Cerebrospinal fluid levels of interleukin-6 and interleukin-12 in children with meningitis

Purpose  Certain cytokines play important roles in the pathophysiology of meningitis. The main purpose of this study was to investigate if the levels of interleukin-6 (IL-6) and interleukin-12 (IL-12) in cerebrospinal fluid (CSF) could be diagnostic predictors of bacterial meningitis in children. Methods  CSF was obtained from 95 patients suspected with meningitis. These cases were classified to the bacterial meningitis (n = 12), aseptic meningitis (n = 41), and nonmeningitis (n = 42) groups. The levels of IL-6 and IL-12 in CSF were measured using the enzyme-linked immmunosorbent assays test. Results  The CSF IL-6 levels in the bacterial meningitis group (45.2 ± 50.0 pg/ml) were significantly higher than those in the aseptic meningitis group (12.9 ± 10.2 pg/ml) and the nonmeningitis group (6.5 ± 7.8 pg/ml; p < 0.05). The CSF IL-12 levels in the bacterial meningitis group (69.8 ± 67.1 pg/ml) were significantly higher than those in the aseptic meningitis group (22.9 ± 10.8 pg/ml) and the nonmeningitis group (15.3 ± 11.2 pg/ml; p < 0.05). With regard to diagnosis, the measurement of CSF IL-6 and IL-12 levels showed sensitivities of 96% and 96%, respectively, and specificities of 51% and 75%, respectively. Conclusion  It is suggested that the CSF IL-6 and IL-12 levels are useful markers for distinguishing bacterial meningitis from aseptic meningitis.     

Plasma CXCL10 correlates with HAND in HIV-infected women

HIV-associated neurocognitive disorder (HAND) is characterized by chronic immune activation. We aimed to identify biomarkers associated with HAND and to investigate their association with cognitive function and sex, in a homogenous cohort of HIV-infected (HIV+) young adults, parenterally infected during early childhood. One hundred forty-four HIV+ Romanian participants (51% women) without major confounders underwent standardized neurocognitive and medical evaluation in a cross-sectional study. IFN-γ, IL-1β, IL-6, CCL2, CXCL8, CXCL10, and TNF-α were measured in plasma in all participants and in cerebrospinal fluid (CSF) in a subgroup of 56 study participants. Biomarkers were compared with neurocognitive outcomes, and the influence of sex and HIV disease biomarkers was assessed. In this cohort of young adults (median age of 24 years), the rate of neurocognitive impairment (NCI) was 36.1%. Median current CD4+ count was 479 cells/mm3 and 36.8% had detectable plasma viral load. Women had better HIV-associated overall status. In plasma, controlling for sex, higher levels of IL-6 and TNF-α were associated with NCI (p < 0.05). Plasma CXCL10 showed a significant interaction with sex (p = 0.02); higher values were associated with NCI in women only (p = 0.02). Individuals with undetectable viral load had significantly lower plasma CXCL10 (p < 0.001) and CCL2 (p = 0.02) levels, and CSF CXCL10 (p = 0.01), IL-6 (p = 0.04), and TNF-α (p = 0.04) levels. NCI in young men and women living with HIV was associated with higher IL-6 and TNF-α in plasma, but not in the CSF. CXCL10 was identified as a biomarker of NCI specifically in women with chronic HIV infection.     

Level of transforming growth factor beta 1 is elevated in cerebrospinal fluid of children with acute bacterial meningitis

