Depression after minor stroke: prevalence and predictors

Background and purpose: Post‐stroke depression (PSD) is one of the most frequent complications of stroke, with a prevalence ranging 20–60%. As PSD seems to be related to stroke severity, we hypothesized that the prevalence of PSD would be lower in patients with minor stroke. Methods: We investigated the prevalence and predictors of PSD over a 30‐month follow‐up period in a cohort of patients with minor ischaemic stroke (NIHSS ≤ 5). Results: We enrolled 105 patients (mean age 64.38 ± 11.2 years, M/F 69/36). PSD was diagnosed in 43 (41%) patients, 40 (93%) of whom had dysthymia; 22% of patients were already depressed at 1 month. The most frequent depressive symptoms (DSs) were working inhibition, indecisiveness, and fatigability. Patients who developed PSD were less educated (P = 0.044) and diabetic (P = 0.006). After excluding patients that were already depressed at 1 month, we performed a logistic regression model to detect predictors of PSD. Crying (P = 0.012, OR 1.067, CI 0.269–4.553) and guilt (P = 0.007, OR 0.037, CI 0.02ì03–0.401) at baseline were two DSs found to be significantly correlated with PSD. Higher educational level (P = 0.022, OR 0.084, CI 0.010–0.698) and diabetes (P = 0.007, OR 14.361, CI 2.040–101.108) were the risk factors significantly correlated with PSD. Conclusion: Post‐stroke depression is frequent even in patients with minor stroke. Early detection of DSs might help to predict long‐term development of PSD. No correlation was observed between lesion site or side and the development of PSD.     

Fluoxetine for poststroke depression ——A randomized placebo controlled clinical trial

BACKGROUND: Studies have demonstrated that poststroke depression(PSD) may be related with the disequilibrium between noradrenaline and 5-hydroxytryptamine (5-HT) caused by cerebral injury. The injured regions involve noradrenergic and 5-hydroxytryptaminergic neurons as well as conduction pathway. The levels of noradrenaline and 5-HT would be decreased. OBJECTIVE: To observe the effect of fluoxetine on preventing against PSD and recovery of neurologic function, and analyze the relationship of fluoxetine and the 5-HT level. DESIGN: A randomized controlled clinical trial. SETTING: Department of Neurology, First Hospital Affiliated to Soochow University. PARTICIPANTS: Ninety consecutive patients, 47 female and 43 male, were recruited who admitted to hospital for recent stroke in the Department of Neurology, First Affiliated Hospital of Soochow University between September 2003 and February 2005. Subjects were aged (64±7 ) years, ranging from 47 to 79 years old. They all met the diagnosis criteria of various cerebrovascular diseases formulated in the 4th National Cerebrovascular Disease Conference and confirmed as stroke by skull CT or MRI; The time from onset to tentative administration was less than 7 days; The patients had clear consciousness, without obvious language disorder. They were randomized into treatment group (n =48) and placebo group (n =42). METHODS: ①All the patients were given routine treatment according to treatment guideline of cerebrovascular disease after admission. Patients in the treatment group and placebo group received 20 mg/d fluoxetine and placebo (component: vitamin C) for 8 weeks, respectively. ② Neurologic deficit was assessed according to 24-item Hamilton Rating Scale for Depression (HAMD) and Activity of Daily Living Scale (ADL) before and at 2,4 and 8 weeks after test, separately; Meanwhile, the levels of platelet 5-HT and plasma 5-HT were determined. Grading criteria of HAMD intergral depression: non-depression < 8 points; mild depression 8–20 points; moderate depression 21–35 points; severe depression > 35 points. ADL was assessed with Barthel index score (full mark 100 points). Higher points indicated better incidence and smaller dependence. Neurologic deficit score was made according to scoring criteria of neurologic deficit formulated in 1995 4th National Cerebrovascular Disease Conference: a score of 0–15 indicated a mild focal neurologic deficit, a score of 16–30 a moderate focal neurologic deficit, and a score of 31–45 a severe focal deficit. MAIN OUTCOME MEASURES: Scores of HAMD, ADL and neurologic deficit, and levels of plasma and platelet 5-HT of patients from 2 groups before, 2,4 and 8 weeks after test. RESULRS: Seventy-three of 90 randomized patients participated in the final analysis. In the treatment group, 11 patients dropped out due to insufficient clinical response (n =4), somatic side effects (n =2), intervening medical illness (n =1), hypomania (n =3), and other reasons (n =2). In the placebo group, 6 patients existed due to insufficient clinical response (n =2), somatic side effects (n =1) and other reasons (n =3). ① Before treatment, there were no significant differences in scores of HAMD, DAL and neurologic deficit in patients between two groups (P > 0.05). After 8 weeks of treatment, the scores of HAMD, DAL and neurologic deficit in the treatment group were significantly different from those in the placebo group (12.6±5.3 vs. 16.3 ±3.7; 8.6±6.4 vs. 11.2±6.4; 60.4±12.5 vs. 52.3±13.5, P < 0.01). ② After 8 weeks of treatment, platelet 5-HT level of patients in the treatment group was significantly lower than that in the placebo group [(325.3± 110.5) mg/L vs. (653.6±138.4) mg/L, P < 0.05], while there were no significant differences in plasma 5-HT between two groups (P > 0.05). CONCLUSION: Early fluoxetine treatment obviously retards PSD. The increase of platelet 5-HT level promotes the recovery of neurologic function.     

