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PubMed1994

Effects of reinforcement history on responding under progressive-ratio schedules of reinforcement.

The effects of experimental history on responding under a progressive-ratio schedule of reinforcement were examined. Sixteen pigeons were divided into four equal groups. Groups 1 to 3 were trained to peck a key for food under a fixed-ratio, variable-ratio, or differential-reinforcement-of-low-rate schedule of reinforcement. After training, these pigeons were shifted to a progressive-ratio schedule, later were shifted back to their original schedule (with decreased rates of reinforcement), and finally were returned to the progressive-ratio schedule. Pigeons in Group 4 (control) were maintained on the progressive-ratio schedule for the entire experiment. To test for potential "latent history" effects, pigeons responding under the progressive-ratio schedule were injected with d-amphetamine and given behavioral-momentum tests of prefeeding and extinction. Experimental histories affected responding in the immediate transition to the progressive-ratio schedule; response rates of pigeons with variable-ratio and fixed-ratio histories were higher than rates of pigeons with differential-reinforcement-of-low-rate and progressive-ratio-only histories. Pigeons with differential-reinforcement-of-low-rate histories, and to a lesser degree pigeons with variable-ratio and fixed-ratio histories, also had shorter postreinforcement pauses than pigeons with only a progressive-ratio history. No consistent long-term effects of prior contingencies on responding under the progressive-ratio schedule were evident. d-Amphetamine and resistance-to-change tests failed to reveal consistent latent history effects. The data suggest that history effects are sometimes transitory and not susceptible to latent influences.

Animals↗

PubMed2000

Progressive-ratio schedules: effects of later schedule requirements on earlier performances.

Four rats were studied with variants of a progressive-ratio schedule with a step size of 6 in which different terminal components followed completion of the 20th ratio: (a) a reversal of the progression, (b) a fixed-ratio 6 schedule, or (c) extinction. Responding in the progressive-ratio components of these schedules was compared to performances under conventional progressive-ratio baselines. Under baseline conditions, postreinforcement pauses increased exponentially as a function of increasing ratio size, whereas running rates showed modest declines. The procedure of linking the progressive-ratio schedule to the reversed progression or to the fixed-ratio component resulted in decreased pausing. Linking the progressive-ratio schedule to the extinction component had the opposite effect, that of producing weakened progressive-ratio performances as evidenced by increased pausing. Subjects whose responses were reinforced on half of the ratios also showed exponential increases; however, pauses were substantially shorter following ratios on which the reinforcer was omitted. The results suggested that progressive-ratio pausing reflects the influence of remote as well as local contingencies.

Animals↗

PubMed1975

Onset and progression of diabetic glomerulosclerosis; a prospective study based on serial renal biopsies.

Clinical factors related to the development and progression of renal lesions were studied in twenty-three diabetics by the use of serial renal biopsies or autopsy. The results were as follows: Most of the juvenile and intermediate type diabetics were poorly controlled, with the glomerular lesion progressing rather rapidly. In contrast, many cases of the adult type were able to be maintained under good control and the renal lesion neither developed nor progressed. Two of the adult type diabetics with poor control showed slowly and slightly progressing renal lesions. The progression of glomerular lesions was significantly related to the control of blood glucose, type of diabetes, age at onset, type of treatment, and degree of obesity, but not to the duration of diabetes or the length of the follow-up period. There was a significant correlation between the type of diabetes and the control of blood glucose over the years. Arteriolar lesions developed concurrently with the progression of the glomerular lesion. Retinopathy also had a tendency to develop in proportion to the progress of glomerular lesions although it was not statistically significant. We have discussed the clinical factors responsible for the progression of diabetic glomerulosclerosis and have suggested that the type of diabetes rather than the degree of control of blood glucose might be more important in determining the development and progression of diabetic glomerulosclerosis. Nevertheless, the possibility remains that successful control of blood glucose may prevent or retard the development of diabetic glomerulosclerosis.

Adult↗

PubMed2001

Rapid progression of albumin excretion is an independent predictor of cardiovascular mortality in patients with type 2 diabetes and microalbuminuria.