We investigated the levels of transforming growth factor beta 1 (TGF-β1) in cerebrospinal fluid (CSF) in children with meningitis, with a view to prognostic relevance. CSF TGF-β1 levels on admission were measured by a sandwich enzyme immunoassay in children with bacterial meningitis (n = 16), aseptic meningitis (n = 12), and control subjects without evidence of central nervous system (CNS) infection (n = 16). Patients were followed up for a mean duration of 13 months, and neurodevelopmental sequelae was determined for those with bacterial meningitis. On admission, CSF TGF-β1 levels were significantly higher in children with bacterial meningitis (mean, standard error, 32.92, 2.36 pg/ml) as opposed to those with aseptic meningitis (25.26, 1.72 pg/ml) (P = 0.0155), or control subjects (20.53, 1.05 pg/ml) (P < 0.0001). The CSF TGF-β1 levels in children with aseptic meningitis were higher than those in the control group, but without significance (P = 0.02). No apparent correlation existed between CSF TGF-β1 levels and CSF protein or cell counts in patients with bacterial meningitis. No significant difference in CSF TGF-β1 levels was found between patients with or without major sequelae following bacterial meningitis. Received: 19 March 1997 Received in revised form: 24 June 1997 Accepted: 20 August 1997     

Comparison of shunt infection incidence in high-risk subgroups receiving antibiotic-impregnated versus standard shunts

Background  Shunt infection is a morbid complication of CSF shunting. Though antibiotic-impregnated shunt (AIS) systems decrease shunt infections by preventing bacterial colonization following device implantation, their effectiveness in populations at high risk for infection has recently been disputed. We set out to determine whether the categorical switch to AIS systems at our institution has resulted in a decreased incidence of shunt infection in high-risk pediatric patients. Methods  We retrospectively reviewed the records from all pediatric patients undergoing CSF shunt procedures at The Johns Hopkins Hospital over a 10-year period between January 1997 and December 2007. During the 5.75 years prior to October 2002, all CSF shunts included standard, non-AIS catheters. During the 4.25 years after October 2002, all CSF shunts included AIS catheters. High-risk subgroups were defined a priori as prematurity (<35 weeks gestational age), shunts placed immediately post-meningitis, conversion of external ventricular drains (EVD) to shunt, and replacement of nosocomial shunt infection in patients requiring prolonged hospital stay (>1 month). Results  A total of 544 pediatric patients underwent 1,072 shunt placement procedures (502 AIS, 570 non-AIS). Of patients with non-AIS catheters, 64 (11.2%) experienced shunt infection, whereas only 16 (3.2%) patients with AIS catheters experienced shunt infection (p < 0.001). AIS versus non-AIS was associated with decreased shunt infection in premature neonates [three (5.5%) vs. seven (20.0%), p = 0.030], acutely following bacterial meningitis [two (5.7%) vs. nine (25.0%), p = 0.043], when converting EVD to shunts [zero (0%) vs. four (13.3%), p = 0.030], and in patients with prolonged hospital stay >1 month [three (5.3%) vs. 12 (18.5%), p = 0.022]. Staphylococcus aureus was the most common infectious agent for both non-AIS (81.3%) and AIS (75.0%) systems. Conclusion  The introduction of AIS catheters into our institutional practice has reduced the incidence of shunt infection in pediatric populations at highest risk for infection. AIS catheters are effective instruments to prevent peri-operative colonization of CSF shunt components. Comments on this article can be found at .     

Effects of B7-H3 on the Inflammatory Response and Expression of MMP-9 in Mice with Pneumococcal Meningitis

B7-H3, a new member of the B7 superfamily, plays a key role in the regulation of T cell-mediated immune responses. Our previous work showed that B7-H3 strongly augmented both LPS- and bacterial lipoprotein-induced NF-κB activation and inflammatory response, and soluble B7-H3 was elevated in CSF and plasma of patients with bacterial meningitis. MMP-9 has been implicated in blood–brain barrier disruption, inflammation, and vasculitis during the pathogenesis of bacterial meningitis. In this study, we report that in a murine model of pneumococcal meningitis, B7-H3 treatment enhances inflammatory response in the meninges, upregulates MMP-9 expression in cerebral parenchyma, and deteriorates clinical disease status indicated by weight loss and impaired movement ability. In vitro results showed that B7-H3 augmented MMP-9 secretion from Streptococcus pneumoniae-stimulated microglia cells. Thus, our data indicate that B7-H3 contributes to the development of pneumococcal meningitis by exaggerating inflammatory responses and upregulating MMP-9 activity in CNS, which ultimately lead to neuronal injury.     