The Efficacy of Group Acceptance and Commitment Therapy for Preventing Post-Stroke Depression: A Randomized Controlled Trial

Background and purposePost-stroke depression (PSD) is a common psychiatric complication of stroke and is associated with the subsequent prognosis, yet still lacking of enough attention. PSD is preventable, and psychotherapy is an alternative prophylactic treatment which needs more solid evidences to confirm its efficacy. In this study, group Acceptance and Commitment Therapy (G-ACT) was performed in acute stroke patients to see if it can effectively relieve depressive symptoms and improve neurological function. The efficacy was also evaluated in stroke patients of different severity.MethodsOne hundred and four hospitalized patients with acute ischemic stroke were enrolled according to the inclusion criteria and exclusion criteria. After baseline evaluation, they were randomly allocated to the intervention (G-ACT) group and the control (usual care) group. Patients in the control group received routine stroke treatment, while those in the intervention group were given additional G-ACT treatment (5 sessions, 45-55 min/session). Both of the two groups were assessed with 24-item Hamilton Depression Scale (HAMD-24), National Institutes of Health Stroke Scale (NIHSS), and Barthel Index (BI) at baseline, 2 weeks, 1 month, and 3 months follow-up. Patients were further divided into the mild stroke group (NIHSS 0-3) and the moderate stroke group (NIHSS 4-9), HAMD scores at different time points were also assessed.ResultsThe HAMD score of G-ACT group was significantly lower than that of control group at 1 month (p = 0.018) and 3 months follow-up (p = 0.001). As to the NIHSS score, there was no significant difference between the two groups within the follow-up period (p > 0.05). The BI score of the two groups was statistically different at 2 weeks (p = 0.033) and 1 month (p = 0.019), while no difference was shown at 3 months (p = 0.191). In acute phase, the HAMD score of moderate stroke patients was significantly higher than that of mild ones (p < 0.001). After G-ACT treatment, both mild and moderate stroke patients showed lower HAMD score at 3 months follow-up (p = 0.004; p = 0.033).ConclusionsG-ACT seems to be a viable and effective treatment for preventing PSD in the acute phase of stroke, while the efficacy of which on improving neurological deficits needs to be further evaluated.     

