In Florence, a patient showed some symptomatic improvement with minor side effects, but further confirmation in a controlled trial is needed. Cyclosporin A does not cause bone marrow depression, but reports of lymphoma development in patients treated with the drug after transplantation, and in those treated with other immunosuppressive drugs, suggest that immunosuppression should be used cautiously. Another approach is based on the finding that suppressor lymphocyte activity is depressed during acute relapses in multiple sclerosis. This has raised the possibility of enhancing suppressor cell activity therapeutically, which is a promising line of investigation. The nature of the disease process in schizophrenia remains unclear. While the diagnosis is based on psychological symptoms and exclusion of other syndromes, the presence of certain symptoms may not indicate a single pathological process. The belief that schizophrenia is primarily a chemical disorder is supported by the observation that symptoms can be exacerbated by drugs affecting specific transmitters. The psychosis seen in some amphetamine abusers may be indistinguishable from acute paranoid schizophrenia. The psychotic changes in animals are associated with increased dopamine release, and similar changes in humans are likely linked to increased dopaminergic transmission. Neuroleptic drugs reduce both schizophrenia symptoms and amphetamine psychosis by increasing dopamine turnover, which is thought to be secondary to dopamine receptor blockade. However, some controversy exists about the extent to which this mechanism explains their antipsychotic effects. Post-mortem studies have shown increased dopamine receptor numbers in some schizophrenia patients, suggesting a possible maladaptive response. The therapeutic effects of dopamine antagonists are delayed, indicating that receptor blockade may allow other changes to occur. The effects of dopamine receptor blockade are limited to positive symptoms, while negative symptoms are more common in chronic schizophrenia and may not respond as well to treatment. Several lines of evidence suggest that schizophrenia may involve two distinct syndromes. The first, associated with acute symptoms, may involve dopaminergic transmission, while the second, characterized by negative symptoms, may involve different pathological processes. The cause of schizophrenia remains unclear, though genetic and viral factors are considered possible contributors.In Florence, a patient showed some symptomatic improvement with minor side effects, but further confirmation in a controlled trial is needed. Cyclosporin A does not cause bone marrow depression, but reports of lymphoma development in patients treated with the drug after transplantation, and in those treated with other immunosuppressive drugs, suggest that immunosuppression should be used cautiously. Another approach is based on the finding that suppressor lymphocyte activity is depressed during acute relapses in multiple sclerosis. This has raised the possibility of enhancing suppressor cell activity therapeutically, which is a promising line of investigation. The nature of the disease process in schizophrenia remains unclear. While the diagnosis is based on psychological symptoms and exclusion of other syndromes, the presence of certain symptoms may not indicate a single pathological process. The belief that schizophrenia is primarily a chemical disorder is supported by the observation that symptoms can be exacerbated by drugs affecting specific transmitters. The psychosis seen in some amphetamine abusers may be indistinguishable from acute paranoid schizophrenia. The psychotic changes in animals are associated with increased dopamine release, and similar changes in humans are likely linked to increased dopaminergic transmission. Neuroleptic drugs reduce both schizophrenia symptoms and amphetamine psychosis by increasing dopamine turnover, which is thought to be secondary to dopamine receptor blockade. However, some controversy exists about the extent to which this mechanism explains their antipsychotic effects. Post-mortem studies have shown increased dopamine receptor numbers in some schizophrenia patients, suggesting a possible maladaptive response. The therapeutic effects of dopamine antagonists are delayed, indicating that receptor blockade may allow other changes to occur. The effects of dopamine receptor blockade are limited to positive symptoms, while negative symptoms are more common in chronic schizophrenia and may not respond as well to treatment. Several lines of evidence suggest that schizophrenia may involve two distinct syndromes. The first, associated with acute symptoms, may involve dopaminergic transmission, while the second, characterized by negative symptoms, may involve different pathological processes. The cause of schizophrenia remains unclear, though genetic and viral factors are considered possible contributors.