Cerebral infarction in bacterial meningitis: predictive factors and outcome

In this study, we analysed the frequency, morphological patterns and clinical characteristics of cerebral ischaemia in bacterial meningitis. We sought to determine predictors for the development of vasculopathy and ischaemic infarction in patients with bacterial meningitis. Consecutive adult patients admitted between March 1998 and February 2009 to a neurological intensive care unit at a university hospital in Germany with the diagnosis of bacterial meningitis were included in the study. Standard criteria were used to define bacterial meningitis. From 68 patients with bacterial meningitis, six patients suffered from cerebral ischaemia (8.8%). In our cohort, reduced level of consciousness on admission (p = 0.01) and lower white blood cell (WBC) count in cerebrospinal fluid (CSF) (p = 0.012) were associated with development of ischaemic cerebrovascular complications. The short-term outcome of all patients was poor (median modified Rankin scale 4.5). In patients presenting with reduced level of consciousness on admission and/or low WBC count in CSF early cerebral imaging including MR angiography or CT angiography are warranted to detect impending cerebrovascular complications.     

Assessing multiple sclerosis activity: is the in vitro production of tumor necrosis factor-α, interleukins 2, 6, 4, and 10, and immunoglobulin G of value?

Tumor necrosis factor (TNF) α, interleukins (IL) 2, 4, 6, and 10, and IgG oligoclonal bands (IgG OB) in vitro production was assessed, after whole-blood stimulation with lipopolysaccharide or concanavalin A, in 61 patients presenting with relapsing-remitting, relapsing-progressive, or chronic progressive multiple sclerosis. Multiple sclerosis patients were receiving no treatment or azathioprine (AZA), cyclosporin, cyclophosphamide, subcutaneous interferon (IFN) β1a, or corticosteroids (CST). Statistical correlations significantly showed that: (a) AZA lowers TNF-α (P = 0.002) and increases IL-4 production (P = 0.0024), and IFN-β1a increases TNF-α and decreases IL-4 levels; (b) CST has a negative effect on TNF-α, IL-6, and IL-4 synthesis; and (c) AZA, IFN-β1a, and CST diminish IgG OB synthesis (P = 0.001). Although our study of the dynamics of TNF-α, IL-2, IL-4, IL-6, and IL-10 in vitro production generally found no statistically significant correlations (partly explained by the limited number of values in the various groups), IL-6 was shown to drop during the periods surrounding relapse (P = 0.05) in the absence of treatment, while TNF-α (P = 0.04) and IL-6 (P < 0.05) dropped before exacerbation in the presence of AZA. In vitro production of TNF-α was closely and positively correlated with that of IL-6, independently of clinical features. The enhanced production of IL-10 detected before or at relapse with AZA and IFN-β1a (trends) may interfere with initiation of the immune reaction and with the development of new CNS lesions. Some discrepancies with previously published results stress the difficulties in studying the state of stimulation of different populations of leukocytes by using a variety of in vitro stimuli and in establishing a correlation between mRNA studies and the amount of final or active protein produced. Received: 16 September 1997 Received in revised form: 21 May 1999 Accepted: 8 June 1999     

The Ca2+/calmodulin-dependent protein kinase II-associated protein complex isolated from chicken retina

