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During rehabilitation after brain damage due to stroke or trauma, or after meningitis, patients often suffer from mental fatigue and decreased capacity for concentration and learning. We hypothesize that one pathogenic cause of these symptoms could be a failure on the part of astroglia to remove glutamate and K+ from synaptic regions during glutamatergic transmission. As astroglial support of neuronal glutamate transmission has been shown to be of utmost importance, such an astroglial failing might lead to a decreased signal-to-noise ratio in glutamatergic neurotransmission, especially when the transmission is intense for a considerable time period. Three aspects of astroglial failing are focused upon: decreased capacity of the astroglial glutamate transporters, depolarization of the astroglial network, and uncoupling of the gap junction coupled astroglial network. It has been shown that several neuroactive substances, present within the nervous system even long after damage or infection, influence upon these three astroglial properties.

Multiple sclerosis (MS) is a demyelinating, central nervous system disease, of putative autoimmune pathogenesis. Although no effective pharmacological therapy has been available for this often disabling disease until recently, several studies have now confirmed that subcutaneous or intramuscular administration of beta-interferon may reduce the frequency and severity of relapses in relapsing MS, and may also inhibit disease progression. Studies are under way to determine the possible efficacy of beta-interferon during the progressive phase of the disease. Three beta-interferon formulations are currently available in Sweden. Another drug, glatiramer acetate, also shown to have some effect on the disease course, is expected to be registered for use in Sweden shortly.

Based on continuous advances in our knowledge of the pathophysiological mechanisms involved in the development of multiple sclerosis and other putatively autoimmune diseases, several new immunological treatment strategies are currently being tested in different parts of the world. In principle, these strategies are designed to interfere with three steps in the presumed pathogenic immunological process: inhibition of lymphocyte recruitment to inflammatory foci in the central nervous system; blocking of antigen-specific activation; and interference with immunological effector mechanisms. Preliminary results are available for some of these treatment strategies.