Disease relevance of Multiple Sclerosis, Chronic Progressive

• In a 24-month prospective study, we used a sensitive enzyme-linked immunosorbent assay to determine levels of TNF-alpha in cerebrospinal fluid and serum in 32 patients with chronic progressive multiple sclerosis and in 20 with stable multiple sclerosis and 85 with other neurologic diseases [1].
• Theiler murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) is a mouse model of chronic-progressive multiple sclerosis (MS) characterized by Th1-mediated CNS demyelination and spastic hindlimb paralysis [2].
• Detailed analysis of the oligodendrocyte myelin glycoprotein gene in four patients with neurofibromatosis 1 and primary progressive multiple sclerosis [3].
• Thirty-seven chronic progressive multiple sclerosis (MS) patients, 20 of whom were taking cyclosporine, were examined for excretion of JC virus (JCV) in the urine [4].

Psychiatry related information on Multiple Sclerosis, Chronic Progressive

• We examined short-term memory (STM) among a group of 23 definite, chronic progressive multiple sclerosis (MS) patients, all of whom had experienced recent significant disease activity, and a control group matched closely on age and education [5].

High impact information on Multiple Sclerosis, Chronic Progressive

• In patients with chronic progressive multiple sclerosis, mean TNF-alpha levels were significantly higher in the cerebrospinal fluid than in corresponding serum samples (52.41 vs. 11.88 U per milliliter; range, 2 to 178 vs. 2 to 39; P less than 0.001) [1].
• Elevated serum interleukin-2 levels in chronic progressive multiple sclerosis [6].
• CD8+ Tact cells were defective in patients with chronic progressive multiple sclerosis (MS) as compared to patients with relapsing-remitting MS or normal controls [7].
• METHODS: 194 patients with worsening relapsing-remitting or secondary progressive multiple sclerosis were assigned placebo or mitoxantrone (5 mg/m(2) [exploratory group] or 12 mg/m(2) intravenously) every 3 months for 24 months [8].
• Cladribine in treatment of chronic progressive multiple sclerosis [9].

Chemical compound and disease context of Multiple Sclerosis, Chronic Progressive

• In relapsing-remitting and secondary-progressive multiple sclerosis, gadolinium enhancement increases the number of detectable active lesions and also probably correlates with pathological activity [10].
• Biased assessment of blinding in a randomized placebo-controlled trial of oral methotrexate in chronic progressive multiple sclerosis [11].
• The time-integrated cortisol response to human corticotropin-releasing hormone (CRH) stimulation was lower in the patients with secondary progressive multiple sclerosis, compared with patients with primary progressive multiple sclerosis and healthy subjects [12].
• One hundred sixty-four patients with chronic progressive multiple sclerosis (MS) have been treated with a regimen of high-dose IV cyclophosphamide and ACTH over the past 6 years [13].
• A phase II study of i.v. methylprednisolone in secondary-progressive multiple sclerosis [14].

Biological context of Multiple Sclerosis, Chronic Progressive

• Primary progressive multiple sclerosis as a phenotype of a PLP1 gene mutation [15].
• Gene expression and genotyping studies implicate the interleukin 7 receptor in the pathogenesis of primary progressive multiple sclerosis [16].
• Allelic association studies with microsatellite markers around the tumour-necrosis factor (TNF) genes have demonstrated significantly different allele distributions of TNF markers (a and b) between relapsing-remitting/secondary progressive multiple sclerosis (MS) (RR/SPMS) patients and normal controls [17].
• In the present study, the role of HLA class II (DRB1, DQA1 and DQB1) alleles and haplotypes was investigated in 43 unrelated Iranian chronic progressive multiple sclerosis (CP-MS) patients compared with 100 healthy individuals [18].

Anatomical context of Multiple Sclerosis, Chronic Progressive

• The sympathetic skin response, a measure of sympathetic nervous system function, is absent in most patients with chronic progressive multiple sclerosis (MS) [19].
• Blood-brain barrier (BBB) breakdown, demonstrable in vivo by enhanced MRI is characteristic of new and expanding inflammatory lesions in relapsing-remitting and chronic progressive multiple sclerosis (MS) [20].
• Central nervous system (CNS) remyelination has been found by light and electron microscopy and immunocytochemistry within fresh lesions from four cases of acute and chronic progressive multiple sclerosis (MS) [21].
• The short-term effect of an immunosuppressive treatment on CSF myelin basic protein in chronic progressive multiple sclerosis [22].
• IgG secretion and Con A suppressor cell function were inversely correlated in MS patients but not in controls, suggesting that in chronic progressive multiple sclerosis a common abnormality underlies both increased response to PWM and decreased induction of suppression by Con A [23].

Gene context of Multiple Sclerosis, Chronic Progressive

• In primary progressive multiple sclerosis, MMP-9 was increased in 57% of CSF samples, but concentrations were below those encountered in the relapsing-remitting form [24].
• TIMPs and other MMPs (MMP-2 and -3) were not upregulated or not detectable (MMP-7) in CSF of patients with relapsing-remitting and primary progressive multiple sclerosis [24].
• Serum cytokine levels in chronic progressive multiple sclerosis: interleukin-2 levels parallel tumor necrosis factor-alpha levels [25].
• CTLA4 exon 1 dimorphism is associated with primary progressive multiple sclerosis [26].
• Serum levels of insulin-like growth factor-1 and insulin-like growth factor binding protein-3 in relapsing and primary progressive multiple sclerosis [27].

Analytical, diagnostic and therapeutic context of Multiple Sclerosis, Chronic Progressive

• A 2-year, placebo-controlled, double-blind, crossover study was started in 1992 to evaluate cladribine, an immunosuppressive drug, in the treatment of chronic progressive multiple sclerosis [28].
• Forty-four patients with chronic progressive multiple sclerosis (MS) were compared with age- and education-matched control groups on a battery of clinical and experimental memory measures [29].
• To assess whether brain tissue loss occurs after profound and sustained suppression of magnetic resonance imaging (MRI) enhancement, we measured brain volume changes from 10 patients with rapidly evolving secondary progressive multiple sclerosis (MS) treated with autologous haematopoietic stem cell transplantation and followed up for 24 months [30].
• 39 patients with chronic-progressive multiple sclerosis were treated with a short course of intensive immunosuppression in high doses of cyclophosphamide and prednisone [31].
• Lymphocytes of chronic progressive multiple sclerosis (MS) patients and healthy persons were isolated by nylon-wool column filtration followed by density centrifugation [32].

References