Activated microglia represent a major source of inflammatory factors in Alzheimer’s disease and a possible source of cytotoxic factors. β-Amyloid (Aβ) peptide, the predominant component in amyloid plaques, has been shown to activate microglia and stimulate their production of inflammatory factors. The present study was performed to analyze the responses of microglia to different forms of Aβ, with regard to release of the proinflammatory cytokines interleukin-1α (IL-1α), IL-1β, tumor necrosis factor-α (TNF-α), IL-6, and interferon-γ (IFN-γ), as well as the IL-1 receptor antagonist (IL-1ra). Primary cultures of microglia from rat neonatal cerebral cortex were incubated with freshly dissolved Aβ_1–40 or Aβ_1–42, Aβ_1–40 fibrils, Aβ_1–40 βamy balls, or vehicle. Aβ_1–40 fibrils did not significantly stimulate any of these cytokines. Freshly dissolved Aβ_1–40 resulted in a marked increase in the release of IL-1β, and freshly dissolved Aβ_1–42 significantly stimulated both IL-1α and IFN-γ secretion. The Aβ_1–40 βamy balls stimulated the secretion of IL-1α and IL-1β. Incubation with Aβ peptides did not affect the secretion of IL-1ra, IL-6, or TNF-α. In the case of IL-1β, the response is correlated with the presence of Aβ peptide as monomers and oligomers.     

TNF-α and TNF-β gene polymorphisms in cerebral infarction

Tumor necrosis factor (TNF) is an important cytokine in the inflammation process of atherosclerosis. Two biallelic polymorphisms in the TNF-α (TNF-α-308) and TNF-β (TNF-β +252) genes have been reported to be associated with TNF production and susceptibility to inflammatory diseases. We investigated two genetic polymorphisms in the TNF locus (TNF-α-308 G→A and TNF-β +252 A→G) as risk factors for cerebral infarction (CI) by determining its prevalence in 294 survivors of CI, and in 581 age-, gender-, and race-matched controls. A significant association was found for the TNF-α and TNF-β genotypes in CI patients compared with controls. A significant increase was found for the TNF-α A allele in controls compared with CI patients (X ²=7.593, p=0.006, odds ratio =1.74, confidence interval =1.17-2.59). In addition, the TNF-α GG genotype increased the relative risk for CI in subjects with the TNF-β AA genotype (X ² = 4.998, P=0.025). As a result, compared to controls, the frequency of the TNF-α AA genotype was decreased, whereas that of TNF-β AA was increased in CI patients. The former implies an association with resistance, whereas the latter suggests an association with susceptibility to the disease. These results show that the TNF-α-308 and TNF-β + 252 locus plays an important role in the etiopathogenesis of CI.     

Analyzing Theoretical Mechanisms of Physical Activity Behavior Change in Breast Cancer Survivors: Results from the Activity Promotion (ACTION) Trial

Background We previously reported that a physical activity (PA) behavior change intervention based on the theory of planned behavior (TPB) increased PA and quality of life in breast cancer survivors. Purpose To examine the effects of our interventions on TPB variables and to determine if PA at 12 weeks follow-up was mediated by TPB variables at 4 weeks. Methods Breast cancer survivors (N = 377) were randomly assigned to receive either a standard public health recommendation for PA (SR group), a step pedometer alone, or one of two TPB-based behavior change interventions consisting of print materials (alone or combined with a step pedometer). For the purpose of this study, we compared the two TPB-based intervention groups (INT group) to the SR group. Results Compared to the SR group, the INT group reported more favorable changes in instrumental attitude (mean difference = 0.13; 95% CI = −0.01 to 0.23; d = 0.19; p = 0.077), intention (mean difference = 0.33; 95% CI = 0.10 to 0.56; d = 0.33; p = 0.006), and planning (mean difference = 0.39; 95% CI = 0.04 to 0.73; d = 0.26; p = 0.027). Mediation analyses indicated that both planning and intention partially mediated the effects of the intervention on PA at 12 weeks. Conclusions Our TPB-based behavior change intervention resulted in small improvements in the TPB constructs that partially mediated the effects of our intervention on PA behavior. Additional research with the TPB is warranted.     

Utility of cerebrospinal fluid cortisol level in acute bacterial meningitis

Background:

Meningitis remains a serious clinical problem in developing as well as developed countries. Delay in diagnosis and treatment results in significant morbidity and mortality. The role and levels of intrathecal endogenous cortisol is not known.