Granulocytes in the subarachnoid space of humans and rabbits with bacterial meningitis undergo apoptosis and are eliminated by macrophages

The contribution of leukocyte apoptosis to the resolution of meningeal inflammation in bacterial meningitis was studied in the cerebrospinal fluid (CSF) and in meningeal infiltrates of humans and rabbits by in situ tailing, flow cytometry, agarose gel electrophoresis, and electron microscopy. In humans, the rate of apoptotic granulocytes was 21.0 ± 20.8% (n = 11) in cytocentrifuge preparations and 3.3 ± 3.4 (n = 14) in putride infiltrates of autopsy cases (P = 0.02). In rabbits, CSF pleocytosis peaked 8 h after the initiation of antibiotic treatment (5311 ± 3122/μl). At this time, the rate of apoptotic granulocytes was 15.2 ± 7.3% in CSF and 1.8 ± 1.4% in the meningeal infiltrates (each group n = 6, P = 0.007). Thereafter, the rate of apoptotic granulocytes in CSF declined below 10%. In humans and rabbits, bands representing internucleosomal fragments of approximately 180 base pairs and multiples thereof were documented on agarose gels. Phagocytosis of apoptotic granulocytes by macrophages was visualized by light and electron microscopy. In conclusion, during resolution of subarachnoid space inflammation in bacterial meningitis, a substantial fraction of granulocytes undergoes apoptosis. These granulocytes are removed by phagocytosis by macrophages. Apoptosis is more frequent in granulocytes floating in the CSF than in adherent cells. Received: 12 February 1998 / Accepted: 29 April 1998     

脑卒中后不同时段抑郁的发生及与预后的关系

目的探讨脑卒中后不同时段抑郁的发生情况及与预后的关系。方法急性期脑卒中病例223例,卒中后72h予HAMD评分,将≥8分者随机分为抗抑郁药物组（干预组）、对照组,〈8分者1月再予评分,将其中≥8分者用相同方法再分为干预组、对照组,〈8分者2月再予评分,将其中≥8分者用相同方法再分为干预组、对照组,将〈8分者3M再次评分,分为≥8分、〈8分组,各组卒中后3月予MoCa、NIHSS评分、mRS分级。分析卒中后不同时段抑郁的发生情况,比较分析各时段对照组3月时MoCa、NIHSS评分、mRS分级。结果卒中后抑郁（PSD）的发生率分别为72h内19.73%,1月时35.03%,2月时53.51%,3月时46.15%;各对照组3月时MoCa评分比较,72h组与其余各组均有明显差异,P均〈0.01;NIHSS评分比较,72h组与1、2月组均有显著差异P均〈0.05;各组预后良好率（mRS分级）比较P均〉0.05。结论卒中后急性期（72h）的发病率偏低,恢复期（2~3月）的发病率较高。急性期PSD对认知功能的影响较小,但抑郁越早发生,对神经功能的恢复影响越大,致残程度越严重。     

卒中后抑郁的相关因素分析

目的探讨卒中后抑郁(PSD)的相关因素。方法采用汉密尔顿抑郁量表(HAMD)在卒中后14 d及90 d对300例脑卒中患者进行评分,并据此分为PSD组及非PSD组,对两组间的卒中部位、美国国立卫生研究院卒中量表(NIHSS)评分、改良Rankin量表评分(mRS)及简易精神状态检查表(MMSE)评分进行比较。结果 140例(46.7%)患者发生PSD;卒中灶多发或位于左侧半球、额颞叶及基底节的患者PSD发生率明显高于卒中灶单发、位于右侧半球、顶枕叶及皮质的患者(均P<0.05);PSD组发病14 d时NIHSS评分、发病14 d及90 d时mRS评分明显高于非PSD组(P<0.05～0.01)。结论 PSD发生与多灶性卒中及卒中灶位于左侧半球、额颞叶、基底节区有关;且与卒中后神经功能缺损程度及残疾程度有关。     