OBJECTIVE: In patients with type 2 diabetes, microalbuminuria is associated with an increase in predominantly cardiovascular mortality. Considerable interindividual variability in the rate of progression of microalbuminuria exists. The prognostic significance of rate of progression of microalbuminuria with regard to cardiovascular and renal clinical end points is, however, unknown. The purpose of this study was to determine the prognostic significance of rate of progression of microalbuminuria for cardiovascular end points and renal function. RESEARCH DESIGN AND METHODS: In a previous prospective cohort study, progression of microalbuminuria (expressed as mean yearly change in albumin-to-creatinine ratio) was assessed in 58 patients with type 2 diabetes. During a median follow-up of 7 years after progression of microalbuminuria was determined, we registered all-cause mortality and coronary heart disease mortality as primary end points and coronary heart disease (fatal or nonfatal), peripheral vascular disease, ischemic stroke, retinopathy, macroalbuminuria, and change in serum creatinine as secondary end points. RESULTS: Seven subjects died during the study; five of these subjects died of coronary heart disease. Cox's regression analysis identified progression of microalbuminuria as a significant predictor of all-cause mortality (hazard ratio 1.46 per point increase in albumin-to-creatinine ratio per year, P < 0.001), coronary heart disease mortality (hazard ratio 2.32, P = 0.006), and macroalbuminuria (hazard ratio 1.79, P < 0.001). Adjustment for multiple cardiovascular risk factors did not affect these results. Identical analyses for baseline level of microalbuminuria instead of progression rate of microalbuminuria did not show significant hazard ratios. In addition, progression of microalbuminuria significantly predicted an increase in serum creatinine (r = 0.29, P = 0.04). CONCLUSIONS: In patients with type 2 diabetes and microalbuminuria, the rate of progression of albumin excretion seems to be a powerful independent predictor of mortality caused mainly by coronary heart disease.

Aged↗

PubMed1996

Detection of Progression of Coronary Artery Disease in the Elderly.

In order to assess the progression of coronary artery disease (CAD) in the elderly, we evaluated 91 patients aged 75 years or older who had undergone 2 consecutive angiograms without intervening revascularization. Progression was defined as an absolute increase in lumen narrowing by at least 20% with minimum stenosis of 50% at second angiogram, or progression to total occlusion of any preexisting lesion. Progression involving at least 1 vessel was observed in 63% of patients. Only 6% of initially normal or insignificantly diseased segments showed progression. In contrast, 72% of segments that progressed to total occlusion had shown an initial narrowing greater than 75%. Progression occurred in 100% of patients with an interval myocardial infarction, but in no patients with symptomatic valvular disease. No regression was observed, while 7 of 36 (19%) of initially occluded segments had recanalized. We conclude that progression of CAD in the elderly occurs at rates similar to those observed in a younger population; however no correlation could be found between the rate of progression and either risk factors or elapsed time between angiographic studies.

Journal Article↗

PubMed2002

Determination of lactic acid level in systemic liquids in children with progressive encephalopathies.

BACKGROUND: This article reports the results of research into the activities of lactic acid concentrations in the body fluids of children with progressive encephalopathies (PE) in comparison to patients with non-progressive encephalopathies (NPE) and those with non-progressive encephalopathies with concomitant epilepsy (NPEE). The study was designed to determine whether there is difference between the serum and CSF lactic acid concentrations in children with progressive encephalopathies (PE), static (non-progressive) encephalopathies (NPE) and non progressive encephalopathies with concomitant epilepsy (NPEE), and whether the clinical status correlates with the concentration of these biochemical markers in children with PE. MATERIAL/METHODS: The assessment involved 138 children of both sexes, whose age ranged between 8 months and 15 years, diagnosed and treated in the Neurology Department at the Pediatric Clinic of the Silesian Medical Academy in Katowice between 1995 and 1997. Lactate concentrations were determined in serum and cerebro-spinal fluid and analyzed statistically. RESULTS: The findings showed higher serum and CSF concentrations in children with PE than in patients who manifested non-progressive forms of encephalopathy. The degree of clinical symptom aggravation in PE children was likewise analyzed and compared to the values of lactate concentrations in body fluids; however, no correlation was found between these parameters. CONCLUSIONS: Children with progressive encephalopathies present higher lactate concentrations in serum and cerebrospinal fluid than patients with static (non-progressive) encephalopathy.

Adolescent↗

PubMedDate not supplied

[Quantification of pharmacological progress by the French National Health Authorities].

