale (HADS). Results Logistic regression analysis showed that college education or above (OR = 0.040) and high level of social support (OR = 0.118) were protective factors for cognitive impairment (P < 0.05). Aged 60 to 88 years (OR = 9.996), severe brain injury (OR = 7.345), headache after injury (OR = 2.159), frequent waking at night or multiple dreams ≥ three times per week (OR = 3.705), severe upper limb dysfunction caused by brain injury (OR = 6.072), depression (OR = 5.202) were risk factors for cognitive impairment (P < 0.05). Conclusion The related factors for cognitive impairment in patients with traumatic brain injury include general factors, disease factors, sleep, psychological and social support and other factors. It is suggested that in addition to the treatment of disease, it is necessary to improve sleep, psychology and social support, to reduce the incidence of cognitive impairment and promote the recovery of disease.

Objective To investigate the correlation between red blood cell distribution width(RDW),systemic immune-inflammation index(SII)and major depressive disorder(MDD).Methods The clinical data of 176 MDD patients hospitalized in the clinical psychology department of our hospital from 2020 to 2022 and 209 non-MDD comparators who were routinely examined in Hebei General Hospital were retrospectively analyzed.Blood analysis was conducted to obtain values of RDW,SII,and red blood cell distribution width/platelet ratio(RPR).The data was used to plot the receiver operator characteristic(ROC)curve to determine the optimal threshold and the area under the curve(AUC)for RDW to discriminate between patients and controls.Result Patients in the MDD group had significantly higher RDW[median and quartiles:13.20(12.70,13.98)vs.12.80(12.40,13.35)],and SII levels[median and quartiles 510.87(350.95,878.12)vs.405.33(313.74,539.92)]compared with those in non-MDD group(P<0.05).There was no significant difference in RPR between the two groups(P>0.05).Multifactorial logistic regression analysis showed that RDW was positively correlated with MDD after adjusting for confounders(OR=3.086,95% CI:1.926-4.944).ROC curve showed that the optimal threshold for RDW to differentiate the risk of developing MDD was 12.85,with an AUC of 0.647(95% CI:0.592-0.702;P<0.001).Conclusion Present study shows that high RDW is a risk factor for the occurrence of MDD and an important parameter for the risk of developing depression.

Studies have suggested that the nucleus accumbens (NAc) is implicated in the pathophysiology of major depression; however, the regulatory strategy that targets the NAc to achieve an exclusive and outstanding anti-depression benefit has not been elucidated. Here, we identified a specific reduction of cyclic adenosine monophosphate (cAMP) in the subset of dopamine D1 receptor medium spiny neurons (D1-MSNs) in the NAc that promoted stress susceptibility, while the stimulation of cAMP production in NAc D1-MSNs efficiently rescued depression-like behaviors. Ketamine treatment enhanced cAMP both in D1-MSNs and dopamine D2 receptor medium spiny neurons (D2-MSNs) of depressed mice, however, the rapid antidepressant effect of ketamine solely depended on elevating cAMP in NAc D1-MSNs. We discovered that a higher dose of crocin markedly increased cAMP in the NAc and consistently relieved depression 24 h after oral administration, but not a lower dose. The fast onset property of crocin was verified through multicenter studies. Moreover, crocin specifically targeted at D1-MSN cAMP signaling in the NAc to relieve depression and had no effect on D2-MSN. These findings characterize a new strategy to achieve an exclusive and outstanding anti-depression benefit by elevating cAMP in D1-MSNs in the NAc, and provide a potential rapid antidepressant drug candidate, crocin.