Biomedical subjects
Publications and source records attributed to A Compston.
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.
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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.
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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.
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This report describes heart disease in a 32-year-old man with the syndrome of chronic progressive external ophthalmoplegia (CPEO). The surface electrocardiogram showed first degree AV block and left bundle-branch block and there was HV prolongation on the His bundle electrogram. Endomyocardial biopsy showed the changes of hypertrophy on light microscopy, and on electron microscopy there were increased numbers of mitochondria which appeared structurally normal. A permanent demand pacemaker was inserted because these patients are prone to develop complete heart block.
Inflammation in the brain selectively damages the myelin sheath resulting in a variety of clinical syndromes of which the most common is multiple sclerosis. In these disorders, the areas of inflammation and demyelination can be identified in life by magnetic resonance imaging. Events occurring at the blood-brain barrier depend on T-cell activation, which increases immune surveillance within the central nervous system. T-cells activated against brain antigens persist to establish the conditions needed for inflammatory demyelination and this depends on local release of cytokines, culminating in removal of oligodendrocytes and their myelin lamellae by macrophages or microglia. These interactions involve binding between receptors present on microglia for the Fc portion of antibody and complement components to corresponding ligands on target cells. Taken together, the evidence from clinical and experimental studies provides a rationale for the issue of immunological treatments in patients with multiple sclerosis.
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Diseases of the human brain and spinal cord are common and often progressive since, unlike peripheral nerve, the adult human central nervous system does not spontaneously repair itself. Studies on development and cell lineages in the nervous system have started to elucidate the scientific basis for this lack of regeneration, and have suggested ways of enhancing repair. At the same time, improved understanding of neurodegenerative processes has provided a rationale for treatments which limit neuronal and glial damage. Cell implantation has been tested, experimentally and in man, and with some prospects for successful restoration of normal cell arrangements in the central nervous system. Taken together, a coherent strategy for limiting the damage and repairing the brain is beginning to emerge. The translation of these ideas into clinical practice is timely and eagerly awaited.
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