The French National Health Authority has delegated to the Transparency Commission (TC) responsibility for defining and quantifying therapeutic progress and for certifying the therapeutic added value of new drugs. It is essential to distinguish between pharmacologic innovation and therapeutic progress. The TC considers that a new product offers therapeutic progress if it: 1) improves patient management, 2) represents a significant clinical breakthrough, and/or 3) meets a previously uncovered need. Therapeutic progress must be supported by quantitative or qualitative clinical evidence of improved therapeutic tolerance, compliance or maintenance. The TC measures progress in terms of the enhancement of therapeutic value (ETV) relative to existing products. Ideally, ETV should be evaluated in head-to-head comparisons, but companies often prefer placebo-controlled studies, meaning that indirect comparisons are unavoidable. ETV is graded in five levels, ranging from I (major progress) to V (no progress), and is attributed for a specific target population. The ETV only measures expected therapeutic progress, to be confirmed in post-registration studies. TC decisions are taken into account by the commission that determines drug prices. One pending economic issue involves "me-too" products. Indeed, scientific committees cannot be expected to regulate market competition--for example, to decide when to inform decision-makers that the number of statins or betablockers on the market is sufficient to cover requirements. Another delicate problem concerns efforts by brand-name drug companies to circumvent generic drugs, notably by introducing fixed-dose combinations. Although the assessment of therapeutic progress is based on objective, verifiable and reproducible criteria, it can only be carried out fairly within a collaborative framework independent of pharmaceutical companies, healthcare insurers and consumer associations.

Drug Costs↗

PubMed1991

[Progression of functional disability in 70 patients with multiple sclerosis].

We have carried out a follow-up study in 70 patients that were included in a follow-up protocol when they met the criteria of MS, so as to evaluate the variations in the disability scale per unit of time of follow-up (index of progression) in relation to the several risk factors. There were 31 females and 39 men followed up for 19.6 +/- 12 months. One half of the patients (35) had their first symptoms between 25 and 45 years of age, in 27 the onset was after age 25 and in 8 after age 45. At the end of follow-up 42 patients were classified as having remitting forms, 12 as progressive forms after a remitting phase and 16 as progressive forms from the onset. Significant differences in the evolutive forms were only found in remitting-progressive forms, which had a quicker progression than the purely remitting and chronic progressive forms. The patients who initially had cerebellar symptoms had a quicker progression than those with any other type of presentation. Whereas patients with late onset had a quicker progression than the group with intermediate onset, the patients with early onset had a slower progression.

Adolescent↗

PubMed1982

Hormonally responsive versus unresponsive progression of prostatic cancer to antiandrogen therapy as studied with the Dunning R-3327-AT and -G rat adenocarcinomas.

The present study has compared the response to antiandrogen therapy of the serially transplantable Dunning R-3327-AT (hereafter called AT) versus Dunning R-3327-G (hereafter called G) rat prostatic adenocarcinoma. Castration or chemical antiandrogen therapy (i.e., cyproterone acetate and diethylstilbestrol) of rats bearing established AT or G tumors results in neither regression of tumor volume nor a cessation of the continuous growth of either tumor. By these criteria, both the AT and G tumors progress following antiandrogen therapy. For the AT tumor, this progression is completely unresponsive to hormonal therapy, and thus such therapy does not increase survival of AT tumor-bearing rats. The AT tumor is therefore an example of hormonally unresponsive progression. In direct contrast, while the G tumor likewise progresses following antiandrogen therapy, this therapy does induce a 1.8-fold decrease in the subsequent growth rate of the G tumor. This positive response during progression of the G tumor results in a 78% increase in the survival of G tumor-bearing rats treated with antiandrogen therapy. The G tumor is therefore an example of hormonally responsive progression. These results indicate neither that prostatic cancers which do not regress or cease growing following antiandrogen therapy can necessarily be considered hormonally unresponsive nor that antiandrogen therapy of such tumors has been completely ineffective, since, as shown in the present study, such progression can be of either a hormonally unresponsive or a responsive type. Regardless of which type of progression occurs, however, additional therapy is required to further increase survival. The present study demonstrates that such additional therapy should probably not include the subsequent use of pharmacological doses of exogenous androgen, since, depending on the type of progression, such treatments can actually decrease survival.

Adenocarcinoma↗

PubMed1995

[Progressive apoplexy. Incidence, risk factors and prognosis--the Copenhagen Stroke Study].

