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Biomedical subjects

A Compston

Publications and source records attributed to A Compston.

At least 73 records · Page 4Linked to original sources
PubMed1992

Epidemiology and genetics of multiple sclerosis.

Epidemiological data suggest an aetiological role for both genetic and environmental factors in multiple sclerosis (MS), but these have yet to be fully characterized. It is probable that MS susceptibility is determined by polygenes but specific loci need to be identified.

Cross-Cultural Comparison↗
PubMed1991

The pathogenesis of demyelinating disease: insights from cell biology.

Cellular and humoral immune mechanisms have been implicated in the pathogenesis of human and experimental demyelinating diseases of the CNS. How these interact in the complex sequence of events that culminates in phagocytosis of myelin by macrophages has yet to be resolved. The relationship between leakage of the blood-brain barrier and demyelination, the reason why recurrent inflammatory demyelination occurs--seemingly in the absence of an antigen-specific immune response--and the lack of effective remyelination all require explanation if a coherent account of immunologically mediated demyelination is to be achieved. One approach to these problems is to study in vitro the developmental and cellular biology of oligodendrocytes--the glial cells responsible for the synthesis and maintenance of CNS myelin. This provides experimental opportunities not offered by more direct investigation of the intact nervous system, but carries the clear disadvantage that observations made in vitro cannot necessarily be extrapolated to humans.

Animals↗
PubMed1990

The effect of methylprednisolone on lymphocyte phenotype and function in patients with multiple sclerosis.

The extent to which symptomatic improvement in patients with multiple sclerosis treated with intravenous methylprednisolone depends on immunological actions of corticosteroids is unknown. In this study the effect of methylprednisolone on circulating T and B cell function has been assessed in vitro and in vivo. Low molar concentrations of methylprednisolone increased pokeweed mitogen-stimulated IgG synthesis by unfractionated lymphocytes in 20 patients with multiple sclerosis and 15 controls. Treatment with methylprednisolone was associated with increased IgG synthesis in a further cohort of 26 affected individuals although dose responsiveness to methylprednisolone was uninfluenced in these patients. Sequential concanavalin A-pokeweed mitogen-induced IgG synthesis by mononuclear cells was also stimulated by methylprednisolone. Phenotypic analysis of paired samples from 12 patients with multiple sclerosis, taken before and after treatment showed no alteration in CD4 or CD8 cells, their suppressor inducer or suppressor subpopulations or activated lymphocytes.

CD4-Positive T-Lymphocytes↗
PubMed1989

Immune mechanisms in the pathogenesis of demyelinating diseases.

The loss of myelin which characterises many human and experimental demyelinating diseases, among them multiple sclerosis, is thought to be immune mediated, but the precise mechanisms responsible remain unknown despite intense research. Normally, myelin in the central nervous system (CNS) is protected from systemic immune responses by the blood brain barrier, which separates nervous tissue from the peripheral circulation. Here we review evidence suggesting that an understanding of the demyelinating disorders may be helped by considering their immune pathogenesis in two stages. The first is damage to the blood brain barrier; this appears to be cell mediated, and allows infiltration into the CNS of other immune effectors. These include complement and also macrophages, which together may mediate the second stage, injury to the myelin/oligodendrocyte complex.

Animals↗
PubMed1988

The 150th anniversary of the first depiction of the lesions of multiple sclerosis.

The clinical and pathological features of multiple sclerosis were fully described, in France and subsequently in England, during the latter half of the XIXth century but clinical descriptions, personal accounts and depictions of the disease had appeared at various times over the previous 50 years. Jean Cruveilhier is usually credited with having first illustrated the lesions of multiple sclerosis in the second tome of his pathological atlas which bears the title date 1835. But the 40 livraisons which make up this work were published separately in parts and documentary evidence contained within the second volume indicates that the putative case of multiple sclerosis cannot have appeared earlier than 1841. Robert Carswell also may have published his pathological atlas in parts but the work was completed by 1838 and so his depiction of the lesions of multiple sclerosis, appearing on plate 4 fig 1, predates Cruveilhier's by at least three years. Curiously, Carswell and Cruveilhier each observed their pathological material in Paris but they cannot have depicted the same individual. 1988 is therefore the 150th anniversary of the depiction of the lesions of multiple sclerosis; the unnamed patient was French, the illustrator a Scotsman.

Brain↗
PubMed1987

Selection of patients for clinical trials.

Since there is no treatment of proven value in patients with MS it is necessary still to select those patients for inclusion in clinical trials who have most to gain and can demonstrate rapidly the effectiveness or not of each new treatment. Experience gained in these trials can be then extrapolated to the disease as a whole.

Clinical Trials as Topic↗
PubMed1986

The modern management of multiple sclerosis.

Many patients with multiple sclerosis and their relatives view the illness as untreatable and inevitably bringing progressive immobility and loss of independence. The optimistic theme of this article is that something can be done for most patients with the disease if disability and expectations are assessed individually.

Combined Modality Therapy↗
PubMed1983

Lymphocyte subpopulations in patients with multiple sclerosis.

Using monoclonal antibodies, peripheral blood helper/inducer (OKT4) and cytotoxic/suppressor (OKT8) lymphocytes were measured in 14 normal controls, 36 patients with multiple sclerosis at different stages of the disease and 15 patients with isolated optic neuritis. Thirty-four of these individuals were studied on two or more occasions at intervals up to 340 days. Patients with multiple sclerosis in relapse had low levels of OKT8 cells (14.07% +/- 3.79) compared with controls (29.42% +/- 4.69) and this abnormality returned to normal within approximately one month of the onset of new symptoms. Further changes occurred with new relapses. Low OKT8 cells were also found in patients with isolated optic neuritis (18.76 +/- 3.71) or progressive multiple sclerosis (19.91% +/- 7.96); the same pattern of recovery was seen in these two groups as in patients with multiple sclerosis in relapse. In 25% patients studied on two or more occasions after an episode of demyelination abnormalities of lymphocyte subpopulations occurred which were not accompanied by new clinical symptoms or signs. Fluctuations of this kind did not occur in controls. The findings have implications for the pathogenesis and management of patients with multiple sclerosis.

Humans↗
PubMed1982

Double-blind controlled trial of immunosuppression in the treatment of multiple sclerosis: final report.

In a double-blind controlled trial 43 patients with relapsing-remitting multiple sclerosis were treated either with anti-lymphocyte globulin, prednisolone, and azathioprine, or with placebo preparations. Treatment began with a combination of the three medicaments but after 1 month was continued for another 14 months with azathioprine (3 mg/kg dialy) only. There was a marginally beneficial effect of immunosuppression on the overall relapse rate and clinical progression. However, there were significant effects on in-vitro lymphocyte function and in the visual evoked potentials in favour of the group receiving suppressive treatment. Placebo-treated patients of the HLA A3 tissue type had significantly more relapses than placebo-treated patients who were not of type HLA A3. Nevertheless, HLA-A3-positive patients treated with immunosuppression had significantly fewer relapses than A3-positive placebo-treated patients.

Adolescent↗