Cop 1 is a random polymer (molecular weight, 14,000 to 23,000) simulating myelin basic protein. It is synthesized by polymerizing L-alanine, L-glutamic acid, L-lysine, and L-tyrosine. It suppresses but does not induce experimental allergic encephalomyelitis, an animal model of multiple sclerosis. It is not toxic in animals. In a double-blind, randomized, placebo-controlled pilot trial, we studied 50 patients with the exacerbating-remitting form of multiple sclerosis, who self-injected either 20 mg of Cop 1 dissolved in 1 ml of saline or saline alone daily for two years. Six of 23 patients in the placebo group (26 percent) and 14 of 25 patients in the Cop 1 group (56 percent) had no exacerbations (P = 0.045). There were 62 exacerbations in the placebo group and 16 in the Cop 1 group, yielding two-year averages of 2.7 and 0.6 per patient, respectively. Among patients who were less disabled on entry (Kurtzke disability score, 0 to 2), there were 2.7 exacerbations in the placebo group and 0.3 in the Cop 1 group over two years. Among patients who were more affected (Kurtzke disability score, 3 to 6), there was an average of 2.7 exacerbations in the placebo group and 1.0 in the Cop 1 group. Over two years, less disabled patients taking Cop 1 improved an average of 0.5 Kurtzke units; those taking placebo worsened an average of 1.2 Kurtzke units. More disabled patients worsened by 0.3 (Cop 1 group) and 0.4 (placebo group) unit. Irritation at injection sites and rare, transient vasomotor responses were observed as side effects. These results suggest that Cop 1 may be beneficial in patients with the exacerbating-remitting form of multiple sclerosis, but we emphasize that the study is a preliminary one and our data require confirmation by a more extensive clinical trial.

The authors used a semistructured interview administered to primary family caregivers to assess the prevalence and nature of psychiatric pathology in 175 well-diagnosed community-residing Alzheimer's disease patients. Symptoms that are indicative of depression in the cognitively intact were virtually ubiquitous in this demented population. A variety of psychotic features were also regularly reported. The implications of these findings for the recognition and treatment of reversible psychiatric impairment are discussed.

This study assessed the impact of attention training on information processing in schizophrenia. Fifty-four inpatients with chronic schizophrenia were randomly assigned to two groups after baseline assessment with the Continuous Performance Test (CPT). Patients in the experimental group participated in individual sessions of computerized attention remediation, while patients in the control group participated in individual sessions during which they viewed video documentaries. After 18 sessions, reassessment with the CPT showed that patients in the experimental group had made significantly more improvement than the control group, which made no significant change. Brief Psychiatric Rating Scale assessments before and after the study phase indicated that both groups improved on the total score but the experimental group made significantly more improvement. These results suggest that it is feasible to use practice and behavioral learning to remediate a core attention deficit in chronic schizophrenia.