偏头痛患者血浆内皮素与环核苷酸水平的变化

目的;研究偏头痛病人血浆内皮素和环核苷酸在发作期和间歇期的水平变化,探讨这些生化因素在偏头痛发生与发展中的作用。方法：空腹抽取偏头痛发作期及间歇期患肘静脉因4ml,测定血浆内皮素及环核苷酸水平,并随机用健康人对照。结果：偏头痛病人发作时,血浆内皮素水平显高于对照组（P＜0．01）及间歇期（P＜0．05）,环磷酸腺苷明显升高（P＜0．01）,环磷酸鸟苷明显下降（P＜0．05）。结论：偏头痛的发病与血浆内皮素密切相关,发作时明显升高。偏头痛存在自主神经功能失调,表现为交感神经功能亢进,副交感神经功能低下。     

偏头痛患者血浆和脑脊液β—内啡肽含量的变化

为探讨偏头痛与β－内啡肽（β－ＥＰ）的关系,本文用放射免疫分析法（ＲＩＡ）测定３０例偏头痛患者血浆和脑脊液β－ＥＰ的含量变化,发现典型偏头痛和普通型偏头痛以及偏头痛各期β－ＥＰ含量均明显降低,提示β－ＥＰ减少是偏头痛的发病机理之一。认为两型偏头痛发病机理相同,间隙期存在鸦片肽功能紊乱,当β－ＥＰ减少到一定程度偏头痛发作。     

偏头痛患者血浆一氧化氮和内皮素含量的相关性研究

目的观察偏头痛患者急性发作期及缓解期血浆一氧化氮(NO)和内皮素(ET)的含量变化及探讨两者在偏头痛发病机制中的作用.方法应用高效液相色谱分析法测定NO的含量,用放射免疫法测定ET的含量.结果偏头痛患者急性发作期血浆NO和ET含量均显著高于正常对照组(P＜0.05),偏头痛缓解期血浆NO降低,与对照组比较无显著差异(P＞0.05).血浆ET含量也降低,但仍高于正常对照组(P＜0.05).急性发作期血浆NO和ET含量呈显著正相关(r=0.564,P＜0.01).还发现偏头痛患者急性发作期血浆NO和ET比值较对照组降低(P＜0.05),而缓解期较对照组增高(P＜0.05).结论偏头痛患者可能存在血浆NO和ET的动态失衡,影响血管的舒缩功能.     

脑梗死、脑出血及偏头痛患者血浆内皮素的动态观察

内皮素 (ｅｎｄｏｔｈｅｌｉｎ ,ＥＴ)是 1988年由Ｙａｎａｇｉｓａｗａ从培养的猪主动脉内皮细胞中分离、纯化所发现 ,是迄今为止发现的最强的缩血管物质[1] ,内皮素在多种疾病的发生和发展中起着重要的作用 ,我们共测定了 10 9例脑梗死 (ＣＩ) ,脑出血 (ＣＨ)以及偏头痛患者的血浆ＥＴ水平 ,并加以分析。1　资料和方法1.1　分组　脑梗死 (ＣＩ)组 30例 ,男性 2 0例 ,女性 10例 ,年龄5 3～ 74岁。脑出血 (ＣＨ)组 2 9例 ,男性 2 2例 ,女性 7例 ,年龄5 0～ 78岁。分 3次抽血 ,第 1次为发病后 3日内、第 2次为发病后第 10～ 13天、第 3次为发…     

偏头痛与血浆内皮素关系的研究

目的：探讨偏头痛与血浆内皮素（ET）关系。方法：应用主免法测定28例偏头痛病人发作期,20例偏头痛间歇和期和20例正常对照组的ET含量。结果：发现偏头痛患发作期ET水平明显高于间歇期与对照组。结论：提示ET在偏头痛发作期脑血管痉挛的发病机理可能起重要作用。偏头痛患血浆内皮素系统可能存在异常。     

偏头痛患者血浆内皮素和氧化低密度脂蛋白水平的研究

目的探讨发作期偏头痛患者血浆内皮素（endothelin,ET）、氧化低密度脂蛋白（ox-LDL）的水平。方法测定30例偏头痛发作期患者（偏头痛组）与30例健康对照者（对照组）血浆ET和ox-LDL的水平。结果偏头痛组血浆ET[（68.19±12.25）ng/L）]水平高于对照组[（58.61±9.18）ng/L]（P〈0.01）,偏头痛组血浆ox-LDL[（13.25±3.15）mg/L]水平高于对照组[（10.06±3.61）mg/L]（P〈0.01）。结论偏头痛发作期患者存在血管舒缩功能障碍和抗氧化体系失衡,易发生脂质过氧化反应,可能是其容易发生心脑血管动脉粥样硬化的原因之一。     

