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Intraventricular hemorrhage (IVH) is a frequent complication of prematurity that is associated with high neonatal mortality and morbidity. IVH is accompanied by red blood cell (RBC) lysis, hemoglobin (Hb) oxidation, and sterile inflammation. Here we investigated whether extracellular Hb, metHb, ferrylHb, and heme contribute to the inflammatory response after IVH. We collected cerebrospinal fluid (CSF) ( = 20) from premature infants with grade III IVH at different time points after the onset of IVH. Levels of Hb, metHb, total heme, and free heme were the highest in CSF samples obtained between days 0 and 20 after the onset of IVH and were mostly non-detectable in CSF collected between days 41 and 60 of post-IVH. Besides Hb monomers, we detected cross-linked Hb dimers and tetramers in post-IVH CSF samples obtained in days 0-20 and 21-40, but only Hb tetramers were present in CSF samples obtained after 41-60 days. Vascular cell adhesion molecule-1 (VCAM-1) and interleukin-8 (IL-8) levels were higher in CSF samples obtained between days 0 and 20 than in CSF collected between days 41 and 60 of post-IVH. Concentrations of VCAM-1, intercellular adhesion molecule-1 (ICAM-1), and IL-8 strongly correlated with total heme levels in CSF. Applying the identified heme sources on human brain microvascular endothelial cells revealed that Hb oxidation products and free heme contribute to the inflammatory response. We concluded that RBC lysis, Hb oxidation, and heme release are important components of the inflammatory response in IVH. Pharmacological interventions targeting cell-free Hb, Hb oxidation products, and free heme could have potential to limit the neuroinflammatory response following IVH.

Cisternal irrigation with thrombolytic agents was used to prevent post-SAH vasospasm, but its role remained inconclusive. To verify effectiveness of papaverine (PPV) in preventing vasospasm, we studied relationship between inflammatory biologic markers and vasospasm. This prospective study included 121 patients with clipped anterior circulation aneurysms that had ruptured, and 372 control patients. Patients were divided into three groups according to cisternal irrigation method: simple drain, papaverine group, and urokinase (UK) group. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were determined in CSF and serum on days 3 and 7 after SAH. The PPV group showed similar incidence of vasospasm with UK group, but lower incidence than the simple drain group. The levels of ICAM-1 and VCAM-1 were significantly higher in the SAH group than in the control group. CSF and serum levels were more elevated on day 7 than day 3, and the degree of elevation were more marked when measured in the CSF than in the serum. However, there was no statistical difference between measured levels of ICAM-1 and VCAM-1, and vasospasm development. PPV cisternal irrigation was similarly effective as UK at preventing vasospasm. Although neither PPV nor UK irrigation could reduce the concentration of adhesion molecules compared with simple drain, we found levels of ICAM-1 and VCAM-1 were specifically elevated in the CSF. Therefore, further research should focus on anti-inflammation as a therapeutic target against cerebral vasospasm and on the CSF as the optimum place where such inflammatory action practically brought about.

Mounting evidence supports the involvement of brain inflammation and the associated blood–brain barrier damage from which spontaneous and recurrent seizures originate. Detection of the soluble form of adhesion molecules (AM) has also been proven to predict outcomes in central nervous system (CNS) disorders. A recent study has shown that expression of AM in brain vessels was upregulated 24 h after kainic acid (KA) induced seizures. The aim of the present study was to investigate soluble AM levels in the cerebrospinal fluid (CSF) and serum of epilepsy patients. Paired CSF and serum samples were analyzed by sandwich enzyme-linked immunosorbent assay (ELISA) to determine the concentrations of soluble vascular cell adhesion molecule-1 (sVCAM-1) and soluble intercellular adhesion molecule-1 (sICAM-1). Increased serum concentrations of sICAM-1 were present in epileptic patients (41 localization-related of unknown etiology, 19 idiopathic generalized). Serum sICAM-1 level in drug-refractory epilepsy was elevated as compared to new diagnosis epilepsy and drug-responsive epilepsy. CSF sVCAM-1 and serum sVCAM-1 concentrations in the epilepsy group were higher as compared to the neurosis group. Moreover, CSF sVCAM-1 and serum sVCAM-1 concentrations in drug-refractory epilepsy were raised as compared to drug-responsive epilepsy and new diagnosis epilepsy. However, there were no significant differences in concentrations of CSF sICAM-1 between the epilepsy and neurosis groups. Our results suggest that sVCAM-1 and sICAM-1 could play an important role in the drug-refractory epilepsy.

