Musical experience and dementia. Hypothesis

BACKGROUND AND AIMS: Cognitively stimulating activities appear to protect against the development of dementing illness--playing a musical instrument may be one of these activities. Consistent with this notion, the aim of this study was to explore the hypothesis that dementia might be less common among orchestral musicians. METHODS: A cross-sectional survey of 23 older orchestral musicians who were former members of a single orchestra was carried out. Prior musical background, family history, and health history were obtained. A cognitive screen was administered in person or by telephone. Musicians were also queried regarding their awareness of living former orchestral colleagues with dementia. RESULTS: The mean age of participants was 76.9 +/- 6.8 (SD). No participant was aware of a living former or current orchestral member with either reported or suspected dementia. CONCLUSIONS: The results are consistent with the hypothesis that dementing illness may be less among orchestral musicians--possibly from a lifetime engaged in a cognitively stimulating endeavor.     

Antibody-mediated interference with annexins in the antiphospholipid syndrome

Targeting of the annexin A5 anticoagulant shield may be a significant mechanism for thrombosis and pregnancy losses in APS. This may occur via high affinity antibodies that recognize phospholipid-binding proteins that are capable of interfering with the assembly of the annexin A5 shield on phospholipid surfaces or via direct recognition of annexin A5 by autoantibodies. In addition, antibodies against other members of the annexin family of proteins may also have pathogenic roles in APS. It is anticipated that further research will elucidate the biologic functions of these proteins and their roles in the aPL disease processes.     

Sensory gating deficit in a subtype of chronic schizophrenic patients

The dual click P50 paradigm has been established as a neurophysiological method to detect gating mechanisms. Studies of schizophrenic patients have shown that an insufficient reduction of the P50 amplitude after the second relative to the first stimulus indicates a deficient sensory gating mechanism. The aim of this study was to compare the P50 responses in the dual click paradigm of healthy volunteers to those of patients with different psychotic disorders, especially with regard to psychopathology and nosology according to ICD-10 and DSM-IV and to the classification system of Leonhard. A total of 34 patients and 12 healthy volunteers were investigated electrophysiologically while they performed the P50 dual click experiment. Patients with prominent negative symptoms and without perceptual abnormalities and patients with a hebephrenic subtype of schizophrenia showed less suppression in the dual click P50 paradigm than did healthy controls. Patients with brief/acute and transient psychotic disorders or cycloid psychoses did not differ from healthy volunteers with regard to suppression in the dual click P50 paradigm. No striking influence of gender, age, duration of disease and present medication was found. The findings confirm the lack of sensory gating measured by the dual click P50 paradigms in some but not all patients with schizophrenia. Both subtype of schizophrenia and current form of psychopathology appear to be related to the presence or absence of abnormal sensory gating.     

Irradiation attenuates neurogenesis and exacerbates ischemia-induced deficits

Increased neurogenesis after cerebral ischemia suggests that functional recovery after stroke may be attributed, in part, to neural regeneration. In this study, we investigated the role of neurogenesis in the behavioral performance of gerbils after cerebral global ischemia. We used ionizing radiation to decrease neural regeneration, and 2 weeks later cerebral global ischemia was induced by bilateral common carotid artery occlusion. One month after the occlusion, the animals were behaviorally tested. Irradiation alone reduced neurogenesis but did not change vascular or dendritic morphology at the time of behavioral testing. Neither did irradiation, ischemia, or combined treatment impair rotor-rod performance or alter open-field activity. Gerbils subjected to both irradiation and ischemia demonstrated impaired performance in the water-maze task, compared with those that received only ischemia, radiation, or no treatment. These impairments after cerebral global ischemia under conditions of reduced neurogenesis support a role for the production of new cells in mediating functional recovery.     

Systemic lupus erythematosus presenting as amyotrophic lateral sclerosis

We report a case of a 27-year-old Omani lady having a 3-year history of progressive skeletal muscle weakness with clinical and skeletal muscle changes of ALS, who during the course of investigations for ALS was found to have SLE. This association is not a simple coincidence but perhaps a causal relationship, opening vistas to explain the autoimmune pathogenesis and justification for immunosuppressive therapy in ALS. SLE presenting as ALS has not been reported earlier.     

Apathy and depression in cross-cultural survivors of traumatic brain injury

The disturbance of motivation and its relationship to depression continues to spark contradictory findings among European and North American populations. Could a cross-cultural study shed some light on the situation? This study aims to detect the prevalence of apathy and to test whether the Apathy Evaluation Scale (AES) can spot the presence or absence of depression in survivors of traumatic brain injury (TBI) in Oman. Eighty subjects who sustained a TBI were given an Arabic version of the AES and were also interviewed with the semistructured Composite International Diagnostic Interview (CIDI). The authors found that the incidence of apathy and depression among Omani people who sustained TBI is similar to that reported elsewhere. The AES has poor discriminatory power in identifying cases of depression. These findings emphasize the importance of developing assessment tools that are culturally sensitive in light of the rising incidence of TBI in developing countries such as Oman.     

The heterogeneity of schizophrenia in disease states

PREVIOUS PRESENTATION: Some of the contents of this paper have been previously presented at the 16th Annual Meeting of the International Society for Technology Assessment in Health Care June 20, 2000 in the Hague, Netherlands and at the 21st Annual Meeting of the Society for Medical Decision Making as a poster on October 3, 1999 in Reno, NV. BACKGROUND: Studies of schizophrenia treatment often oversimplify the array of health outcomes among patients. Our objective was to derive a set of disease states for schizophrenia using the Positive and Negative Symptom Assessment Scale (PANSS) that captured the heterogeneity of symptom responses. METHODS: Using data from a 1-year clinical trial that collected PANSS scores and costs on schizophrenic patients (N=663), we conducted a k-means cluster analyses on PANSS scores for items in five factor domains. Results of the cluster analysis were compared with a conceptual framework of disease states developed by an expert panel. Final disease states were defined by combining our conceptual framework with the empirical results. We tested its utility by examining the influence of disease state on treatment costs and prognosis. RESULTS: Analyses led to an eight-state framework with varying levels of positive, negative, and cognitive impairment. The extent of hostile/aggressive symptoms and mood disorders correlated with severity of disease states. Direct treatment costs for schizophrenia vary significantly across disease states (F=27.47, df=7, p<0.0001), and disease state at baseline was among the most important predictors of treatment outcomes. CONCLUSION: The disease states we describe offer a useful paradigm for understanding the links between symptom profiles and outcomes.     

Cerebral vasospasm

The cellular mechanisms responsible for cerebral vasospasm (CVS) occurring after subarachnoid hemorrhage (SAH) have been of major interest over the past 50 years. The present review describes how each of the discrete anatomic components that comprise the cerebral artery may contribute to the pathology of CVS. The blood extravasated after SAH is hemolyzed and undergoes degradation with resultant production of free radicals, known to be powerful initiators of vascular damage. An inflammatory response is generated activating both leukocytes and platelets with subsequent release of inflammatory agents. The cerebral artery affected by CVS undergoes phenotypic change involving both the endothelial and smooth muscle cells. In the endothelium the production of nitric oxide and prostacyclin is affected. In the smooth muscle cells signal transduction pathways that enhance the function of the contractile proteins and induce the upregulation of contractile receptors are activated. In parallel, there is evidence that nervous reflex pathways involving the trigeminal ganglion and the hypothalamus are activated. However, the relative contributions of each of the systems are speculative. Therapy may be directed at disrupting the cascade leading from the SAH insult to CVS or at overcoming the dysfunction incurred by CVS; possible therapeutical interventions are considered.