Objective:

To study the cerebrospinal fluid (CSF) cortisol levels and to evaluate its role as a diagnostic and therapeutic marker in acute bacterial meningitis.

Materials and Methods:

Thirty patients with acute bacterial meningitis with no prior treatment were evaluated. Cortisol levels were compared with 20 patients with aseptic (viral) meningitis and 25 control subjects.

Results:

Mean CSF cortisol level was 13.85, 3.47, and 1.05 in bacterial meningitis, aseptic meningitis, and controls, respectively. Mean CSF cortisol level in bacterial meningitis was significantly higher as compared to controls (P < 0.001). There was significant difference in CSFcortisol levels in bacterial and aseptic meningitis (P < 0.001).

Conclusions:

Cortisol levels in CSF are highly elevated in patients with acute bacterial meningitis. This suggests that intrathecalcortisol may serve as a valuable, rapid, relatively inexpensive diagnostic marker in discriminatingbetween bacterial and aseptic meningitis. This helps in earlier institution of appropriate treatment and thereby decreasing morbidity and mortality.     

Doxepin concentrations in plasma and cerebrospinal fluid

Doxepin—like other antidepressant drugs (ADs)—shows a variable antidepressant effect in clinical practice. The cause for this variability is as yet unclear; however, pharmacokinetic factors such as the variable permeability of doxepin into the cerebrospinal fluid (CSF), may contribute to the difference in therapeutic efficacy. We measured and correlated the concentration of doxepin and its active metabolite nordoxepin in both the plasma and CSF. Plasma and CSF samples were taken simultaneously from 21 patients who were treated with doxepin due to different clinical indications. The plasma concentration of both doxepin and nordoxepin correlated significantly with the oral dosage of doxepin (doxepin: r = +0.66, p < 0.001; nordoxepin: r = +0.78, p < 0.0001; Spearman’s correlation). Furthermore, we found significant correlations between the plasma and CSF concentrations of both doxepin (r = +0.71; p < 0.001; Pearson’s correlation) and nordoxepin (r = +0.74; p < 0.001). These highly significant correlations between the plasma and CSF concentrations indicate a constant CSF permeability of doxepin and its active metabolite nordoxepin.     

α-MSH Rescues Neurons from Excitotoxic Cell Death

This study investigates the effects of alpha-melanocyte-stimulating hormone (α-MSH), on neurodegeneration, gliosis and changes in the neurotrophic protein brain-derived neurotrophic factor (BDNF) and in pro-inflammatory cytokines, following kainic acid (KA)-induced excitotoxic damage in the rat. Male Sprague-Dawley rats were treated with α-MSH (intraperitoneally, i.p.) at 20 min, and 24 and 48 h following administration of 10 mg/kg KA (i.p.). The animals were sacrificed at 30 min, 4 h, 24 h and 72 h after KA-administration and the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) were analysed in samples of hippocampus and hypothalamus. Levels of BDNF were analysed in the hippocampus. Stereological quantification showed a markedly reduced number of viable neurons in the CA1 pyramidal cell layer upon KA-administration as compared to animals injected with vehicle (p < 0.05, 79,587 ±  25,554 vs. 145,254 ± 27,871). The number of viable neurons upon administration of α-MSH was significantly higher than upon KA alone (p < 0.05, 119,776 ± 33,158, KA+α-MSH vs. 79,587 ± 27,554, KA + Saline). Astrocyte activation due to the KA-induced excitotoxicity was reduced, and the KA-induced increase in IL-1β levels was delayed by the treatment with α-MSH. In conclusion, the degree of reduction in cell viability in the hippocampus CA1 pyramidal cell layer upon KA-induced excitotoxicity was similar to that seen previously upon global cerebral ischaemia. Furthermore, the administration of α-MSH resulted in a similar increase in cell viability, supporting the hypothesis that administration of α-MSH has rescuing effects on neurons subjected to excitotoxic insults.     