先兆型偏头痛血浆内皮素和脑血流变化的临床研究

为研究先兆型偏头痛血浆内皮素(ET-l)含量和头痛侧脑血流的变化情况,探讨先兆型偏头痛发病机制,我们对36例先兆型偏头痛患者血浆ET-1含量及头痛侧大脑中动脉平均血流速度进行了动态观察.     

急性颅脑损伤患者内皮素含量变化及临床意义

目的：探讨急性颅脑损伤患者内皮素含量变化的意义。方法：采用放免法动态测定53例急性颅脑损伤患者血浆及脑脊液内皮素含量，以观察内皮素水平在颅脑损伤组和正常对照组中的变化。结果：颅脑损伤患者急性期血浆及脑脊液内皮素含量显著高于对照组，且与病情轻重程度明显相关。结论：内皮素参与急性颅脑损伤后继发性病理生理损害，钙拮抗剂成为治疗颅脑损伤的有效途径，血浆或脑脊液内皮素动态含量，可能是判断颅脑损伤患者预后的重要因素。     

急性颅脑损伤患者内皮素含量变化及临床意义

目的：探讨急性颅脑损伤患者内皮素含量变化的意义。方法：采用放免法动态测定５３例急性颅脑损伤患者血冰及脑脊液内皮素含量，以观察内皮素水平在颅脑损伤组和正常对照组中的变化。结果，颅脑损伤患者急性期血浆及脑脊液内皮素含量显著高于对照组，且与病情轻重程度明显相关，结论：内皮素参与急性颅脑损伤后继发性病理生理损害，钙拮抗剂成为治疗颅脑损伤的有效途径，血浆或脑脊液内皮素动态含量，可能是判断颅脑损伤患者预后的重     

Neuroexcitatory amino acid levels in plasma and cerebrospinal fluid during migraine attacks

A current hypothesis for migraine suggests that neuroexcitatory amino acids may participate in the triggering of attacks. To investigate this possibility we measured glutamic and aspartic acid level in plasma and cerebrospinal fluid (CSF) of patients with common and classic migraine during attacks, making comparisons with controls suffering from stress. Plasma levels of amino acids in migraine patients were lower than in controls. CSF concentrations of glutamic acid were higher in migraineurs than in controls. Our results suggest an excess of neuroexcitatory amino acids in the CNS of migraine patients during attacks, possibly favoring a state of neuronal hyperexcitability.     

脑脊液置换对蛛网膜下腔出血患者血清一氧化氮及内皮素的影响

目的：了解脑脊液置换对蛛网膜下腔出血（ＳＡＨ）患者外周血一氧化氮（ＮＯ）和内皮素（ＥＴ）的影响。方法：对１７例ＳＡＨ患者进行脑脊液置换，并对治疗前后的ＮＯ和ＥＴ水平进行观察。结果：脑脊液置换后第４日和第７日外周血ＮＯ水平分别由（４．４５±１．０２）μｍｏｌ／Ｌ升高至（８．０１±１．０１）μｍｏｌ／Ｌ和（７．９３±１．８７）μｍｏｌ／Ｌ，差异有极显著性（Ｐ均＜０．０１）；ＥＴ水平由（１２．３２±２．２７）ｎｇ／Ｌ下降至（５．５６±０．７５）ｎｇ／Ｌ和（６．０２±１．１０）ｎｇ／Ｌ，差异有极显著性（Ｐ均＜０．０１）。结论：脑脊液置换是治疗ＳＡＨ的有效方法。     

Glial cell line-derived neurotrophic factor and somatostatin levels in cerebrospinal fluid of patients affected by chronic migraine and fibromyalgia