急性缺血性卒中后抑郁的相关危险因素分析

目的探讨急性缺血性卒中后抑郁(PSD)的发生率及其相关危险因素。方法 185例经CT或MRI证实的急性缺血性卒中患者根据精神障碍诊断和统计手册第5版(DSM-V)标准和24项Hamilton抑郁量表(HAMD)评分分为PSD组和non-PSD组;分析PSD社会人口学资料、血管危险因素、相关生化指标、NIHSS、Barthel指数(BI)、MMSE等相关因素对PSD的影响。结果本组PSD发生率为40.54%(75例),主要以轻、中度抑郁为主;与non-PSD组比较,PSD组患者糖尿病发生率高(P=0.044),神经功能缺损程度重、日常生活活动能力差(P=0.000,P=0.001),MMSE评分降低(P=0.000),而超敏C-反应蛋白(hs-CRP)和同型半胱氨酸(Hcy)水平升高(P=0.000,P=0.006);其中BI、MMSE评分与HAMD评分呈负相关(均P0.05),而NIHSS评分、hs-CRP和Hcy与HAMD评分呈正相关(均P0.05);Logistic回归分析提示,低MMSE评分、高NIHSS评分及高hs-CRP和Hcy水平可能是急性缺血性PSD的独立危险因素。结论 PSD主要以轻、中度抑郁为主;PSD与糖尿病病史、认知功能障碍、神经功能缺损程度、hs-CRP和Hcy水平密切相关。     

Effectiveness of a new gelatin sealant system for dural closure

Abstract

Objectives:

Watertight dural closure is imperative after neurosurgical procedures because inadequately treated leakage of cerebrospinal fluid (CSF) can have serious consequences. In this study, the authors test the use of a new gelatin glue as a dural sealant in in vitro and in vivo canine models of transdural CSF leakage.

Methods:

The in vitro model was sutured semicircles of canine dura mater and artificial dural substitute. The sutures were sealed with gelatin glue (n = 20), fibrin glue (n = 20), or a polyethylene glycol (PEG)-based hydrogel sealant (n = 20). Each sample was set in a device to measure water pressure, and pressure was increased until leakage occurred. Bonding strength was subjectively evaluated. The in vivo model was dogs who underwent dural excision and received either no sealant (control group; n = 5) or gelatin glue sealant (n = 5) before dural closure. Twenty-eight days post-surgery, the maximum intracranial pressure was measured at the cisterna magna using Valsalva maneuver and tissue adhesion was evaluated.

Results:

The water pressure at which leakage occurred in the in vitro model was higher with gelatin glue (76·5 ± 39·8 mmHg) than with fibrin glue (38·3 ± 27·4 mmHg, P < 0·001) or the PEG-based hydrogel sealant (46·3 ± 20·9 mmHg, P = 0·007). Bonding strength was higher for the gelatin glue than fibrin glue (P < 0·001) or PEG-based hydrogel sealant (P = 0·001). The maximum intracranial pressure in the in vivo model was higher for the gelatin glue group (59·0 ± 2·2 mmHg) than the control group (13·8 ± 4·0 mmHg, P < 0·001). Tissue adhesion was lower for the gelatin glue group than the control group (P = 0·005).

Discussion:

The new gelatin glue provides an effective watertight closure when used as an adjunct to sutured dural repair.     

脑卒中后抑郁患者检测SEP与血浆5-羟色胺的临床意义

目的探讨脑卒中后抑郁(post-stroke depression,PSD)患者体感诱发电位(somatosensory evoked potential,SEP)与血浆5-羟色胺(5-hydroxytryptamine,5-HT)水平的变化及其相关性,为脑卒中后抑郁的诊断及预后提供科学依据。方法单纯脑卒中组(n=19)、脑卒中后抑郁组(n=17),采用汉密尔顿抑郁量表(Hamilton Depression Scale,HAMD)判断抑郁程度,另设正常对照组(n=12),检测3组体感诱发电位N9、N13、N20的潜伏期及波幅;检测各组血浆5-HT含量,比较分析3组体感诱发电位和血浆5-HT含量。结果脑卒中患者、脑卒中后抑郁患者正中神经测定N20的潜伏期及波幅异常率较正常人高(P0.05);脑卒中后抑郁组血浆中5-HT含量明显低于正常对照组或脑卒中组,差异显著均有统计学意义(P0.05);脑卒中后抑郁患者HAMD评分与N20潜伏期呈正相关、与N20波幅呈负相关,N9波幅、N9潜伏期、N13波幅、N13潜伏期、N20波幅无相关;脑卒中后抑郁组HAMD评分与血浆中5-HT含量呈负相关。结论脑卒中后抑郁患者血浆中5-HT含量明显低于正常人或脑卒中患者,并且脑卒中后抑郁患者及脑卒中患者正中神经测定N20波幅及潜伏期异常率明显高于正常组。因此,检测脑卒中患者的SEP中N20波幅、潜伏期及血浆5-HT水平,将对脑卒中后抑郁的诊断及预后具有很好的临床意义。     