Effect of induced hyperglycemia on brain cell membrane function and energy metabolism during the early phase of experimental meningitis in newborn piglets

This study was done to elucidate the mechanism of hypoglycorrhachia and elevated lactate concentrations leading to neuronal dysfunction in neonatal meningitis, and to determine the effects of induced hyperglycemia on these disturbances. Thirty-eight newborn piglets were divided into three groups: 12 in the control group (CG), 12 in the normoglycemic meningitis group (NG), and 14 in the hyperglycemic meningitis group (HG). Meningitis was induced by intracisternal injection of 108 cfu of Escherichia coli. Hyperglycemia (blood glucose 300–400 mg dl⁻¹) was induced and maintained for 60 min before induction of meningitis and throughout the experiment using modified glucose clamp technique. CSF-to-blood glucose ratio decreased significantly in NG. In HG, baseline CSF-to-blood glucose ratio was lower than two other groups, but increased at 1 h after induction of meningitis. CSF lactate concentration was increased progressively in both meningitis groups, and positively correlated with CSF leukocyte numbers (r=0.41, p<0.001) and TNF-α level (r=0.43, p<0.001). Brain glucose concentration was significantly increased in HG and showed inverse correlation with CSF leukocyte numbers (r=−0.59, p<0.01). Brain lactate concentration was not significantly different among three groups and positively correlated with the CSF TNF-α level (r=0.51, p<0.05). Lipid peroxidation products were increased in NG. Na⁺,K⁺-ATPase activity, ATP/PCr concentrations were not different among three groups. Increased intracranial pressure, CSF pleocytosis (214±59 vs. 437±214/mm³, p<0.02) and increased lipid peroxidation products observed in NG were reduced in HG. These results suggest that hypoglycorrhachia and elevated lactate concentration in the CSF during meningitis originates primarily from the increased anaerobic glycolysis in the subarachnoid space, induced by TNF-α and leukocytes. Induced hyperglycemia attenuates the inflammatory responses of meningitis and might be beneficial by providing an increased glucose delivery to meet its increased demand in meningitis.     

Effects of Mindfulness-Based Stress Reduction Intervention on Psychological Well-being and Quality of Life: Is Increased Mindfulness Indeed the Mechanism?

Background  Although several studies have reported positive effects of mindfulness-based stress reduction (MBSR) intervention on psychological well-being, it is not known whether these effects are attributable to a change in mindfulness. Purpose  The aim of this study is to compare the effects of MBSR to a waiting-list control condition in a randomized controlled trial while examining potentially mediating effects of mindfulness. Methods  Forty women and 20 men from the community with symptoms of distress (mean age 43.6 years, SD = 10.1) were randomized into a group receiving MBSR or a waiting-list control group. Before and after the intervention period, questionnaires were completed on psychological well-being, quality of life, and mindfulness. Results  Repeated measures multiple analysis of variance (MANCOVAs) showed that, compared with the control group, the intervention resulted in significantly stronger reductions of perceived stress (p = 0.016) and vital exhaustion (p = 0.001) and stronger elevations of positive affect (p = 0.006), quality of life (p = .009), as well as mindfulness (p = 0.001). When mindfulness was included as a covariate in the MANCOVA, the group effects on perceived stress and quality of life were reduced to nonsignificance. Conclusion  Increased mindfulness may, at least partially, mediate the positive effects of mindfulness-based stress reduction intervention.     

Clinical,laboratory, and neuroimaging characteristics of fatigue in HIV-infected individuals