The aim of the present study was to verify cerebrospinal fluid (CSF) levels of glial cell line-derived neurotrophic factor (GDNF) and somatostatin, both measured by sensitive immunoassay, in: 16 chronic migraine (CM) patients, 15 patients with an antecedent history of migraine without aura diagnosed as having probable chronic migraine (PCM) and probable analgesic-abuse headache (PAAH), 20 patients affected by primary fibromyalgia syndrome (PFMS), and 20 control subjects. Significantly lower levels of GDNF and somatostatin were found in the CSF of both CM and PCM + PAAH patients compared with controls (GDNF =P < 0.001, P < 0.002; somatostatin = P < 0.002, P < 0.0003), without significant difference between the two groups. PFMS patients, with and without analgesic abuse, also had significantly lower levels of both somatostatin and GDNF (P < 0.0002, P < 0.001), which did not differ from those of CM and PCM + PAAH patients. A significant positive correlation emerged between CSF values of GDNF and those of somatostatin in CM (r = 0.70, P < 0.02), PCM + PAAH (r = 0.78, P < 0.004), and PFMS patients (r = 0.68, P < 0.008). Based on experimental findings, it can be postulated that reduced CSF levels of GDNF and somatostatin in both CM and PCM + PAAH patients can contribute to sustained central sensitization underlying chronic head pain. The abuse of simple or combination analgesics does not seem to influence the biochemical changes investigated, which appear to be more strictly related to the chronic pain state, as demonstrated also for fibromyalgia.     

Cerebrospinal fluid sodium increases in migraine

BACKGROUND: Pharmaceuticals with calcium- or sodium-channel-blocking activity have proven useful for migraine prophylaxis, and calcium channel, sodium transporter, and sodium channel gene mutations have been found in familial hemiplegic migraine. However, it is not known whether calcium or sodium homeostasis is altered in migraine. OBJECTIVE: To compare levels of sodium, calcium, potassium, and magnesium in cerebrospinal fluid (CSF) and blood plasma between migraineurs and controls. METHODS: We recruited 20 migraineurs without aura and 11 controls prospectively, and studied migraineurs in sick (MH(+)) and well (MH(-)) states. We collected lumbar CSF and venous blood plasma, quantified elements with ion-selective electrodes or colorimetry, and determined osmolality by depression of freezing point. We compared levels of Na(+), Ca(2+), K(+), and Mg among and also within subjects who were studied in both MH(+) and MH(-) states. RESULTS: Mean CSF Na(+) levels were increased by 3 mmol/L in MH(+) compared with MH(-) and by 4 mmol/L compared to controls (P < 0.005). In 4 subjects who were sampled in both MH(+) and MH(-) states, mean CSF Na(+) concentration increased by 2 mmol/L in the MH(+) state compared with the MH(-) state (P < 0.05). Simultaneous plasma Na(+) levels did not differ among the 3 clinical groups, nor did osmolality, total Ca and Ca(2+), K(+), and total Mg levels in CSF. CONCLUSIONS: Compared to both controls and the MH(-) state, CSF Na(+) concentration increased in MH(+) independently from other clinical or pharmacological fluctuations, CSF concentrations of Ca(2+), Mg, and K(+), and blood plasma Na(+) levels. These results implicate a deviation of Na(+) homeostasis in migraine. The modestly elevated extracellular Na(+) in MH(+) may cause the neural changes that underlie clinical features of migraine.     

Cerebrospinal fluid cytokine levels in migraine, tension-type headache and cervicogenic headache

Cytokines have been measured in cerebrospinal fluid (CSF) from headache patients [infrequent episodic tension-type headache (TTH) and migraine with or without aura, all during attack, and cervicogenic headache] and compared with levels in pain-free individuals. Both proinflammatory [interleukin (IL)-1β, tumour necrosis factor-α and monocyte chemoattractant protein-1 (MCP-1)] and anti-inflammatory cytokines [IL-1 receptor antagonist (IL-1ra), IL-4, IL-10 and transforming growth factor-β1 (TGF-β1)] were included. There were significant group differences in IL-1ra, TGF-β1 and MCP-1 in episodic TTH and migraine compared with controls, and a significant difference in MCP-1 between cervicogenic headache and migraine with aura. Intrathecal MCP-1 correlated with IL-1ra, IL-10 and TGF-β1 in episodic TTH, and MCP-1 with IL-10 in migraine with aura. Cytokine increases were modest compared with those often accompanying serious neurological conditions, and may represent a mild response to pain. We believe this to be the first comparative study of CSF cytokine levels in connection with headache.     