A small sodium channel blocking factor in the cerebrospinal fluid is preferentially found in Guillain-Barré syndrome: a combined cell physiological and HPLC study

The cerebrospinal fluid (CSF) of patients with Guillain-Barré syndrome (GBS) contains a low molecular weight factor with sodium channel blocking activity. This study investigated whether such activity also exists in the CSF of patients with other neurological diseases. Further, using high-performance liquid chromatography (HPLC) we tested whether the electrophysiological effect of the CSF is correlated with the size of the corresponding peak in the chromatograms. The existence of sodium channel blocking activity was tested in 27 native CSF samples of three groups of patients (group 1: GBS, n = 13; group 2: other inflammatory diseases, n = 8; group 3: controls, n = 6). NH15-CA2 neuroblastoma × glioma cells in the whole-cell recording configuration was used as a system for assaying the sodium channel blocking activity of CSF specimens. CSF shifted the steady-state inactivation curve of the sodium channels reversibly by –10.2 ± 4.4 mV in group 1, –6.7 ± 3.9 mV in group 2, and – 3.5 ± 2.8 mV in group 3 (P < 0.01). The shift was greater in demyelinating (9.3 ± 4.7 mV) than in nondemyelinating (5.6 ± 3.9 mV) diseases (P < 0.04). HPLC analysis of CSFs showed a well separated peak containing the substance responsible for the electrophysiological effect at about 41 min elution time. The peak covered the molecular weight range of 600–800 Da. Sodium channel blocking activity of CSFs and areas of the corresponding peak in the chromatograms were well correlated. We conclude that sodium current inhibition by a low molecular weight factor is generally present but increased in GBS. Received: 2 March 1999 Received in revised form: 7 May 1999 Accepted: 17 May 1999     

Intrathecal levels of IL-6, IL-11 and LIF in Alzheimer's disease and frontotemporal lobar degeneration

Cerebrospinal fluid (CSF) levels of interleukin (IL)-6, IL-11 and leukaemia inhibitory factor (LIF) were evaluated in 43 patients with Alzheimer's disease (AD) and 24 patients with frontotemporal lobar degeneration (FTLD) as compared with 30 agematched controls (CON), and correlated with clinical and demographic data and with CSF biomarkers amyloid beta (Aβ)42, total tau and tau phosphorylated at position 181 (P-tau). CSF IL-11 mean levels were significantly increased in AD and FTLD as compared with CON (6.5 ± 4.6 and 6.6 ± 5.1 versus 3.1 ± 3.3 pg/ml, P = 0.009). IL-6 mean levels did not differ between patients and CON (P > 0.05),whereas LIF levels were not detectable in patients or in CON. In AD patients, a significantly positive correlation between MMSE scores and IL-11 CSF concentration was observed (r = 0.344, P = 0.028). No correlations with CSF Aβ42, total tau and P-tau were found. IL-11, but not IL-6 levels are increased in AD and FTLD, and the highest peaks were observed in patients with a less severe degree of cognitive deterioration, therefore suggesting a role of this cytokine in early phases of neurodegeneration.     