Clinical progression after arrival to hospital is frequent in acute stroke patients. Risk factors and mechanisms behind progression have remained largely unknown. This prospective, community-based study of 1006 acute stroke patients was undertaken to uncover factors of importance in the development of stroke-in-progression (SIP), and to assess the impact of SIP on prognosis. The diagnosis of progression was based on the Scandinavian Neurological Stroke Scale (SSS). Patients were divided according to whether progression occurred early (within 36 hours from stroke onset) or late (within the first week from onset). A marked progression developed in 32%. The following risk factors for early progression were identified: Systolic blood pressure on admission decreased the relative risk by 0.66 per 20 mmHg elevation (95% CI 0.55-0.83) and diabetes increased the relative risk by 1.9 (95% CI 1.1-3.3). Stroke severity was the only risk factor found in late progression (OR 1.4 per 20-point increase in stroke severity (95% CI 1.1-1.7)). These relations were independent of age, sex, blood glucose, heart disease and other stroke risk factors. SIP doubled mortality (0.001) and numbers discharged to nursing homes (0.001), and was associated with increased neurological deficits and decreased functional ability (0.0001) in survivors. These findings suggest that a causal relationship exists between the systemic blood pressure and the development of progression in the early phase of stroke and that this relationship is enhanced in patients with diabetes. The impact of SIP on prognosis is severe and lasting.

Aged↗

PubMed1994

[Progression of coronary sclerosis after smoking cessation].

Cigarette smoking is an established risk factor for the development of coronary artery disease, but whether cessation of heavy smoking influences progression of coronary artery disease is unclear. In 390 patients (359 men, 31 women; 52.4 +/- 6.7 SD years) with coronary artery disease, two coronary angiograms were performed at an interval of 62.4 +/- 23.5 months. Smoking habits were obtained by questionnaires. Progression of coronary artery disease was defined as the sum of new stenoses, progression of existing stenoses and new coronary occlusions. Multivariate classification analyses of risk factor profile revealed cigarette smoking (amount per day and length of time) as the most relevant factor for progression of coronary artery disease. Non-smokers had a progression score of 0.96 (95% confidence interval: 0.63-1.28) over the observation period. Former smokers (20.2 +/- 11.8 cigarettes/day for 19.4 +/- 7.6 years) who quit about 10 years before the first angiogram showed a progression of 2.20 (95% confidence interval: 1.77-2.63; p < 0.01) compared to non-smokers. Those smokers (23.8 +/- 9.2 cigarettes/day for 31.3 +/- 7.0 years) who quit at the time of the first angiogram showed a progression of 2.47 (95% confidence interval: 1.97-2.97; p < 0.001). Current smokers (20.5 +/- 9.7 cigarettes/day for 34.8 +/- 8.5 years) had a progression of 3.17 (95% confidence interval: 2.35-3.99; p < 0.001). The data indicate that former heavy cigarette smoking continues to act as a significant risk factor for progression of coronary artery disease even after cessation. This does not mean that current cigarette smokers should not stop.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

The role of CA 125 and conventional examinations in diagnosing progressive carcinoma of the ovary.

The clinical significance of the serum marker CA 125 and conventional examinations in diagnosing progressive disease was evaluated in 98 patients. The examinations included CA 125, gynecologic and complete physical examination, abdominal computed tomography (CT), roentgenogram of the chest, second look operation and serum biochemistry profile. Progressive disease occurred in 49 patients and the time to progression was a median of 12 months (range of four to 52 months). At the time of progression, an elevated CA 125 was found in 73 percent of the patients, and in 63 percent of the patients, CA 125 increase preceded clinical progression for a median of four and one-half months (range of 0.5 to 29.5 months). A positive gynecologic examination at progression was found in 67 percent of the patients, physical examination and abdominal CT scan were positive in 30 percent, intervention operation in 14 percent and roentgenogram of the chest in 12 percent of the patients. With the combination of serum CA 125, gynecologic and general physical examination, progressive disease could be diagnosed in 92 percent of the patients. The false-positive rate in the 49 patients with no evidence of disease was 1.6 percent for CA 125, 2.0 percent for gynecologic examination, 4.0 percent for physical examination, 14.0 percent for CT scan and 2.0 percent for roentgenograms of the chest. Serum CA 125 is the most reliable examination to detect progressive disease early. With the combined use of serum CA 125 and the gynecologic and general physical examination, progression of the disease can be detected in about 90 percent of the patients.

Adenocarcinoma↗

PubMed1995

Progressive hemifacial atrophy. A natural history study.