多梗死性痴呆患者血浆、脑脊液胰岛素含量与智能水平的相关性研究

Vasculardementia（VD）isanacquiredsyndromeofmentalim－pairmentresultingfromcerebralbloodvesseldisease．Multi－infarctdementia（MID）isamostcommonformofVD，butlimitedinformationisavailableonthepathophysiology．However，itisunclearwhethercentralandplasmainsulinlevelsareabnormalinMIDandwhethertheseabnormalitiesarerelatedtotheseverityofdementia．WethereforeinvestigatedtheplasmaandCSFinsulinlevelsin５５MIDand７２CItogainfurtherinsightintothepathophysiologyofMID．１Subjectsandmothods１．１S…     

Cerebrospinal fluid analyses in migraine patients and controls

To investigate the role of central neurotransmitters in the pathogenesis of migraine, we measured cerebrospinal fluid (CSF) levels of certain amino acids (glycine, taurine, glutamine) and metabolites of biogenic amines (5-hydroxyindoleacetic acid and homovanillic acid) in 38 migraine patients and compared them with the levels from 10 headache-free controls. The levels of taurine, glycine and glutamine were significantly higher in the migraine patients (p < 0.0001 for taurine and glycine; p < 0.0009 for glutamine); there were no significant differences among the three migraine subgroups (infrequent migraine, frequent migraine and transformed migraine). In seven patients subsequently treated with divalproex sodium, CSF taurine levels decreased significantly from pretreatment baseline values. These data support the concept that migraine is at least in part a disorder of central neurotransmission.     

Vasoactive peptide levels in the plasma of young migraine patients with and without aura assessed both interictally and ictally

We measured, by RIA methods, ictal and interictal levels of substance P (SP), calcitonin-gene related peptide (CGRP) and neurokinin A (NKA) in the plasma of 30 young migraine patients with aura (MPA) and 45 migraine patients without aura (MWA), and compared the results with those of 30 age-matched controls. There were no significant differences between the levels of these vasoactive peptides in the control group and the levels in both migraine groups studied in headache-free periods. An elevation of CGRP levels in plasma was found during attacks in MPA and, to a lesser extent, in MWA ( p < 0.03 and p < 0.05, respectively). A significant increase in NKA levels was also demonstrated in the MPA and MWA groups ( p < 0.02 and p < 0.04, respectively). These data suggest, although indirectly, that CGRP and NKA could be involved in the pathogenesis of migraine attacks in juvenile migraine patients.     

Decreased cerebrospinal fluid cytochrome c levels in patients with amyotrophic lateral sclerosis

Objective. There is evidence showing impaired mitochondrial energy production and increased oxidative damage to mitochondria in amyotrophic lateral sclerosis (ALS). It is known that a lack of cytochrome c (CyC) in the mitochondrial intermembrane space can increase free radical release from mitochondria through interruption of the electron transport. CyC also plays a role in the apoptotic cell death which is suspected in ALS. The aim of the study was to measure cerebrospinal fluid (CSF) and serum CyC levels in patients with ALS. Material and methods. Forty ALS patients were diagnosed according to the El Escorial criteria of ALS. The clinical state of the patients was measured using the Amyotrophic Lateral Sclerosis Functional Rating Scale [ALSFRS]. Results. It was shown that overall CyC levels were significantly decreased by 46?% in the CSF of patients with ALS compared with controls (p<0.05), and not affected in serum of patients with ALS (p>0.05). There was no significant difference in CyC levels in relation to the clinical parameters of the disease (p>0.05). Conclusions. The study indicates that CyC may play a role in the pathogenesis of ALS. A possible mechanism is that increased neurodegeneration in ALS caused by free radical production decreases the concentrations of CyC.     

急性脑血管病患者血清和脑脊液三碘甲状腺原氨酸、甲状腺素及促甲状腺激素含量的变化及其临床意义

对６５例急性脑血管病（ＡＣＶＤ）患者血清与脑脊液（ＣＳＦ）中三碘甲状腺原氨酸（Ｔ３）、甲状腺素（Ｔ４）及促甲状腺激素（ＴＳＨ）的含量进行了测定，发现脑出血组与脑梗塞组血清与ＣＳＦ中Ｔ３、Ｔ４明显低于正常对照组（Ｐ均＜０．０１），ＴＳＨ则明显高于对照组（Ｐ＜０．０５）；且脑出血组Ｔ３、Ｔ４明显低于脑梗塞组，ＴＳＨ则高于脑梗塞组；病情轻重与甲状腺激素的变化明显相关（Ｐ＜０．０５）；治疗前后甲状腺激素水平明显不同，治疗后Ｔ３、Ｔ４明显升高（Ｐ均＜０．０５），以Ｔ３升高最明显（Ｐ＜０．０１）。作者并就其改变机制及临床意义进行了初步讨论。