强化心理治疗联合万拉法新对卒中后抑郁患者神经缺损的影响

目的 探讨强化心理治疗联合万拉法新对急性卒中后抑郁患者神经缺损的影响.方法 将126例急性脑卒中后并发早发性抑郁症患者按入选顺序随机分为对照组、万拉法新组和强化心理治疗+万拉法新组(联合治疗组),每组各42例.在治疗前,治疗4周、6周及90 d随访时对各组患者分别采用汉密尔顿(HAMD)抑郁量表、美国国立卫生研究院卒中(NIHSS)量表及Barthel指数量表进行疗效评价.结果 治疗前3组患者NIHSS评分及Barthel指数评分差异无统计学意义(P>0.05),治疗4周、6周及90 d随访时联合治疗组HAMD评分、NIHSS评分及Barthel指数评分较对照组、万拉法新组明显改善,差异均有统计学意义(P<0.05).结论 强化心理治疗作为抗抑郁药物治疗的辅助措施能显著增加卒中后抑郁患者的康复机会,疗效也更持久和稳定,能明显提高卒中患者的生活质量.     

强化心理治疗联合万拉法新对卒中后抑郁患者神经缺损的影响

目的 探讨强化心理治疗联合万拉法新对急性卒中后抑郁患者神经缺损的影响.方法 将126例急性脑卒中后并发早发性抑郁症患者按入选顺序随机分为对照组、万拉法新组和强化心理治疗+万拉法新组(联合治疗组),每组各42例.在治疗前,治疗4周、6周及90 d随访时对各组患者分别采用汉密尔顿(HAMD)抑郁量表、美国国立卫生研究院卒中(NIHSS)量表及Barthel指数量表进行疗效评价.结果 治疗前3组患者NIHSS评分及Barthel指数评分差异无统计学意义(P>0.05),治疗4周、6周及90 d随访时联合治疗组HAMD评分、NIHSS评分及Barthel指数评分较对照组、万拉法新组明显改善,差异均有统计学意义(P<0.05).结论 强化心理治疗作为抗抑郁药物治疗的辅助措施能显著增加卒中后抑郁患者的康复机会,疗效也更持久和稳定,能明显提高卒中患者的生活质量.     

Changes in the activity and protein levels of CSF acetylcholinesterases in relation to cognitive function of patients with mild Alzheimer’s disease following chronic donepezil treatment

Summary. Objectives. To evaluate long-term changes in acetylcholinesterase (AChE) activity in CSF and blood following donepezil treatment in relation to the concentration of donepezil and cognition in AD patients. Methods. CSF or blood (or both) samples of a total of 104 patients with mild AD were used [MMSE score 23 ± 0.4; age 75 ± 1 years (mean ± SEM); n = 53 for CSF and n = 51 for plasma/red blood cell (RBC) samples]. The patients were treated with 5 or 10 mg/day donepezil and clinically followed for 2 years. The CSF and RBC AChE activities were measured by the Ellman’s direct colorimetric assay. Protein levels of two variants of AChE (“read-through” AChE-R and synaptic AChE-S) were determined by an ELISA-like method. Results. The plasma donepezil concentration was dose-dependent (between 30 and 60 ng/mL in the 5-mg and 10-mg group, respectively). The CSF donepezil concentration was 10 times lower than the plasma level and showed dose- and time-dependent kinetics. The RBC AChE inhibition was moderate (19–29%). CSF AChE-S inhibition was estimated to 30–40% in the 5-mg and 45–55% in the 10-mg group. Positive correlations were observed between the CSF AChE inhibition, an increased protein level of the AChE-R variant and MMSE examination. Patients with high AChE inhibition (≥45%) showed a stabilized MMSE test result after up to two years, while a significant decline was observed in AD patients with lower AChE inhibition (≤30%). Conclusions. An increase in the protein level of the AChE-R variant corresponded to a high AChE inhibition in CSF and favored less cognitive deterioration.     