Background: The pathophysiology of ischemic cerebral lesions following aneurysmal subarachnoid hemorrhage (SAH) is poorly understood. There is growing evidence that inflammatory reactions could be involved in the pathogenesis of such delayed occurring ischemic lesions. The aim of this study was to evaluate adhesion molecules with regard to these lesions following SAH. Methods: Serum and cerebrospinal fluid (CSF) samples were taken daily from 15 patients up to day 9 after SAH and evaluated for intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1). Results: CSF and serum samples correlated well during nearly the whole time course (p < 0.0001). A secondary increase in ICAM-1 and VCAM-1 in the serum and CSF correlated with an increase in flow velocity in the transcranial Doppler (p > 0.0001 and p < 0.007) but not to a delayed lesion in the CT scan. Conclusion: We believe that inflammatory processes are involved in the pathogenesis of cerebral vasospasm but they might only be a part of a multifactorial pathogenesis.

It has been hypothesized that immunoactivation may contribute to brain damage and affect outcome after traumatic brain injury (TBI). In order to determine the role of inflammation after TBI, we studied the interrelationship of the immune mediators sICAM-1 and IL-6 with the levels of S-100β and neuronal specific enolase (NSE), both recognized markers of brain damage. In addition, the extent and type of cerebral injury and the neurological outcome were related to these measured markers of injury. An evident elevation of S-100β (range of means: 2.7-81.4 ng/mL) and NSE (range of means: 2.0-81.3 ng/mL) was observed in CSF of all 13 patients during the first 3 post-traumatic days and decreased over 2 weeks. In parallel, the production of sICAM-1 (range of means: 0.7-11.9 ng/mL) and IL-6(range of means: 0.1-8.2 ng/mL) was also markedly enhanced in CSF. The CSF means of S-100β and NSE per patient correlated with IL-6 (r = 0.60, p < 0.05; and r = 0.64,p < 0.05, respectively), whereas the corresponding means in serum showed a significant correlation only between NSE and IL-6 (r = 0.56, p < 0.05). Maximal CSF values of NSE and sICAM-1 correlated with each other (r = 0.57, p < 0.05). The contusion sizes assessed on the CT scans correlated with the means of S-100β (r = 0.63, p < 0.05) and NSE (r = 0.71, p < 0.05) in CSF and with the mean of S-100β in serum, although not statistically significant (r = 0.52, p = 0.06), but not with serum NSE. Interestingly, linear regression analysis demonstrated that means of S-100β in CSF (r = 0.78, p = 0.002) and serum (r = 0.82, p < 0.001) correlated with the GOS. These results indicate that the elevation of these parameters in CSF depends on the extent of injury and that S-100β may be a predictor of outcome after TBI, whereas NSE reflects better the inflammatory response.

Numerous recent studies have reported a significant inflammatory reaction in the brain and the systemic circulation following traumatic brain injury (TBI), infection, or neoplasm of the brain with a sequential release of pro- and anti-inflammatory mediators. Although there is growing knowledge and understanding of the mechanisms leading to the often poor outcome of these patients, only a limited database exists on the physiological expression of pro- and anti-inflammatory cytokines and molecules in plasma and particularly in cerebrospinal fluid (CSF). Therefore, we analyzed paired plasma/CSF samples of healthy human volunteers for the physiological concentrations of Interleukin(IL)-6, IL-8, IL-10, soluble TNF-receptors (sTNF-R) p55 and p75, soluble ICAM (sICAM), and soluble E-selectin (sE-selectin). A physiological release of IL-6, IL-8, IL-10, and sTNF-R p55 and p75 was detected in plasma and CSF. In contrast, sICAM and sE-selectin were only detectable in plasma. Pro- and anti-inflammatory mediators exhibited different concentration patterns in plasma and CSF, suggesting a pro-inflammatory predisposition in the central nervous system.