Fatigue is among the most common symptoms reported by HIV-infected individuals. Previous reports suggest that the prevalence of fatigue varies by disease status with rates close to 80% in patients with AIDS. However, most studies have not been conducted in the setting of a controlled trial and have not assessed the association of fatigue with cellular markers of brain activity. Data for this study were derived from baseline and longitudinal evaluations in ACTG A5090, a randomized, double-blind, placebo-controlled trial of the Selegiline Transdermal System for the treatment of HIV-associated cognitive impairment. Fatigue was assessed using the Fatigue Severity Scale with scores of >4 considered “fatigued”. Participants in a substudy underwent brain magnetic resonance spectroscopy (MRS) imaging, an in vivo method for assessing brain metabolites associated with neuronal and glia activity. Differences between fatigued and non-fatigued participants were evaluated with respect to demographics and clinical characteristics, plasma and CSF HIV-1 RNA concentration, CD4 counts, and brain metabolites. One hundred and twenty-eight participants were enrolled (88% male, median age = 45 years) and 82 participants (64%, 95% confidence interval 55%, 72%) were fatigued at baseline. MRS was conducted in 62 of the 128 participants. Fatigued participants were significantly younger (p = 0.011), had lower Karnofsky scores (p = 0.032), and had higher levels of depressive symptoms on the Center for Epidemiologic Studies Depression (CES-D) scale (p < 0.001) than non-fatigued participants. Statistically significant differences between fatigued and non-fatigued groups were not detected for plasma and CSF HIV-1RNA concentration, CD4 counts, or on neuropsychological tests. MRS revealed significantly lower levels of the cellular energy marker total creatine (p = 0.002) in the basal ganglia of fatigued participants. Statistically significant differences in other brain metabolites were not detected. Longitudinal data showed that fatigue persisted and worse fatigue at baseline was predictor of future fatigue. Among the cognitive tests, baseline Stroop score was associated with future fatigue. Fatigue was present in 64% of A5090 study participants and persisted during the 24 weeks of follow-up. Fatigue was associated with worse functional performance and depressive mood. Lower cellular energy levels in the basal ganglia, as measured by MRS total creatine concentration, suggest energy dysmetabolism in this brain region. This observation, taken together with the association between fatigue and neuropsychological tests of frontal lobe performance is consistent with the hypothesis of a striatal–cortical circuitry involvement in the symptoms of fatigue.     

Evaluation of Cerebellar and Cerebral Volume in Migraine with Aura: A Stereological Study

Migraine is associated with an increased risk of deep white matter lesions and subclinical posterior circulation infarcts. A significant association between deep white matter hyperintensities and cerebral atrophy is true for various neurological diseases; it was not specifically proven in migraine. The aim of this study was to evaluate the cerebellar and cerebral volume and volume ratios for cerebellum using the Cavalieri principle. We also aimed to examine whether migraine with aura causes cerebellar and cerebral atrophy. Twenty three right-handed patients with migraine with aura diagnosed by means of the International Headache Society criteria and 24 age-matched subjects whose only health problem was headache due to rhinosinusitis and tension type headache were included in the study. Measurements of the cerebellar and cerebral volumes as well as cerebellar/cerebral volume ratios were made using Cavalieri’s principle by utilizing the point-counting methods. There were no significant differences between the volumes of cerebrum, cerebellum, and the ratio of cerebellum to cerebrum for males (p = 0.05, p = 0.10, and p = 0.64, respectively) and for females (p = 0.18, p = 0.89, and p = 0.24, respectively). Our results suggest that patients with migraine with aura do not have a significant difference in cerebellar and cerebral volumes and cerebellar/cerebral volume ratios compared to the non-migraine group.     

NF-κB activation in cerebrospinal fluid cells from patients with meningitis

Abstract

We examined whether or not NF-κB, a factor that regulates expression of the genes that code for pro-inflammatory cytokines, is activated in cerebrospinal fluid (CSF) cells to investigate the production of pro-inflammatory cytokines by CSF cells in patients with meningitis. Western blotting demonstrated that NF-κB was more activated in CSF cells of patients with bacterial meningitis than in those of patients with aseptic meningitis. NF-κB was hardly activated in carcinomatous meningitis. The NF-κB activation in CSF cells of patients with meningitis tended to be correlated with the CSF interleukin-6 concentration. Our data suggested that CSF cells produce pro-inflammatory cytokines through NF-κB activation in meningitis, and that increased NF-κB activation in CSF cells indicate infectious meningitis rather than carcinomatous meningitis.