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D A Compston

Publications and source records attributed to D A Compston.

118 records · Page 7Linked to original sources
PubMed1986

Cerebrospinal fluid C9 in demyelinating disease.

We measured CSF and plasma concentrations of C9, IgG, and albumin in 91 patients with demyelination and 73 controls with other neurologic diseases. The C9 index was reduced and IgG index increased in patients with multiple sclerosis and those with isolated demyelinating lesions, irrespective of disease activity; abnormalities were less marked in patients with isolated lesions than in those with MS. Humoral mechanisms may not be responsible for initiating demyelination, but activation of the complement system could amplify tissue damage and account for some symptomatic recovery.

Complement C9↗
PubMed1984

Terminal component of complement (C9) in cerebrospinal fluid of patients with multiple sclerosis.

An immunoradiometric assay was used to measure the concentration of the terminal component of complement (C9) in cerebrospinal fluid (CSF) and plasma from 35 patients with multiple sclerosis and 55 controls with other neurological diseases. There was a highly significant reduction in cerebrospinal fluid C9 concentration in patients with multiple sclerosis (0.26 +/- 0.02 microgram/ml) compared with controls (1.52 +/- 0.20 micrograms/ml; p less than 0.0005). As a single protein measurement C9 seemed to be more useful as an aid to clinical diagnosis than CSF IgG; the C9 index was also a better discriminator than IgG index between the two groups of patients. Reduced CSF C9 concentration in patients with multiple sclerosis implies C9 consumption due to formation of membrane attack complexes, which could mediate myelin damage and cause more widespread but reversible loss of function, accounting for the transient symptoms characteristic of the disease.

Adolescent↗
PubMed1984

Peripheral blood lymphocyte sub-populations and multiple sclerosis.

Serial studies of lymphocyte sub-populations in patients with multiple sclerosis (MS) show periodic reductions in OKT8 cells (%). This alteration is neither immunologically nor disease-specific and also occurs in some apparently healthy normal individuals. In twice-monthly serial studies of lymphocyte sub-populations carried out over a 6-month period, we have found significant reductions in OKT8 cells on at least 2 occasions in 9/9 patients, 7/7 spouses and 3/11 siblings, but rarely in unrelated controls living in the same city. Abnormalities in these unaffected people occurred at the same time as those seen in their affected relative. Cyclical reduction in OKT8 cells is probably one factor associated with susceptibility to MS, perhaps only abnormal in terms of the frequency and duration with which it occurs, and may be related to environmental conditions affecting patients with MS and their close contacts but not most other unaffected individuals.

Antibodies, Monoclonal↗
PubMed1982

Histocompatibility antigens and post-encephalitic Parkinsonism.

Twenty-one patients with Parkinsonism secondary to von Economo's encephalitis were typed for HLA-A, B, C and DR antigens. No differences were found in the phenotype frequencies of these antigens compared with controls. This finding fails to support the hypothesis of genetic susceptibility to post-encephalitic Parkinsonism.

Gene Frequency↗
PubMed1978

Strong association between HLA-DRW2 and antibody-mediated Goodpasture's syndrome.

In a study of HLA types in Caucasian patients with nephritis due to antibodies to glomerular basement membrane, antigen frequencies at A, B, or CW loci were normal. However, 15 out of 17 (88%) patients to whom DRW types were definitely assigned had HLA-DRW2 compared with 32 out of 100 Caucasian blood-donors. This difference is highly significant.

Anti-Glomerular Basement Membrane Disease↗
PubMed1978

Factors influencing the risk of multiple sclerosis developing in patients with optic neuritis.

One-hundred and forty-six patients who had presented with optic neuritis but without evidence of demyelination elsewhere in the nervous system, and in whom no specific cause could be identified, were reassessed clinically between one month and twenty-three years after the onset. Fifty-eight patients (40 per cent) had developed MS. All 146 patients were HLA-typed. Three factors were identified which were significantly associated with the development of MS: positive typing for the HLA antigen BT 101, winter onset of the initial attack of optic neuritis in BT 101-positive patients only, and recurrent attacks of optic neuritis. The application of these results to the individual patient is of limited use. However, recurrent attacks of optic neuritis should be given the same significance in the clinical classification of MS as episodes of demyelination occurring elsewhere in the central nervous system in a patient with a previous attack of optic neuritis. The results suggest that optic neuritis is caused by two different environmental agents or groups of agents and that the agent which is most common in the winter leads to the development of MS in the genetically susceptible individual. The agent more common in the summer is much less likely to cause MS in either suscetible or non-susceptible individuals. The biological role of the HLA system in the handling of foreign antigens is discussed and it is suggested that the presence of the HLA antigens associated with MS confers a specific disadvantage on individuals in the ability to handle infection by the MS causative agent and that this allows damaging immunological processes to develop.

Diagnosis, Differential↗
PubMed1976

B-lymphocyte alloantigens associated with multiple sclerosis.

6 B-lymphocyte alloantigens have been provisionally identified with lymphocytotoxic antisera reacting, after absorption, specifically with B but not T cells. 3 of these antigens appear to form part of an allelic series. The frequency of HLA and B-lymphocyte antigens was then studied in 59 patients with multiple sclerosis (M.S.). 1 of the B-cell antigens, BT 101, was found in 49 out of 59 patients (83%), compared with 10 out of 30 normal individuals (33%), giving a relative risk of 9-8 times to the association. 2 other B-cell alloantigens and HLA-B7 showed lesser but significant positive associations with M.S. Apart from providing possible clues to the pathogenesis of M.S., the association between BT 101 and M.S. may allow screening for susceptible individuals who are thought to be at special risk.

Adolescent↗
PubMedDate not supplied

Immunocytochemical localization of the terminal complement complex in multiple sclerosis.

Granular deposits of C9 and the terminal complement complex, measuring 0.3-1.2 microns, have been demonstrated immunocytochemically in association with capillary endothelial cells, predominantly within plaques and adjacent white matter, in tissue obtained at autopsy from 5/7 patients with multiple sclerosis (MS) and one individual with subacute sclerosing panencephalitis but not from 7/7 controls. This finding suggests that the evolution of focal tissue damage in MS may involve complement activation associated with passage of humoral and cellular mediators of the immune system through the blood-brain barrier.

Adolescent↗