根据Brunnstrom分期制定针对性康复方案对脑卒中患者康复效果的影响

目的探讨Brunnstrom分期制定针对性康复方案对脑卒中患者康复效果的影响作用。方法选取90例脑卒中患者采用随机数字表法分为实验组和对照组各45例,实验组依据Brunnstrom分期制定针对性康复方案,对照组给予常规康复治疗方法。结果康复治疗前实验组和对照组的Fugl-Meyer运动功能评分法(FAM)、改良Barthel指数(MBI)、运动功能评估量表(MAS)、美国国立卫生研究院神经功能缺损量表(NIHSS)评分和脑卒中专用生存质量量表(SS-QOL)评分差异均不具有统计学意义(P0.05)。康复治疗后实验组的FAM评分(48.2±7.6)分、MBI评分(58.2±11.6)分、MAS评分(33.7±6.2)分和SS-QOL评分(44.8±5.3)分均高于对照组的(29.6±5.7)分、(53.6±9.8)分、(29.6±5.7)分和(40.2±5.0)分,差异均具有统计学意义(P0.05);实验组NIHSS评分(13.5±3.8)分显著低于对照组的(15.7±4.0)分,差异具有统计学意义(P0.05)。结论 Brunnstrom分期制定针对性康复方案较常规康复治疗对脑卒中患者具有更加显著的康复效果,具有提高患者生活质量的作用。     

Nonenzymatic derived lipid peroxide, 8-iso-PGF2α, participates in the pathogenesis of delayed cerebral vasospasm in a canine SAH model

Abstract

We studied whether 8-iso-PGF_2α, nonenzymatic arachidonyl peroxide, participated in the pathogenesis of delayed vasospasm using a canine subarachnoid hemorrhage (SAH) model. Fourteen adult mongrel dogs were divided into two groups, two-hemorrhage SAH group (n = 8) and control group (n = 6). The contents of 8-iso-PGF _2α in CSF, the basilar artery segment, and subarachnoid clot were measured by enzyme immunoassay kit. The CSF 8-iso-PGF_2α content on Day 7 in the SAH group was 67.9 ± 29.9 pg ml^-1 (n = 8), which was significantly higher than 27.1 ± 13.8 (n = 8) on Day 0 in the SAH group, and 33.2 ± 14.4 pg ml^-1 (n = 5) on Day 7 in the control group. The 8-iso-PGF_2α content in the basilar artery segment with spasm on Day 7 in the SAH group was 13.5 ± 1.9 pg mg^-1 wet weight (n = 8), significantly higher than 8.7 ± 1.9 (n = 6) in the control group. The 8-iso-PGF_2α content in subarachnoid clot was 1.7 ± 1.4 ng g^-1 wet weight (n = 8). Significant elevation of the 8-iso-PGF_2α contents in the CSF and the basilar artery segment occurred on Day 7 in the SAH group. The subarachnoid clot enclosed the basilar artery on Day 7, contained a considerable amount of 8-iso-PGF_2α. These results suggested that 8-iso-PGF_2α could play a crucial role in the pathogenesis of the delayed cerebral vasospasm. [Neurol Res 2002; 24: 301-306]     

Distribution of growth hormone and thyroid-stimulating hormone in cerebrospinal fluid and pathological compartments of the central nervous system

Human growth hormone (HGH) radio-immunoassay (RIA) was adapted for an accurate measurement of immunoreactive HGH concentrations in the CSF in different cases of hypothalamic-somatotropin dysfunctions.In control subjects (n = 43) mean HGH levels were 0.35 ± 0.03 ng/ml in CSF and 1.95 ± 0.2 ng/ml in plasma with a $\text{CSF}\text{plasma}$ ratio of 17%. The thyroid-stimulating hormone (TSH) RIA gave in controls mean basal levels of 2.65 ± 0.2 μU/ml in CSF and 5.95 ± 0.3 μU/ml in plasma with a $\text{CSF}\text{plasma}$ ratio of 44%. HGH and TSH concentrations in CSF and plasma show a very good correlation; but the regression curves for both hormones are distinctly different and appear specific for each polypeptide hormone.Hypothalamic-somatotropin hyperreactivity was reported in diabetic retinopathy (DR). CSF and plasma HGH concentrations in a group of diabetic patients with progressing retinopathy (n = 27) were not different from those in normal subjects (respectively 0.35 ± 0.05 in CSF and 2.10 ± 0.25 ng/ml in plasma with a $\text{CSF}\text{plasma}$ ratio of 16%). The HGH regression curve obtained in diabetics is similar to that of controls. These data do not substantiate the hypothesis of an HGH hyperreactivity in diabetic retinopathy.In somatotropin hypersecretion (acromegaly) without adenoma suprasellar extension, higher HGH concentrations recorded in CSF than in plasma cannot be attributed to an anatomical break-down of the CSF blood-brain barrier and suggest an active transport process of pituitary hormones to the CNS.HGH and TSH concentrations were measured in the cystic fluid of CNS tumors. In 1 case of a cystic dysembryoma, the HGH and TSH of CF were considerably increased. In gliomas (n = 8) the HGH and TSH cystic fluid concentrations were more elevated (respectively 0.72 ± 0.2 ng/ml and 3.6 ± 0.7 μU/ml) than in the CSF of controls.     