PURPOSE: To describe two very different natural history courses in 2 patients with hemifacial atrophy. Progressive hemifacial atrophy (Parry-Romberg syndrome, Romberg syndrome, PHA) is characterized by slowly progressive atrophy, frequently involving only one side of the face, primarily affecting the subcutaneous tissue and fat. The onset usually occurs during the first 2 decades of life. The cause and pathophysiology are unknown. Ophthalmic involvement is common, with progressive enophthalmos a frequent finding. Pupillary disturbances, heterochromia, uveitis, pigmentary disturbances of the ocular fundus, and restrictive strabismus have also been reported. Neurologic findings may be present, but the natural history and progression of ocular findings are often not described in the literature. METHODS: We studied the records and present findings of 2 patients with progressive hemifacial atrophy who were observed in our institution over a 10-year period. RESULTS: Both patients showed progression of ophthalmic findings, primarily on the affected side. One patient has had chronic uveitis with secondary cataract and glaucoma, in addition to retinal pigmentary changes. She also had a third-nerve paresis of the contralateral eye and mild seizure activity. The other patient had mild uveitis, some progression of unilateral retinal pigmentary changes, and a significant increase in hyperopia in the affected eye, in addition to hypotony at age 19 without a clear cause, but with secondary retinal and refractive changes. CONCLUSION: Ocular manifestations of progressive hemifacial atrophy are varied, but can progress from mild visual impairment to blindness.

Adult↗

PubMed1997

[Mode of progression of visual field defects and risk factors in glaucoma patients].

A study of glaucoma was conducted at 17 institutions to clarify the mode of progression of visual field defects in specific types of glaucoma, including primary open angle glaucoma (POAG), primary angle closure glaucoma (PACG), and normal tension glaucoma (NTG). Staging of glaucoma was done by the Kosaki Classification or the Aulhorn Classification and the mode of progression was assessed by life-stable method. The progressive and non-progressive groups of patients in each glaucoma stage were compared with respect to age, intraocular pressure, refraction, and optic disc cupping. A total of 656 eyes were investigated in 656 patients (301 men and 355 women) with a mean age of 58.0 years. The average follow-up period was 5.8 years for the study using the Kosaki Classification and 4.0 years for that done with the Aulhorn Classification. The progression of visual field defects was rapid in the early stage but slow in the middle and late stages in the study by the Kosaki Classification, and it was slow in the late stages in the study by the Aulhorn Classification. The time for progression from stage Ia to stage VI was 43.3 years in the study by the Kosaki Classification and the time for progression from stage 0 to stage 6 was 47.2 years in the study by the Aulhorn Classification. The progressive and non-progressive groups differed significantly with respect to intraocular pressure at various stages.

Female↗

PubMed1998

Breast cancer metastasis-associated genes: role in tumour progression to the metastatic state.

Breast cancer patients usually do not die of their primary cancers; they die of metastatic disease. Thus understanding the progression of breast cancer to the metastatic state and the changes that take place in highly malignant breast cells are important goals that could eventually result in new therapeutic approaches to highly progressive breast disease. Changes in the expression of certain genes or alterations in gene structures and encoded products can result in benign tumour cells progressing to the metastatic state. Experimentally, this has been performed by transferring dominantly acting oncogenes into susceptible cells and then testing the malignant properties of these cells in suitable animal models, but such rapid qualitative changes occur in vivo only rarely, and the natural progression of mammary cells to the metastatic state is thought to occur through a slow stepwise process that can take several years. Some of the slow stepwise changes in mammary cancer progression can be reversible and need not involve dominantly acting oncogenes or tumour suppressor genes, consistent with clinical observations. An important element of the natural progression of mammary tumours to malignancy may be their ability to circumvent microenvironmental controls that regulate growth and cellular diversity, a process that appears to involve mainly quantitative changes in gene expression, resulting in loss of normal cellular regulation. One of the important mechanisms of cellular regulation in epithelial tissues, such as those found in the breast, is mediated by intercellular junctional communication. Alterations in gene expression can result in loss of gap-junctional communication, concomitant with cellular diversification and progression. It is thought that the highly malignant cancer cells that have slowly evolved in vivo with only a few qualitative changes in gene structure have undergone extensive cycles of diversification and the accumulation of several quantitative changes in the expression of various genes that encode products related to malignancy. We have identified some of the genes that are related to progression and metastasis in breast cancer. For example, one of these genes, a novel gene called mta1 (in rodents) or MTA1 (in humans) appears to be involved in mammary cell motility and growth regulation. Thus highly malignant cellular phenotypes can arise rapidly due to specific qualitative changes in critical controlling genes, or more slowly via less critical qualitative genetic changes coupled with other cellular changes, such as loss of intercellular communication, and changes in gene expression, such as in the MTA1 gene, resulting in cellular diversification and ultimately tumour progression to the metastatic state.

