Prevalence of multiple sclerosis in a south London borough.

A survey of multiple sclerosis in the London Borough of Sutton, population 169,600, yielded 195 cases, giving an overall prevalence of 115/100,000. This is the third highest prevalence for a first survey of a geographical area in the United Kingdom, exceeded only by 127/100,000 in north east Scotland and 134/100,000 in Shetland. On the classification system of Allison and Millar, three quarters of the cases were classified as probable multiple sclerosis, 15% as early probable and latent multiple sclerosis, and 10% as possible multiple sclerosis. The mean age was 49 years, the mean age at onset was 34 years, and the mean duration of the disease was 15.4 years. The age standardised female to male ratio was 2:1. The prevalence found in this survey does not differ significantly from that recorded in the first north east Scotland survey. This study suggests that, firstly, the prevalence of multiple sclerosis in south east England is probably about 100/100,000 and, secondly, the latitudinal effect on the prevalence of multiple sclerosis in the United Kingdom is less appreciable than previously believed.     

Feeding of school children in a London borough.

A survey of 12 schools in a London borough showed that the protein and energy content of the average school meal was below the standard set by the Department of Health and Social Security for all age groups. Failure to meet the standards resulted from inadequate food purchases, poor menu planning and portion control, and several management problems. A 24-hour recall questionnaire showed that 5% of the pupils were "poorly" fed. These pupils were, however, no worse off than their "adequately" fed peers with regard to absences from school or academic attainment measured by reading quotient, but there was some slight difference in height and weight. The percentage of children having no breakfast increased from 4% in the infant schools to 21% in the senior schools. Two per cent of the senior pupils regularly ate no lunch.     

Prevalence of multiple sclerosis in Saskatoon.

In an epidemiologic survey based on a search of all available medical records for 1955 to 1980 at the city''s three general hospitals the prevalence in Saskatoon of probable multiple sclerosis was found to be 111/100,000 and that of combined probable and possible multiple sclerosis 134/100,000 on Jan. 1, 1977. The average annual incidence over the three decades was 4.8/100,000. These prevalence and incidence rates were two to three time greater than those reported for other Canadian cities. Of the 150 individuals with probable multiple sclerosis 87 were living in Saskatoon at the time of onset of the disease; thus, the prevalence of the disease among residents was 64/100,000. The prevalence was 77/100,000 among Saskatchewan-born residents, including those born in Saskatoon, and 48/100,000 among immigrants from other provinces and outside Canada.     

Prevalence of celiac disease in multiple sclerosis

Background  

Celiac disease (CD) is a common systemic disease related to a permanent intolerance to gluten and is often associated with different autoimmune and neurological diseases. Its mean prevalence in the general population is 1-2% worldwide. Our aim was to study the prevalence of celiac disease in a prospective series of Multiple Sclerosis (MS) patients and their first-degree relatives.     

Prevalence of multiple sclerosis in north-east Scotland.

An epidemiological study of multiple sclerosis (MS) in north-east Scotland was carried out based on data correct on 1 December 1970. The prevalence of MS was 127 cases/100 000 population, which is greater than in any other surveyed area with a comparable population. The disease was not spread homogeneously within the region, and in one district one in 400 people was affected. The geographical distributions of MS and the presence of HLA antigens A3 and B7,which are associated with the disease, are remarkably similar, and the prevalence of B7 in north-east Scotland is higher than elsewhere. This may partly explain the high prevalence of MS in this area, but the essential additional environmental factor remains to be established.     

Prevalence of multiple sclerosis in five rural Suffolk practices.

OBJECTIVE--To determine a point prevalence of multiple sclerosis in part of Suffolk. DESIGN--Multiple source search for patients with multiple sclerosis in five general practices. Patients were reviewed and categorised by using general practice notes. SETTING--Five rural general practices in Suffolk, 12 May 1988. SUBJECTS--31,379 patients registered with five practices. MAIN OUTCOME MEASURES--Multiple sclerosis diagnosed by a specialist. RESULTS--The search produced a provisional list of 62 eligible patients with multiple sclerosis. Review of case notes showed that 48 had probable disease, 10 early disease, and four possible disease. The probable cases gave a crude prevalence of 153/100,000 population (95% confidence interval 109/100,000 to 196/100,000). CONCLUSIONS--Although the results should be interpreted cautiously because of the small sample size, they suggest that the prevalence of multiple sclerosis in Suffolk is higher than has been estimated from hospital data.     

Common mistakes in infant feeding: survey from London borough.

A survey of infant-feeding practices among 265 mothers of 12-week-old infants in a London borough showed that only 18 gave breast milk alone, 236 giving bottle feeds, and 197 solids. Serious mistakes in feed preparation were common, and only 51 mothers followed manufacturers'' instructions exactly. Most mothers (239) had attended a well-baby clinic, but clinic staff gave conflicting advice on infant feeding. Health workers must pay greater attention to educating mothers on the details of infant feeding if the risks of hypernatraemia and obesity are to be reduced.     