Association of post stroke depression with social factors,insomnia, and neurological status in Chinese elderly population

The purpose of this study was to investigate the association of post stroke depression (PSD) with social factors, insomnia, and neurological status among elderly Chinese patients with ischemic stroke. Six hundred and eight patients over 60 years of age, who had suffered from a first episode of ischemic stroke within 7 days, were enrolled into the study. They were divided into PSD and non-PSD groups according to the Self-rating Depression Scale (SDS) scores. The association of PSD with social factors, insomnia, and neurological status was analyzed using multivariable logistic regression analysis. Compared with the patients who did not develop PSD, those with PSD reported adverse life events more frequently, and more subjects with PSD lived alone, had left carotid artery infarction and cortical infarction (P < 0.05), history of insomnia, and high National Institute of Health Stroke Scale (NIHSS) scores and low Barthel Index (BI) scores (P < 0.01). The multivariable logistic regression analysis showed that the occurrence of PSD was associated with a history of insomnia (HR = 1.59, 95 % CI 1.12–2.36, P < 0.01), NIHSS scores (HR = 2.45, 95 % CI 1.42–3.91, P < 0.01) and BI scores (HR = 2.56, 95 % CI 1.39–4.25, P < 0.01). Insomnia and the degree of neurological deficit were associated with PSD in an elderly population of Chinese people.     

不同时段脑卒中后抑郁的药物干预治疗对比研究

目的使用HAMD、MoCA、SAS和NIHSS四项量表综合评价脑卒中后72 h、1和2月发生脑卒中后抑郁(post-stroke depression,PSD)患者的抗抑郁药物干预效果,为不同时段的PSD药物干预提供临床研究依据。方法入选脑卒中病例223例,于脑卒中后72 h予HAMD评分,≥8分者随机分为72 h对照组和72 h治疗组;余患者于脑卒中后1月再次予HAMD评分,评分≥8分者随机分为1月对照组、1月治疗组;余患者于脑卒中后2月再次予HAMD评分,评分≥8分者同前再随机分为2月对照组、2月治疗组;各组均予常规药物及相同的康复治疗方案,治疗组加用帕罗西汀20 mg/d治疗。对以上各组病例于脑卒中后3个月随访,进行HAMD(24项版)量表、SAS量表、MoCA量表及NIHSS量表的评分。结果 (1)72 h治疗组与对照组比较,HAMD评分无显著差异(P>0.05),而MoCa、SAS和NIHSS评分均有显著差异(P≤0.01);1月治疗组与对照组比较,SAS评分无显著差异(P>0.05),而HAMD、SAS和NIHSS评分均有显著差异(P<0.01),2月治疗组与对照组的四项量表评分比较均有显著差异(P<0.01);(2)72 h、1月和2月治疗组在第3个月随访时的MoCa、SAS、HAMD及NIHSS评分均无显著差异(P>0.05)。结论 (1)脑卒中后不同时间出现PSD患者的抗抑郁干预效果有时间段差异,PSD出现时间越晚,抗抑郁治疗达到明显效果所需的时间越短;(2)脑卒中患者发生PSD后及早予抗抑郁药物治疗,不仅可改善抑郁,对焦虑、认知和神经功能康复也有积极效果。