Several studies have reported a positive correlation between levels of soluble adhesion molecules in serum or cerebrospinal fluid and cranial MRI activity. We performed a cross-sectional study in 46 patients with newly diagnosed MS and determined levels of soluble intercellular adhesion molecule-1 (sICAM-1) as well as vascular cell adhesion molecule-1 (sVCAM-1) in correlation to the number and area of gadolinium enhancing lesions on cranial magnetic resonance images (MRI). The data revealed a significant positive correlation between sVCAM-1 serum levels and gadolinium enhancing lesions. In addition, CSF to serum ratios for sICAM-1 and sVCAM-1 correlated to MRI activity. In patients with a single enhancing lesion (SEL) there was a negative correlation between the QsCAM and the distance of the SEL to the ventricles. As these adhesion molecules are stable and markers of disease activity in MS, we further investigated sVCAM-1 serum levels during treatment with interferon beta-1b (Betaferon®). Significant increases in serum levels for sVCAM-1 in patients receiving Betaferon were associated with a favourable treatment response after 1 year in 17 out of 19 patients and correlated to decreased MRI activity, whereas stable or reduced sVCAM-1 levels occured more often in non-responders (five out of six patients). Therefore it can be hypothezised that soluble adhesion molecules are released from cerebral endothelial cells as an early immunoregulatory activity of the immune system to reduce cellular traffic across the blood brain barrier and this is further enhanced by IFN-beta treatment.

In this study the aim was to evaluate the intrathecal sICAM-1 production in multiple sclerosis (MS) patients during relapse and remission. In addition to this, we assessed whether there is a correlation between intrathecal sICAM-1 production and other disease activity markers such as IgG index and gadolinium enhancement in magnetic resonance imaging (MRI). Twenty four relapsing-remitting MS patients were included in the study. Serum and cerebrospinal fluid (CSF) samples were obtained both during relapse and remission. The soluble form of ICAM (sICAM) was measured by the ELISA method in serum and CSF. Cranial MRI with triple dose gadolinium injection was performed for each patient both during relapse and remission. Serum levels of sICAM-1 (245.23 +/- 92.88 ng/ml) were higher during relapse than those in remission (219.90 +/- 110.94 ng/ml), but the difference was not statistically significant. In relapse periods CSF levels of sICAM-1 (1.304 +/- 0.92 ng/ml) were higher than those in remission (1.06 +/- 0.86 ng/ml), but this was not significant. However, during relapse periods patients had significantly higher sICAM-1 index values (1.76 +/- 0.60) than those found during remission periods (1.01 +/- 0.44) (p < 0.05). The IgG index values were higher in relapse periods than in remission (0.88 +/- 0.37 vs. 0.67 +/- 0.28) (p < 0.005). On T1 weighted images following triple dose Gd injection, at least two or more enhancing lesions were present in 22/24 of the patients (91%) in relapse and 4/24 of the patients (19%) in remission. There was strong correlation both between the sICAM-1 index and Gd enhancement (r =0 .72 p < 0.05) and sICAM-1 index and IgG index in relapse (r = 0.69 p < 0.05). In conclusion, there is association between high sICAM-1 and IgG indices, as well as between high sICAM-1 index and Gd enhancing MRI lesions in relapsing MS patients.

[...]ICH may initiate an inflammatory process leading to secondary brain damage, as has been suggested in human ischaemic stroke, 4 as well as for experimental ICH and subarachnoid haemorrhage in animal models. 1, 3 With regard to the second hypothesis, it would be interesting to investigate the effects of early anti-inflammatory treatment in patients with ICH and an initial highly increased concentration of adhesion molecules in their ventricular CSF samples.

In this controlled study, we investigated the serum and cerebrospinal fluid (CSF) levels of soluble intercellular adhesion molecule-1 (sICAM-1) in relapsing-remitting multiple sclerosis (RRMS) patients and changes in the levels of this adhesion molecule during interferon-beta1b (IFN-beta1b) treatment. We also investigated the changes in the levels of sICAM-1 in correlation with disease activity and with findings on magnetic resonance images (MRI). The study included 24 patients (16 females and 8 males) who were confirmed to have RRMS based on the criteria of Poser et al. Sixteen of the patients received IFN-beta1b (Betaseron, Berlex Laboratories, Schering AG Germany, Berlin) treatment, and 8 did not receive this therapy. The levels of sICAM-1 in the MS patients' serum and CSF were significantly higher than levels in individuals with noninflammatory neurologic disease (p = 0.0081 and p = 0.0001, respectively). In the first 3 months of the study, MS patients treated with IFN-beta1b showed a significant rise in sICAM-1 levels (p = 0.0023), whereas their untreated counterparts showed no significant change. Neither of the groups showed a significant correlation between sICAM-1 level and disease activity demonstrated by MRI or between sICAM-1 level and clinical disease activity. The findings suggest that IFN-beta1b treatment may have a short-term upregulating effect on sICAM-1.