Glutamate excitotoxicity in a model of multiple sclerosis

Glutamate excitotoxicity mediated by the AMPA/kainate type of glutamate receptors damages not only neurons but also the myelin-producing cell of the central nervous system, the oligodendrocyte. In multiple sclerosis, myelin, oligodendrocytes and some axons are lost as a result of an inflammatory attack on the central nervous system. Because glutamate is released in large quantities by activated immune cells, we expected that during inflammation in MS, glutamate excitotoxicity might contribute to the lesion. We addressed this by using the AMPA/kainate antagonist NBQX to treat mice sensitized for experimental autoimmune encephalomyelitis, a demyelinating model that mimics many of the clinical and pathologic features of multiple sclerosis. Treatment resulted in substantial amelioration of disease, increased oligodendrocyte survival and reduced dephosphorylation of neurofilament H, an indicator of axonal damage. Despite the clinical differences, treatment with NBQX had no effect on lesion size and did not reduce the degree of central nervous system inflammation. In addition, NBQX did not alter the proliferative activity of antigen-primed T cells in vitro, further indicating a lack of effect on the immune system. Thus, glutamate excitotoxicity seems to be an important mechanism in autoimmune demyelination, and its prevention with AMPA/kainate antagonists may prove to be an effective therapy for multiple sclerosis.     

Prevalence of grey matter pathology in early multiple sclerosis assessed by magnetization transfer ratio imaging

The aim of the study was to assess the prevalence, the distribution and the impact on disability of grey matter (GM) pathology in early multiple sclerosis. Eighty-eight patients with a clinically isolated syndrome with a high risk developing multiple sclerosis were included in the study. Forty-four healthy controls constituted the normative population. An optimized statistical mapping analysis was performed to compare each subject''s GM Magnetization Transfer Ratio (MTR) imaging maps with those of the whole group of controls. The statistical threshold of significant GM MTR decrease was determined as the maximum p value (p<0.05 FDR) for which no significant cluster survived when comparing each control to the whole control population. Using this threshold, 51% of patients showed GM abnormalities compared to controls. Locally, 37% of patients presented abnormalities inside the limbic cortex, 34% in the temporal cortex, 32% in the deep grey matter, 30% in the cerebellum, 30% in the frontal cortex, 26% in the occipital cortex and 19% in the parietal cortex. Stepwise regression analysis evidenced significant association (p = 0.002) between EDSS and both GM pathology (p = 0.028) and T2 white matter lesions load (p = 0.019). In the present study, we evidenced that individual analysis of GM MTR map allowed demonstrating that GM pathology is highly heterogeneous across patients at the early stage of MS and partly underlies irreversible disability.     

Apoptosis in multiple sclerosis

Several recent studies have provided evidence that apoptosis is an important feature in the pathogenesis of multiple sclerosis (MS), an autoimmune disease of the central nervous system. Apoptosis presumably plays a role in the immunoregulation via activation-induced T-cell death (AICD) and in local processes of tissue damage. In this review the dual role of apoptosis in the MS pathogenesis and its relevance regarding therapeutic concepts is discussed.     

Riedel's thyroiditis in a patient with multiple sclerosis

Our patient developed Riedel's thyroiditis soon after having an exacerbation of multiple sclerosis (MS). MS has been associated with other autoimmune diseases, including thyroiditis, and both Hashimoto's thyroiditis and subacute thyroiditis have been described in connection with MS. Yet, we are not aware of any other patient reported to have concomitant MS and Riedel's thyroiditis. The association between MS and Riedel's thyroiditis remains obscure but may reflect an autoimmune disorder common to both diseases.     

Antigen-specific therapies in multiple sclerosis

Multiple sclerosis is the major neurological disease of young adults in the western world, affecting about 1 per 1,000. It is characterised by chronic or recurrent lesions of inflammatory damage in the white matter of the central nervous system. Within such lesions, the protective myelin sheath is stripped off axons by infiltrated macrophages which leads to impaired conductivity. The inflammatory process most likely starts by activation of helper T cells directed against local myelin antigens. Currently, efforts are directed at specifically blocking such myelin-reactive helper T cells in order to control the disease. In this chapter, immunological features of multiple sclerosis and the experimental animal model for the disease, experimental allergic encephalomyelitis, are discussed. Next, an overview is presented on myelin antigens that have been suggested to play a role as target antigens in MS. Finally, strategies are discussed that are currently employed to selectively block the activation of T-cells reactive against myelin antigens.     

Insulin counter-regulation in multiple sclerosis

Fasting hypoglycemia is frequently observed in patients with Multiple Sclerosis (S.M.) showing orthostatic hypotension and defective thermoregulation, although they never complicate in hypoglycemic coma. The aim of this study was to evaluate glucose homeostasis in S.M. patients. Both insular and counter-insular regulating mechanisms were investigated by determination of glucose, insulin, C-peptide and cortisol plasmatic levels during OGTT, and subsequently by evaluating glucagon plasmatic levels after arginine administration (30 g., i.v.). Our results suggest that the increased susceptibility of S.M. patients to undergo fasting hypoglycemia could be related to some alterations in counter-insular mechanisms, generally included among neurovegetative modifications in S.M. patients and probably due to orthosympathetic function impairment.