Breast Neoplasms↗

PubMed1998

Homozygous deletions at chromosome 9p21 involving p16 and p15 are associated with histologic progression in follicle center lymphoma.

Low-grade follicle center lymphoma (LGFCL) is characterized genetically by the t(14;18) translocation and an indolent clinical course. Histologic progression from LGFCL to an aggressive diffuse large B-cell lymphoma (DLCL) occurs in 60% to 80% of cases, and this transformation is associated with the accumulation of secondary genetic alterations. Using 10 polymorphic microsatellite markers spanning the chromosome 9p21 region harboring the p15 (p15(INK4B)/MTS-2/CDKN2B) and p16 (p16(INK4A)/MTS-1/CDKN2) tumor-suppressor gene loci, we analyzed 11 matched pairs of LGFCL and their corresponding progressed DLCL biopsies for loss of heterozygosity and homozygous deletions at 9p21. A comparative multiplex polymerase chain reaction assay was also used for the detection of homozygous deletions. Deletions were identified in 8 of the 11 cases studied (73%): 6 homozygous (54%) and 2 hemizygous (18%). The deletions were identified exclusively in the progressed DLCL biopsies. Immunohistochemical studies showed an excellent correlation with the results from the genetic analyses. Of the 9 matched pairs of LGFCL and progressed DLCL with interpretable immunohistochemical staining, 9 of 9 (100%) of the LGFCL showed diffuse reactivity for p16. Four of the 9 (44%) immunohistochemically evaluable cases of progressed DLCL showed loss of or, in 1 case, markedly diminished p16 expression. All 4 of these cases correspondingly showed homozygous deletions at 9p21. Five of the 9 progressed DLCL cases showed p16 expression and demonstrated retention of one or both 9p21 alleles by genetic analysis. This is the first longitudinal series examining sequential biopsy specimens of low-grade and progressed FCL for genetic loss at 9p21 encompassing the p16 and p15 loci. The high frequency and exclusive occurrence of deletions involving p16 in the progressed DLCLs suggests that genetic loss at 9p21 targeting p16 and/or p15 is an important secondary genetic event in the histologic progression of FCL.

Carrier Proteins↗

PubMed1996

Predictive value of p53 mutations analyzed in bladder washings for progression of high-risk superficial bladder cancer.

To assess the value of p53 mutations in predicting the progression of superficial bladder cancer [transitional cell carcinoma (TCC)] and to define exactly when p53 mutations occur in the process of tumor progression, 80 consecutive bladder washings from 26 high-risk (indicated by quantitative karyometric analysis) superficial TCC patients were examined by single-strand conformation polymorphism. Six of 13 patients who experienced clinical progression (progression to T2 or higher) were found to have a p53 mutation in one or more of their bladder washings. In the control group (no progression to invasive disease), only 1 of 13 patients had a p53 mutation. For these high-risk superficial TCC patients, the occurrence of a p53 mutation has a positive predictive value of 86% for the progression of disease. A negative predictive value of 63% was observed. Moreover, because p53 mutations were found in samples prior to progression (mean, 8 months), they could identify patients who need changes in their treatment strategies to prevent progression to invasive disease. Despite these promising results, it is obvious that to increase not only the positive predictive value but especially the negative predictive value of this procedure to predict progression, additional prognostic markers are still needed.

Aged↗

PubMed2004

The pathogenesis of primary progressive multiple sclerosis: antibody-mediated attack and no repair?

Primary progressive multiple sclerosis (MS) differs from the more common form of MS which has an initial relapsing-remitting course in a number of ways, including pathological features, clinical course, differential diagnosis and response to treatment. The lesions in primary progressive MS tend to be more diffuse, less inflammatory and less likely to remyelinate than those occurring in relapsing-remitting MS and secondary progressive MS; there are also fewer focal lesions in the brain in primary progressive MS. Recent evidence suggests that antibodies to central nervous system (CNS) antigens have an important role in disease progression. Such antibodies could cause demyelination, inhibit remyelination and cause axonal destruction. Ongoing immune attack by autoantibody and lack of CNS repair could be responsible for the gradually increasing disability in primary progressive MS. Further research on the B-cell and autoantibody response in primary progressive MS might lead to advances in diagnosis and treatment. Inhibition of autoantibody production by inducing B-cell apoptosis with rituximab is a potential new therapy for primary progressive MS.

Autoantibodies↗